PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 29216949-0 2017 [Effects of N-butylphthalide on the expressions of calpain 1 and CaMK II in hippocampus in rats with acute severe carbon monoxide poisoning]. 3-n-butylphthalide 12-28 calpain 1 Rattus norvegicus 51-60 28990110-9 2017 Furthermore, butylphthalide significantly increased the level of SOD, reduced MDA levels, and reduced TNF-alpha, IL-1beta, and IL-6 levels in the hippocampus when compared with the DM group. 3-n-butylphthalide 13-27 tumor necrosis factor Rattus norvegicus 102-111 28990110-9 2017 Furthermore, butylphthalide significantly increased the level of SOD, reduced MDA levels, and reduced TNF-alpha, IL-1beta, and IL-6 levels in the hippocampus when compared with the DM group. 3-n-butylphthalide 13-27 interleukin 1 beta Rattus norvegicus 113-121 28990110-9 2017 Furthermore, butylphthalide significantly increased the level of SOD, reduced MDA levels, and reduced TNF-alpha, IL-1beta, and IL-6 levels in the hippocampus when compared with the DM group. 3-n-butylphthalide 13-27 interleukin 6 Rattus norvegicus 127-131 28842949-0 2017 Dl-3-n-butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF-kappaB signalling. 3-n-butylphthalide 0-21 toll-like receptor 4 Rattus norvegicus 120-124 28842949-0 2017 Dl-3-n-butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF-kappaB signalling. 3-n-butylphthalide 0-21 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 125-134 29228686-0 2017 Dl-3n-butylphthalide reduces epileptiform activity through GluA2-lacking calcium-permeable AMPARs in epilepsy models. 3-n-butylphthalide 0-20 glutamate ionotropic receptor AMPA type subunit 2 Homo sapiens 59-64 28849056-6 2017 Phosphorylation of JNK and p38 was significantly inhibited following treatment with NBP. 3-n-butylphthalide 84-87 mitogen-activated protein kinase 8 Mus musculus 19-22 28849056-6 2017 Phosphorylation of JNK and p38 was significantly inhibited following treatment with NBP. 3-n-butylphthalide 84-87 mitogen-activated protein kinase 14 Mus musculus 27-30 29228686-0 2017 Dl-3n-butylphthalide reduces epileptiform activity through GluA2-lacking calcium-permeable AMPARs in epilepsy models. 3-n-butylphthalide 0-20 glutamate ionotropic receptor AMPA type subunit 2 Homo sapiens 91-97 29077149-0 2017 Effects of dl-3-n-butylphthalide on serum VEGF and bFGF levels in acute cerebral infarction. 3-n-butylphthalide 11-32 vascular endothelial growth factor A Homo sapiens 42-46 29077149-0 2017 Effects of dl-3-n-butylphthalide on serum VEGF and bFGF levels in acute cerebral infarction. 3-n-butylphthalide 11-32 fibroblast growth factor 2 Homo sapiens 51-55 28214984-0 2017 DL-3-n-Butylphthalide (NBP) Provides Neuroprotection in the Mice Models After Traumatic Brain Injury via Nrf2-ARE Signaling Pathway. 3-n-butylphthalide 0-21 nuclear factor, erythroid derived 2, like 2 Mus musculus 105-109 29077149-1 2017 OBJECTIVE: To observe the curative effect of dl-3-n-Butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on levels of serum vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). 3-n-butylphthalide 45-66 vascular endothelial growth factor A Homo sapiens 157-191 29077149-1 2017 OBJECTIVE: To observe the curative effect of dl-3-n-Butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on levels of serum vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). 3-n-butylphthalide 45-66 vascular endothelial growth factor A Homo sapiens 193-197 29077149-1 2017 OBJECTIVE: To observe the curative effect of dl-3-n-Butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on levels of serum vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). 3-n-butylphthalide 45-66 fibroblast growth factor 2 Homo sapiens 203-233 29077149-1 2017 OBJECTIVE: To observe the curative effect of dl-3-n-Butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on levels of serum vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). 3-n-butylphthalide 45-66 fibroblast growth factor 2 Homo sapiens 235-239 29077149-1 2017 OBJECTIVE: To observe the curative effect of dl-3-n-Butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on levels of serum vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). 3-n-butylphthalide 68-71 vascular endothelial growth factor A Homo sapiens 157-191 29077149-1 2017 OBJECTIVE: To observe the curative effect of dl-3-n-Butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on levels of serum vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). 3-n-butylphthalide 68-71 vascular endothelial growth factor A Homo sapiens 193-197 29077149-1 2017 OBJECTIVE: To observe the curative effect of dl-3-n-Butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on levels of serum vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). 3-n-butylphthalide 68-71 fibroblast growth factor 2 Homo sapiens 203-233 29077149-1 2017 OBJECTIVE: To observe the curative effect of dl-3-n-Butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on levels of serum vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). 3-n-butylphthalide 68-71 fibroblast growth factor 2 Homo sapiens 235-239 28214984-0 2017 DL-3-n-Butylphthalide (NBP) Provides Neuroprotection in the Mice Models After Traumatic Brain Injury via Nrf2-ARE Signaling Pathway. 3-n-butylphthalide 23-26 nuclear factor, erythroid derived 2, like 2 Mus musculus 105-109 26773175-1 2016 This study investigates the impacts of n-butylphthalide (NBP) on the expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGF-beta1) in rats with focal cerebral ischemia. 3-n-butylphthalide 39-55 vascular endothelial growth factor A Rattus norvegicus 83-117 29931921-7 2017 Butylphthalide could prolong asth-matic incubation period (53.3 +-13.2 33.1 +-13.0), improve asthmatic behaviors, reduce NO in serum (78.71 +-19.40 84.75 +-20.97) and ET-1 in bronchoalveolar lavage fluid (24.30 +-5.80 28.50 +-6.31) (P < 0.05, 0.01). 3-n-butylphthalide 0-14 endothelin-1 Cavia porcellus 167-171 29931921-8 2017 CONCLUSIONS: Butylphthalide has some effects of anti-asthma and one of the mechanisms is to relieve abnormal increase of NO and ET-1. 3-n-butylphthalide 13-27 endothelin-1 Cavia porcellus 128-132 27833554-3 2016 In this study, we investigated the effects of N-butylphthalide (NBP) on the expressions of zonula occludens-1 (ZO-1), claudin-5 and aquaporin-4 (AQP-4) proteins in a CO poisoning rat model. 3-n-butylphthalide 46-62 tight junction protein 1 Rattus norvegicus 91-109 27833554-3 2016 In this study, we investigated the effects of N-butylphthalide (NBP) on the expressions of zonula occludens-1 (ZO-1), claudin-5 and aquaporin-4 (AQP-4) proteins in a CO poisoning rat model. 3-n-butylphthalide 46-62 tight junction protein 1 Rattus norvegicus 111-115 27833554-3 2016 In this study, we investigated the effects of N-butylphthalide (NBP) on the expressions of zonula occludens-1 (ZO-1), claudin-5 and aquaporin-4 (AQP-4) proteins in a CO poisoning rat model. 3-n-butylphthalide 46-62 claudin 5 Rattus norvegicus 118-127 27833554-3 2016 In this study, we investigated the effects of N-butylphthalide (NBP) on the expressions of zonula occludens-1 (ZO-1), claudin-5 and aquaporin-4 (AQP-4) proteins in a CO poisoning rat model. 3-n-butylphthalide 46-62 aquaporin 4 Rattus norvegicus 132-143 27468961-0 2016 N-Butylphthalide (NBP) ameliorated cerebral ischemia reperfusion-induced brain injury via HGF-regulated TLR4/NF-kappaB signaling pathway. 3-n-butylphthalide 0-16 hepatocyte growth factor Rattus norvegicus 90-93 27468961-0 2016 N-Butylphthalide (NBP) ameliorated cerebral ischemia reperfusion-induced brain injury via HGF-regulated TLR4/NF-kappaB signaling pathway. 3-n-butylphthalide 0-16 toll-like receptor 4 Rattus norvegicus 104-108 27015680-0 2016 Butylphthalide Suppresses Neuronal Cells Apoptosis and Inhibits JNK-Caspase3 Signaling Pathway After Brain Ischemia /Reperfusion in Rats. 3-n-butylphthalide 0-14 mitogen-activated protein kinase 8 Rattus norvegicus 64-67 27015680-0 2016 Butylphthalide Suppresses Neuronal Cells Apoptosis and Inhibits JNK-Caspase3 Signaling Pathway After Brain Ischemia /Reperfusion in Rats. 3-n-butylphthalide 0-14 caspase 3 Rattus norvegicus 68-76 27015680-2 2016 Therefore, the aim of this study was to investigate the neuroprotective mechanisms of BP against ischemic brain injury induced by cerebral I/R through inhibition of the c-Jun N-terminal kinase (JNK)-Caspase3 signaling pathway. 3-n-butylphthalide 86-88 caspase 3 Rattus norvegicus 169-207 27015680-6 2016 Furthermore, the expression of p-JNK, p-Bcl2, p-c-Jun, FasL, and cleaved-caspase3 was also decreased in the rats treated with BP. 3-n-butylphthalide 126-128 mitogen-activated protein kinase 8 Rattus norvegicus 33-36 27015680-6 2016 Furthermore, the expression of p-JNK, p-Bcl2, p-c-Jun, FasL, and cleaved-caspase3 was also decreased in the rats treated with BP. 3-n-butylphthalide 126-128 Fas ligand Rattus norvegicus 55-59 27015680-6 2016 Furthermore, the expression of p-JNK, p-Bcl2, p-c-Jun, FasL, and cleaved-caspase3 was also decreased in the rats treated with BP. 3-n-butylphthalide 126-128 caspase 3 Rattus norvegicus 73-81 27015680-7 2016 In summary, our results imply that BP could remarkably improve the survival of CA1 pyramidal neurons in I/R-induced brain injury and inhibit the JNK-Caspase3 signaling pathway. 3-n-butylphthalide 35-37 carbonic anhydrase 1 Rattus norvegicus 79-82 27015680-7 2016 In summary, our results imply that BP could remarkably improve the survival of CA1 pyramidal neurons in I/R-induced brain injury and inhibit the JNK-Caspase3 signaling pathway. 3-n-butylphthalide 35-37 mitogen-activated protein kinase 8 Rattus norvegicus 145-148 27015680-7 2016 In summary, our results imply that BP could remarkably improve the survival of CA1 pyramidal neurons in I/R-induced brain injury and inhibit the JNK-Caspase3 signaling pathway. 3-n-butylphthalide 35-37 caspase 3 Rattus norvegicus 149-157 26827641-0 2016 Dl-3-n-butylphthalide-induced upregulation of antioxidant defense is involved in the enhancement of cross talk between CREB and Nrf2 in an Alzheimer"s disease mouse model. 3-n-butylphthalide 0-21 cAMP responsive element binding protein 1 Mus musculus 119-123 26827641-0 2016 Dl-3-n-butylphthalide-induced upregulation of antioxidant defense is involved in the enhancement of cross talk between CREB and Nrf2 in an Alzheimer"s disease mouse model. 3-n-butylphthalide 0-21 nuclear factor, erythroid derived 2, like 2 Mus musculus 128-132 26827641-5 2016 Dl-NBP treatment reduced oxidative stress in the APP/PS1 mouse brain and alleviated learning and memory deficits. 3-n-butylphthalide 0-6 presenilin 1 Mus musculus 53-56 26827641-6 2016 Dl-NBP supplementation meliorated synaptic plasticity, diminished soluble amyloid beta and amyloid beta oligomer in the APP/PS1 mouse brain. 3-n-butylphthalide 0-6 presenilin 1 Mus musculus 124-127 26827641-7 2016 Dl-NBP administration caused an increase of cyclic adenosine monophosphate-response element binding protein (CREB)-binding protein (CBP)-associated Ser133-phosphorylated CREB (p-CREB) protein. 3-n-butylphthalide 0-6 cAMP responsive element binding protein 1 Mus musculus 44-107 26827641-7 2016 Dl-NBP administration caused an increase of cyclic adenosine monophosphate-response element binding protein (CREB)-binding protein (CBP)-associated Ser133-phosphorylated CREB (p-CREB) protein. 3-n-butylphthalide 0-6 CREB binding protein Mus musculus 109-130 26827641-7 2016 Dl-NBP administration caused an increase of cyclic adenosine monophosphate-response element binding protein (CREB)-binding protein (CBP)-associated Ser133-phosphorylated CREB (p-CREB) protein. 3-n-butylphthalide 0-6 CREB binding protein Mus musculus 132-135 26827641-7 2016 Dl-NBP administration caused an increase of cyclic adenosine monophosphate-response element binding protein (CREB)-binding protein (CBP)-associated Ser133-phosphorylated CREB (p-CREB) protein. 3-n-butylphthalide 0-6 cAMP responsive element binding protein 1 Mus musculus 109-113 26827641-7 2016 Dl-NBP administration caused an increase of cyclic adenosine monophosphate-response element binding protein (CREB)-binding protein (CBP)-associated Ser133-phosphorylated CREB (p-CREB) protein. 3-n-butylphthalide 0-6 cAMP responsive element binding protein 1 Mus musculus 170-174 26827641-9 2016 We demonstrate that the Dl-NBP-triggered upregulation of antioxidant defenses is involved in the enhancement of cross talk between CREB and nuclear factor erythroid 2-related factor 2 via CBP. 3-n-butylphthalide 24-30 cAMP responsive element binding protein 1 Mus musculus 131-135 26827641-9 2016 We demonstrate that the Dl-NBP-triggered upregulation of antioxidant defenses is involved in the enhancement of cross talk between CREB and nuclear factor erythroid 2-related factor 2 via CBP. 3-n-butylphthalide 24-30 nuclear factor, erythroid derived 2, like 2 Mus musculus 140-183 26827641-9 2016 We demonstrate that the Dl-NBP-triggered upregulation of antioxidant defenses is involved in the enhancement of cross talk between CREB and nuclear factor erythroid 2-related factor 2 via CBP. 3-n-butylphthalide 24-30 CREB binding protein Mus musculus 188-191 28131710-0 2017 DL-3-n-butylphthalide-Edaravone hybrids as novel dual inhibitors of amyloid-beta aggregation and monoamine oxidases with high antioxidant potency for Alzheimer"s therapy. 3-n-butylphthalide 0-21 amyloid beta precursor protein Homo sapiens 68-80 28131710-2 2017 A series of DL-3-n-butylphthalide-Edaravone hybrids were designed, synthesized and evaluated as novel dual inhibitors of amyloid-beta aggregation and monoamine oxidases. 3-n-butylphthalide 12-33 amyloid beta precursor protein Homo sapiens 121-133 27833554-3 2016 In this study, we investigated the effects of N-butylphthalide (NBP) on the expressions of zonula occludens-1 (ZO-1), claudin-5 and aquaporin-4 (AQP-4) proteins in a CO poisoning rat model. 3-n-butylphthalide 46-62 aquaporin 4 Rattus norvegicus 145-150 29926617-3 2016 RESULTS: Butylphthalide significantly improved pulmonary function, lowered asthmatic behavior score, inhibited the activity of ECE-1, and reduced ET-1 gene expression level in lung tissue. 3-n-butylphthalide 9-23 endothelin-converting enzyme 1 Cavia porcellus 127-132 29926617-3 2016 RESULTS: Butylphthalide significantly improved pulmonary function, lowered asthmatic behavior score, inhibited the activity of ECE-1, and reduced ET-1 gene expression level in lung tissue. 3-n-butylphthalide 9-23 endothelin-1 Cavia porcellus 146-150 29926617-4 2016 CONCLUSIONS: Butylphthalide has an anti-asthma effect and the mechanisms involve inhibition of ECE-1 activity and lowering of ET-1geng expression. 3-n-butylphthalide 13-27 endothelin-converting enzyme 1 Cavia porcellus 95-100 26773175-1 2016 This study investigates the impacts of n-butylphthalide (NBP) on the expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGF-beta1) in rats with focal cerebral ischemia. 3-n-butylphthalide 39-55 vascular endothelial growth factor A Rattus norvegicus 119-123 26773175-1 2016 This study investigates the impacts of n-butylphthalide (NBP) on the expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGF-beta1) in rats with focal cerebral ischemia. 3-n-butylphthalide 39-55 transforming growth factor, beta 1 Rattus norvegicus 129-161 26773175-1 2016 This study investigates the impacts of n-butylphthalide (NBP) on the expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGF-beta1) in rats with focal cerebral ischemia. 3-n-butylphthalide 39-55 transforming growth factor, beta 1 Rattus norvegicus 163-172 25722681-0 2012 Hypoxia inducible factor-1alpha mediates protection of DL-3-n-butylphthalide in brain microvascular endothelial cells against oxygen glucose deprivation-induced injury. 3-n-butylphthalide 55-76 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-31 26056974-0 2015 Effects of N-butylphthalide on the activation of Keap1/Nrf-2 signal pathway in rats after carbon monoxide poisoning. 3-n-butylphthalide 11-27 Kelch-like ECH-associated protein 1 Rattus norvegicus 49-54 26056974-0 2015 Effects of N-butylphthalide on the activation of Keap1/Nrf-2 signal pathway in rats after carbon monoxide poisoning. 3-n-butylphthalide 11-27 NFE2 like bZIP transcription factor 2 Rattus norvegicus 55-60 26056974-10 2015 The expressions of Keap1, Nrf-2 and NQO-1 proteins significantly increased at 1, 3 and 7 day after NBP administration as compared with the CO poisoning group (P<0.01). 3-n-butylphthalide 99-102 Kelch-like ECH-associated protein 1 Rattus norvegicus 19-24 26056974-10 2015 The expressions of Keap1, Nrf-2 and NQO-1 proteins significantly increased at 1, 3 and 7 day after NBP administration as compared with the CO poisoning group (P<0.01). 3-n-butylphthalide 99-102 NFE2 like bZIP transcription factor 2 Rattus norvegicus 26-31 26056974-10 2015 The expressions of Keap1, Nrf-2 and NQO-1 proteins significantly increased at 1, 3 and 7 day after NBP administration as compared with the CO poisoning group (P<0.01). 3-n-butylphthalide 99-102 NAD(P)H quinone dehydrogenase 1 Rattus norvegicus 36-41 26056974-11 2015 These findings suggest that N-butylphthalide may protect mitochondrial function, balance the expressions of anti-apoptosis genes and pro-apoptosis genes, be in part associated with activation of Keap1-Nrf-2/antioxidant response element (ARE) signaling pathway, and play a neuroprotective role in brain damage after acute CO poisoning. 3-n-butylphthalide 28-44 Kelch-like ECH-associated protein 1 Rattus norvegicus 195-200 26056974-11 2015 These findings suggest that N-butylphthalide may protect mitochondrial function, balance the expressions of anti-apoptosis genes and pro-apoptosis genes, be in part associated with activation of Keap1-Nrf-2/antioxidant response element (ARE) signaling pathway, and play a neuroprotective role in brain damage after acute CO poisoning. 3-n-butylphthalide 28-44 NFE2 like bZIP transcription factor 2 Rattus norvegicus 201-206 26234133-2 2015 Butylphthalide was incubated with selective inhibitors of CYP450, and its metabolic rate was determined to identify the metabolizing isoenzymes of NBP in rat (normal and induced rats) and human liver microsomes. 3-n-butylphthalide 0-14 NUBP iron-sulfur cluster assembly factor 1, cytosolic Homo sapiens 147-150 26234133-3 2015 The in vitro inhibition effect of butylphthalide on 6 main liver microsomal CYP450 isoenzymes was evaluated by using probe drugs; the induction and inhibition activities in vivo of butylphthalide on CYP450 isoenzymes were evaluated by NBP ig dosing (160 mg x kg(-1)) and iv dosing (20 mg x kg(-1)) in rats. 3-n-butylphthalide 34-48 NUBP iron-sulfur cluster assembly factor 1, cytosolic Homo sapiens 235-238 26234133-3 2015 The in vitro inhibition effect of butylphthalide on 6 main liver microsomal CYP450 isoenzymes was evaluated by using probe drugs; the induction and inhibition activities in vivo of butylphthalide on CYP450 isoenzymes were evaluated by NBP ig dosing (160 mg x kg(-1)) and iv dosing (20 mg x kg(-1)) in rats. 3-n-butylphthalide 181-195 NUBP iron-sulfur cluster assembly factor 1, cytosolic Homo sapiens 235-238 25812770-0 2015 Effects of N-Butylphthalide on the expressions of Nogo/NgR in rat brain tissue after carbon monoxide poisoning. 3-n-butylphthalide 11-27 reticulon 4 Rattus norvegicus 50-54 25812770-0 2015 Effects of N-Butylphthalide on the expressions of Nogo/NgR in rat brain tissue after carbon monoxide poisoning. 3-n-butylphthalide 11-27 reticulon 4 receptor Rattus norvegicus 55-58 26248419-0 2015 [Effect of 3-n-butylphthalide pretreatment on expression of the HSP70 after brain ischemia/reperfusion]. 3-n-butylphthalide 11-29 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 64-69 26248419-1 2015 OBJECTIVE: To explore the effect of 3-n-butylphthalide pretreatment on the delayed neuronal death(DND) and the expreesion of heat shock protein70 (HSP70) in rat hippocampus after ischemia/ reperfusion. 3-n-butylphthalide 36-54 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 147-152 26248419-8 2015 CONCLUSION: 3-n-butylphthalide (NBP) prevents the neurons from ischemia/reperfusion injury through upregulating the expression of HSP70. 3-n-butylphthalide 12-30 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 130-135 26248419-8 2015 CONCLUSION: 3-n-butylphthalide (NBP) prevents the neurons from ischemia/reperfusion injury through upregulating the expression of HSP70. 3-n-butylphthalide 32-35 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 130-135 25734213-0 2015 DL-3-n-butylphthalide inhibits platelet activation via inhibition of cPLA2-mediated TXA2 synthesis and phosphodiesterase. 3-n-butylphthalide 0-21 phospholipase A2 group IVA Homo sapiens 69-74 24468743-0 2014 Bioactivation of 3-n-butylphthalide via sulfation of its major metabolite 3-hydroxy-NBP: mediated mainly by sulfotransferase 1A1. 3-n-butylphthalide 17-35 sulfotransferase family 1A member 1 Homo sapiens 108-128 22507239-0 2012 DL-3-n-Butylphthalide protects rat bone marrow stem cells against hydrogen peroxide-induced cell death through antioxidation and activation of PI3K-Akt pathway. 3-n-butylphthalide 0-21 AKT serine/threonine kinase 1 Rattus norvegicus 148-151 22800896-18 2012 Furthermore, we found that treating SOD1-G93A mice with DL-NBP (60 mgxkg(-1)xd(-1)) slowed the rate of MUNE reduction (P < 0.01). 3-n-butylphthalide 56-62 superoxide dismutase 1, soluble Mus musculus 36-40 22800896-20 2012 Treating mice with DL-NBP (60 mgxkg(-1)xd(-1)) significantly reduced CD11b immunoreactivity compared with vehicle control mice (P < 0.05). 3-n-butylphthalide 19-25 integrin alpha M Mus musculus 69-74 22800896-22 2012 CONCLUSIONS: The post-disease-onset administration of DL-NBP significantly prolonged survival and improved motor performance in SOD1-G93A mice. 3-n-butylphthalide 54-60 superoxide dismutase 1, soluble Mus musculus 128-132 22286127-0 2012 dl-3n-Butylphthalide promotes angiogenesis via the extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase/Akt-endothelial nitric oxide synthase signaling pathways. 3-n-butylphthalide 0-20 mitogen-activated protein kinase 1 Homo sapiens 51-92 22286127-0 2012 dl-3n-Butylphthalide promotes angiogenesis via the extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase/Akt-endothelial nitric oxide synthase signaling pathways. 3-n-butylphthalide 0-20 AKT serine/threonine kinase 1 Homo sapiens 127-130 22286127-0 2012 dl-3n-Butylphthalide promotes angiogenesis via the extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase/Akt-endothelial nitric oxide synthase signaling pathways. 3-n-butylphthalide 0-20 nitric oxide synthase 3 Homo sapiens 131-164 22286127-1 2012 We have previously demonstrated that dl-3n-butylphthalide (NBP) has a potential angiogenic activity. 3-n-butylphthalide 37-57 NUBP iron-sulfur cluster assembly factor 1, cytosolic Homo sapiens 59-62 24442989-0 2014 The effect of butylphthalide on the brain edema, blood-brain barrier of rats after focal cerebral infarction and the expression of Rho A. 3-n-butylphthalide 14-28 ras homolog family member A Rattus norvegicus 131-136 24442989-1 2014 The aim of this study was to explore the effect of butylphthalide on the brain edema, blood-brain barrier of rats of rats after focal cerebral infarction and the expression of Rho A. 3-n-butylphthalide 51-65 ras homolog family member A Rattus norvegicus 176-181 24442989-8 2014 The butylphthalide could reduce the brain edema, protect the blood-brain barrier, and decrease the expression of Rho A around the infarction. 3-n-butylphthalide 4-18 ras homolog family member A Rattus norvegicus 113-118 25206879-5 2014 3-N-butylphthalide administration improved the neuronal morphology in the cerebral cortex and hippocampus of rats with chronic cerebral ischemia, increased choline acetyltransferase activity, and decreased malondialdehyde and amyloid beta levels, and greatly improved cognitive function. 3-n-butylphthalide 0-18 choline O-acetyltransferase Rattus norvegicus 156-181 25722681-1 2012 Studies have demonstrated that DL-3-n-butylphthalide can significantly alleviate oxygen glucose deprivation-induced injury of human umbilical vein endothelial cells at least partly associated with its enhancement on oxygen glucose deprivation -induced hypoxia inducible factor-1alpha expression. 3-n-butylphthalide 31-52 hypoxia inducible factor 1 subunit alpha Homo sapiens 252-283 25722681-2 2012 In this study, we hypothesized that DL-3-n-butylphthalide can protect against oxygen glucose deprivation-induced injury of newborn rat brain microvascular endothelial cells by means of upregulating hypoxia inducible factor-1alpha expression. 3-n-butylphthalide 36-57 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 198-229 25722681-5 2012 Real-time RT-PCR reaction results showed that DL-3-n-butylphthalide reduced apoptosis by inhibiting downregulation of pro-apoptotic gene caspase-3 mRNA expression and upregulation of apoptosis-executive protease bcl-2 mRNA expression; however, DL-3-n-butylphthalide had no protective effects on brain microvascular endothelial cells after knockdown of hypoxia inducible factor-1alpha by small interfering RNA. 3-n-butylphthalide 46-67 caspase 3 Homo sapiens 137-146 25722681-5 2012 Real-time RT-PCR reaction results showed that DL-3-n-butylphthalide reduced apoptosis by inhibiting downregulation of pro-apoptotic gene caspase-3 mRNA expression and upregulation of apoptosis-executive protease bcl-2 mRNA expression; however, DL-3-n-butylphthalide had no protective effects on brain microvascular endothelial cells after knockdown of hypoxia inducible factor-1alpha by small interfering RNA. 3-n-butylphthalide 46-67 BCL2 apoptosis regulator Homo sapiens 212-217 25722681-5 2012 Real-time RT-PCR reaction results showed that DL-3-n-butylphthalide reduced apoptosis by inhibiting downregulation of pro-apoptotic gene caspase-3 mRNA expression and upregulation of apoptosis-executive protease bcl-2 mRNA expression; however, DL-3-n-butylphthalide had no protective effects on brain microvascular endothelial cells after knockdown of hypoxia inducible factor-1alpha by small interfering RNA. 3-n-butylphthalide 46-67 hypoxia inducible factor 1 subunit alpha Homo sapiens 352-383 25722681-6 2012 These findings suggest that DL-3-n-butylphthalide can protect brain microvascular endothelial cells against oxygen glucose deprivation-induced injury by upregulating bcl-2 expression and downregulating caspase-3 expression though hypoxia inducible factor-1alpha pathway. 3-n-butylphthalide 28-49 BCL2 apoptosis regulator Homo sapiens 166-171 25722681-6 2012 These findings suggest that DL-3-n-butylphthalide can protect brain microvascular endothelial cells against oxygen glucose deprivation-induced injury by upregulating bcl-2 expression and downregulating caspase-3 expression though hypoxia inducible factor-1alpha pathway. 3-n-butylphthalide 28-49 caspase 3 Homo sapiens 202-211 25722681-6 2012 These findings suggest that DL-3-n-butylphthalide can protect brain microvascular endothelial cells against oxygen glucose deprivation-induced injury by upregulating bcl-2 expression and downregulating caspase-3 expression though hypoxia inducible factor-1alpha pathway. 3-n-butylphthalide 28-49 hypoxia inducible factor 1 subunit alpha Homo sapiens 230-261 22906269-0 2012 The therapeutic effect of (DL)-3-n-butylphthalide in rats with chronic cerebral hypoperfusion through downregulation of amyloid precursor protein and matrix metalloproteinase-2. 3-n-butylphthalide 26-49 matrix metallopeptidase 2 Rattus norvegicus 150-176 22906269-6 2012 Western blot analysis indicated that, in comparison with the sham-operated control group, protein levels of Abeta40 and MMP-2 were significantly increased in the cerebral cortex of hypoperfused rats, and treatment with DL-NBP prevented this hypoperfusion-induced increase in Abeta40 and MMP-2. 3-n-butylphthalide 220-226 matrix metallopeptidase 2 Rattus norvegicus 120-125 22906269-6 2012 Western blot analysis indicated that, in comparison with the sham-operated control group, protein levels of Abeta40 and MMP-2 were significantly increased in the cerebral cortex of hypoperfused rats, and treatment with DL-NBP prevented this hypoperfusion-induced increase in Abeta40 and MMP-2. 3-n-butylphthalide 220-226 matrix metallopeptidase 2 Rattus norvegicus 288-293 21706121-2 2011 Compound 7e inhibited the adenosine diphosphate (ADP), thrombin (TH) and arachidonic acid (AA)-induced in vitro platelet aggregation, superior to NBP and aspirin, released moderate levels of NO, and improved aqueous solubility relative to NBP. 3-n-butylphthalide 239-242 coagulation factor II Rattus norvegicus 55-63 22493886-0 2012 [Effect of butylphthalide on levels of glutamate and expression of NR2B in the hippocampus of rats with alcohol addiction]. 3-n-butylphthalide 11-25 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 67-71 20800583-0 2010 DL-3-n-butylphthalide prevents neuronal cell death after focal cerebral ischemia in mice via the JNK pathway. 3-n-butylphthalide 0-21 mitogen-activated protein kinase 8 Mus musculus 97-100 20197608-0 2010 [Effect of butylphthalide on the expression of GFAP and VEGF in the hippocampus of rats with Alzheimer"s disease]. 3-n-butylphthalide 11-25 glial fibrillary acidic protein Rattus norvegicus 47-51 20855262-0 2010 [Butylphthalide improves learning and memory abilities of rats with Alzheimer"s disease possibly by enhancing protein disulfide isomerase and inhibiting P53 expressions]. 3-n-butylphthalide 1-15 prolyl 4-hydroxylase subunit beta Rattus norvegicus 110-137 20855262-0 2010 [Butylphthalide improves learning and memory abilities of rats with Alzheimer"s disease possibly by enhancing protein disulfide isomerase and inhibiting P53 expressions]. 3-n-butylphthalide 1-15 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 153-156 20855262-1 2010 OBJECTIVE: To determine the effect of butylphthalide on the expressions of protein disulfide isomerase (PDI) and P53 in the brain tissue of rats with Alzheimer"s disease (AD). 3-n-butylphthalide 38-52 prolyl 4-hydroxylase subunit beta Rattus norvegicus 75-102 20855262-1 2010 OBJECTIVE: To determine the effect of butylphthalide on the expressions of protein disulfide isomerase (PDI) and P53 in the brain tissue of rats with Alzheimer"s disease (AD). 3-n-butylphthalide 38-52 prolyl 4-hydroxylase subunit beta Rattus norvegicus 104-107 20855262-1 2010 OBJECTIVE: To determine the effect of butylphthalide on the expressions of protein disulfide isomerase (PDI) and P53 in the brain tissue of rats with Alzheimer"s disease (AD). 3-n-butylphthalide 38-52 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 113-116 20855262-6 2010 In comparison with the model group, the rats in the butylphthalide group showed significantly increased PDI-positive cells in the hippocampus and decreased expression of P53 in the cortex (P < 0.01). 3-n-butylphthalide 52-66 prolyl 4-hydroxylase subunit beta Rattus norvegicus 104-107 20855262-6 2010 In comparison with the model group, the rats in the butylphthalide group showed significantly increased PDI-positive cells in the hippocampus and decreased expression of P53 in the cortex (P < 0.01). 3-n-butylphthalide 52-66 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 170-173 20855262-7 2010 CONCLUSION: Butylphthalide improves the learning and memory abilities of rats with experimental AD, the mechanism of which may involve inhibition of P53 expression and enhancement of PDI expression in the brain tissues. 3-n-butylphthalide 12-26 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 149-152 20855262-7 2010 CONCLUSION: Butylphthalide improves the learning and memory abilities of rats with experimental AD, the mechanism of which may involve inhibition of P53 expression and enhancement of PDI expression in the brain tissues. 3-n-butylphthalide 12-26 prolyl 4-hydroxylase subunit beta Rattus norvegicus 183-186 20483006-0 2010 3-n-Butylphthalide (NBP) reduces apoptosis and enhances vascular endothelial growth factor (VEGF) up-regulation in diabetic rats. 3-n-butylphthalide 0-18 vascular endothelial growth factor A Rattus norvegicus 56-90 20483006-0 2010 3-n-Butylphthalide (NBP) reduces apoptosis and enhances vascular endothelial growth factor (VEGF) up-regulation in diabetic rats. 3-n-butylphthalide 0-18 vascular endothelial growth factor A Rattus norvegicus 92-96 20197608-0 2010 [Effect of butylphthalide on the expression of GFAP and VEGF in the hippocampus of rats with Alzheimer"s disease]. 3-n-butylphthalide 11-25 vascular endothelial growth factor A Rattus norvegicus 56-60 20197608-6 2010 The positive cells of GFAP in the hippocampus of the butylphthalide group decreased and the expression of VEGF increased significantly, compared with the model group(P<0.05). 3-n-butylphthalide 53-67 glial fibrillary acidic protein Rattus norvegicus 22-26 20197608-7 2010 CONCLUSION: Butylphthalide may protect the neuron-vascular unit of the hippocampus of Alzheimer model rats by inhibiting the expression of GFAP and increasing the expression of VEGF. 3-n-butylphthalide 12-26 glial fibrillary acidic protein Rattus norvegicus 139-143 20197608-7 2010 CONCLUSION: Butylphthalide may protect the neuron-vascular unit of the hippocampus of Alzheimer model rats by inhibiting the expression of GFAP and increasing the expression of VEGF. 3-n-butylphthalide 12-26 vascular endothelial growth factor A Rattus norvegicus 177-181 17723347-6 2006 Two compounds were found to bind to HSA and human blood serum, their binding degrees were consistent with ferulic acid and 3-butylphthalide, the active compounds in Rhizoma Chuangxiong. 3-n-butylphthalide 123-139 albumin Homo sapiens 36-39 19726301-0 2009 [Butylphthalide improves learning and memory abilities of rats with Alzheimer"s disease possibly by inhibiting P38 mitogen-activated protein kinase and enhancing extra-cellular signal regulated kinase expressions]. 3-n-butylphthalide 1-15 mitogen activated protein kinase 14 Rattus norvegicus 111-147 19726301-1 2009 OBJECTIVE: To determine the effect of butylphthalide on the expressions of p38 mitogen-activated protein kinase and extra-cellular signal regulated kinases (ERKs) in the brain tissue of rats with Alzheimer"s disease (AD). 3-n-butylphthalide 38-52 mitogen activated protein kinase 14 Rattus norvegicus 75-111 19726301-6 2009 In comparison with the model group, the rats in the butylphthalide group showed significantly decreased P38-positive cells in the hippocampus and increased expression of ERK in the cortex (P<0.01). 3-n-butylphthalide 52-66 mitogen activated protein kinase 14 Rattus norvegicus 104-107 19726301-6 2009 In comparison with the model group, the rats in the butylphthalide group showed significantly decreased P38-positive cells in the hippocampus and increased expression of ERK in the cortex (P<0.01). 3-n-butylphthalide 52-66 Eph receptor B1 Rattus norvegicus 170-173 19726301-7 2009 CONCLUSIONS: Butylphthalide improves the learning and memory abilities of rats with experimental AD, the mechanism of which may involve inhibition of P38 expression and enhancement of ERK expression in the brain tissues. 3-n-butylphthalide 13-27 mitogen activated protein kinase 14 Rattus norvegicus 150-153 19726301-7 2009 CONCLUSIONS: Butylphthalide improves the learning and memory abilities of rats with experimental AD, the mechanism of which may involve inhibition of P38 expression and enhancement of ERK expression in the brain tissues. 3-n-butylphthalide 13-27 Eph receptor B1 Rattus norvegicus 184-187 19726345-0 2009 [Effect of butylphthalide on the expression of S100 and glial fibrillary acidic protein in a rat model of Alzheimer disease]. 3-n-butylphthalide 11-25 glial fibrillary acidic protein Rattus norvegicus 47-87 19726345-4 2009 RESULTS: The number of cells positive for S100 and GFAP in the hippocampus in butylphthalide group were significantly higher than that in the control group (P/0.01), but lower than that in the model group (P/0.05). 3-n-butylphthalide 78-92 glial fibrillary acidic protein Rattus norvegicus 51-55 19726345-5 2009 CONCLUSION: The expression of S100 protein and glial fibrillary acidic protein increased significantly in the hippocampal astrocytes of rats with AD, and butylphthalide can inhibit the increase of their expression. 3-n-butylphthalide 154-168 glial fibrillary acidic protein Rattus norvegicus 47-78 19626991-0 2009 [Effects of dl-3n-butylphthalide on the expression of VEGF and bFGF in transient middle cerebral artery occlusion rats]. 3-n-butylphthalide 12-32 vascular endothelial growth factor A Rattus norvegicus 54-58 19626991-0 2009 [Effects of dl-3n-butylphthalide on the expression of VEGF and bFGF in transient middle cerebral artery occlusion rats]. 3-n-butylphthalide 12-32 fibroblast growth factor 2 Rattus norvegicus 63-67 19626991-1 2009 OBJECTIVE: To investigate the effect of dl-3n-butylphthalide (NBP) on the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in protein and mRNA levels in the treatment of cerebral infarction with transient middle cerebral artery occlusion (MCAO) in rats. 3-n-butylphthalide 40-60 vascular endothelial growth factor A Rattus norvegicus 88-122 19626991-1 2009 OBJECTIVE: To investigate the effect of dl-3n-butylphthalide (NBP) on the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in protein and mRNA levels in the treatment of cerebral infarction with transient middle cerebral artery occlusion (MCAO) in rats. 3-n-butylphthalide 40-60 vascular endothelial growth factor A Rattus norvegicus 124-128 19626991-1 2009 OBJECTIVE: To investigate the effect of dl-3n-butylphthalide (NBP) on the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in protein and mRNA levels in the treatment of cerebral infarction with transient middle cerebral artery occlusion (MCAO) in rats. 3-n-butylphthalide 40-60 fibroblast growth factor 2 Rattus norvegicus 134-164 19626991-1 2009 OBJECTIVE: To investigate the effect of dl-3n-butylphthalide (NBP) on the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in protein and mRNA levels in the treatment of cerebral infarction with transient middle cerebral artery occlusion (MCAO) in rats. 3-n-butylphthalide 40-60 fibroblast growth factor 2 Rattus norvegicus 166-170 18390208-0 2008 [Effects of dl-3-n-butylphthalide on expression of VEGF and bFGF in rat brain with permanent focal cerebral ischemia]. 3-n-butylphthalide 12-33 vascular endothelial growth factor A Rattus norvegicus 51-55 18390208-0 2008 [Effects of dl-3-n-butylphthalide on expression of VEGF and bFGF in rat brain with permanent focal cerebral ischemia]. 3-n-butylphthalide 12-33 fibroblast growth factor 2 Rattus norvegicus 60-64 18390208-1 2008 OBJECTIVE: To study the effects of dl-3n-butylphthalide (NBP) on the protein and mRNA expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in rats brain with permanent middle cerebral artery occlusion (MCAO). 3-n-butylphthalide 35-55 vascular endothelial growth factor A Rattus norvegicus 100-134 18390208-1 2008 OBJECTIVE: To study the effects of dl-3n-butylphthalide (NBP) on the protein and mRNA expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in rats brain with permanent middle cerebral artery occlusion (MCAO). 3-n-butylphthalide 35-55 vascular endothelial growth factor A Rattus norvegicus 136-140 18390208-1 2008 OBJECTIVE: To study the effects of dl-3n-butylphthalide (NBP) on the protein and mRNA expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in rats brain with permanent middle cerebral artery occlusion (MCAO). 3-n-butylphthalide 35-55 fibroblast growth factor 2 Rattus norvegicus 146-176 18390208-1 2008 OBJECTIVE: To study the effects of dl-3n-butylphthalide (NBP) on the protein and mRNA expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in rats brain with permanent middle cerebral artery occlusion (MCAO). 3-n-butylphthalide 35-55 fibroblast growth factor 2 Rattus norvegicus 178-182 17593816-0 2007 [The effect of butylphthalide on expression of NGF and BDNF in ischemia stroke tissue of rat cerebrum]. 3-n-butylphthalide 15-29 nerve growth factor Rattus norvegicus 47-50 17593816-0 2007 [The effect of butylphthalide on expression of NGF and BDNF in ischemia stroke tissue of rat cerebrum]. 3-n-butylphthalide 15-29 brain-derived neurotrophic factor Rattus norvegicus 55-59 17593816-12 2007 In butylphthalide group, there was a significant expression up-regulation to BDNF, NGF, BDNF mRNA and NGF mRNA in the peripheral around infarction and cornu ammonis or hippocampus area (P<0. 3-n-butylphthalide 3-17 brain-derived neurotrophic factor Rattus norvegicus 77-81 17593816-12 2007 In butylphthalide group, there was a significant expression up-regulation to BDNF, NGF, BDNF mRNA and NGF mRNA in the peripheral around infarction and cornu ammonis or hippocampus area (P<0. 3-n-butylphthalide 3-17 nerve growth factor Rattus norvegicus 83-86 17593816-12 2007 In butylphthalide group, there was a significant expression up-regulation to BDNF, NGF, BDNF mRNA and NGF mRNA in the peripheral around infarction and cornu ammonis or hippocampus area (P<0. 3-n-butylphthalide 3-17 brain-derived neurotrophic factor Rattus norvegicus 88-92 17593816-12 2007 In butylphthalide group, there was a significant expression up-regulation to BDNF, NGF, BDNF mRNA and NGF mRNA in the peripheral around infarction and cornu ammonis or hippocampus area (P<0. 3-n-butylphthalide 3-17 nerve growth factor Rattus norvegicus 102-105 17593816-16 2007 CONCLUSION: Comparing to control group, butylphthalide can significantly up-regulate the expressions of BDNF and NGF in genetic transcription level, and protect from the ischemia injury. 3-n-butylphthalide 40-54 brain-derived neurotrophic factor Rattus norvegicus 104-108 17593816-16 2007 CONCLUSION: Comparing to control group, butylphthalide can significantly up-regulate the expressions of BDNF and NGF in genetic transcription level, and protect from the ischemia injury. 3-n-butylphthalide 40-54 nerve growth factor Rattus norvegicus 113-116 10374632-1 1998 AIM: To study the effect of dl-3-n-butylphthalide (NBP) on regional cerebral blood flow (rCBF) in forcal cerebral ischemia rats. 3-n-butylphthalide 28-49 CCAAT/enhancer binding protein zeta Rattus norvegicus 89-93 10678142-7 1999 dl-NBP 100 mg.kg-1 increased rCBF in caudate nucleus by 26% at 15 min and by 36% at 180 min respectively after SAH. 3-n-butylphthalide 0-6 CCAAT/enhancer binding protein zeta Rattus norvegicus 29-33 12016907-0 1998 [Effect of dl-3-N-butylphthalide on the expression of hsp70 mRNA and c-fos in transient cerebral ischemic and reperfused rat brain]. 3-n-butylphthalide 11-32 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 54-59 12016907-0 1998 [Effect of dl-3-N-butylphthalide on the expression of hsp70 mRNA and c-fos in transient cerebral ischemic and reperfused rat brain]. 3-n-butylphthalide 11-32 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 69-74 34837757-0 2022 Dl-3-N-Butylphthalide Attenuates Hypoxic Injury of Neural Stem Cells by Increasing Hypoxia-Inducible Factor-1alpha. 3-n-butylphthalide 0-21 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 83-114 8446516-2 1993 Of these compounds p-mentha-2,8-dien-1-ol,3-n-butyl phthalide, and sedanolide exhibited high activities to induce the detoxifying enzyme glutathione S-transferase (GST) in the target tissues of female A/J mice. 3-n-butylphthalide 42-61 hematopoietic prostaglandin D synthase Mus musculus 137-162 8446516-2 1993 Of these compounds p-mentha-2,8-dien-1-ol,3-n-butyl phthalide, and sedanolide exhibited high activities to induce the detoxifying enzyme glutathione S-transferase (GST) in the target tissues of female A/J mice. 3-n-butylphthalide 42-61 hematopoietic prostaglandin D synthase Mus musculus 164-167 8446516-3 1993 3-n-Butyl phthalide and sedanolide (20 mg/dose every two days for a total of 3 doses) increased GST activity 4.5-5.9 and 3.2-5.2 times over the controls in the mouse liver and small intestinal mucosa, respectively. 3-n-butylphthalide 0-19 hematopoietic prostaglandin D synthase Mus musculus 96-99 8446516-9 1993 The data indicating that 3-n-butyl phthalide and sedanolide were both active in tumor inhibition and GST assays suggested a correlation between the inhibitory activity and the GST-inducing ability. 3-n-butylphthalide 25-44 hematopoietic prostaglandin D synthase Mus musculus 101-104 8446516-9 1993 The data indicating that 3-n-butyl phthalide and sedanolide were both active in tumor inhibition and GST assays suggested a correlation between the inhibitory activity and the GST-inducing ability. 3-n-butylphthalide 25-44 hematopoietic prostaglandin D synthase Mus musculus 176-179 33971083-7 2021 Results showed that the inclusion of hydroxypropyl-beta-cyclodextrin with butylphthalide significantly improved the pharmacokinetic behavior of free body HP-beta-CD and NBP in vivo. 3-n-butylphthalide 74-88 ACD, shelterin complex subunit and telomerase recruitment factor Rattus norvegicus 157-164 34837757-12 2022 The HIF-1alpha - VEGF pathway may be implicated in this protective effect of dl-NBP. 3-n-butylphthalide 77-83 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 4-14 34837757-12 2022 The HIF-1alpha - VEGF pathway may be implicated in this protective effect of dl-NBP. 3-n-butylphthalide 77-83 vascular endothelial growth factor A Rattus norvegicus 17-21 34987460-8 2021 The butylphthalide group showed lower MMP-9 (130 +- 59 vs. 188 +- 65, p = 0.001) and higher VEGF (441 +- 121 vs. 378 +- 70, p = 0.034) levels on day 6 compared with the conventional treatment group. 3-n-butylphthalide 4-18 vascular endothelial growth factor A Homo sapiens 92-96 34987460-0 2021 Butylphthalide Combined With Conventional Treatment Attenuates MMP-9 Levels and Increases VEGF Levels in Patients With Stroke: A Prospective Cohort Study. 3-n-butylphthalide 0-14 matrix metallopeptidase 9 Homo sapiens 63-68 34987460-0 2021 Butylphthalide Combined With Conventional Treatment Attenuates MMP-9 Levels and Increases VEGF Levels in Patients With Stroke: A Prospective Cohort Study. 3-n-butylphthalide 0-14 vascular endothelial growth factor A Homo sapiens 90-94 34987460-2 2021 To explore whether butylphthalide combined with conventional treatment can change the levels of MMP-9 and VEGF and the National Institutes of Health Stroke Scale (NIHSS) scores of patients with stroke. 3-n-butylphthalide 19-33 matrix metallopeptidase 9 Homo sapiens 96-101 34987460-2 2021 To explore whether butylphthalide combined with conventional treatment can change the levels of MMP-9 and VEGF and the National Institutes of Health Stroke Scale (NIHSS) scores of patients with stroke. 3-n-butylphthalide 19-33 vascular endothelial growth factor A Homo sapiens 106-110 34987460-8 2021 The butylphthalide group showed lower MMP-9 (130 +- 59 vs. 188 +- 65, p = 0.001) and higher VEGF (441 +- 121 vs. 378 +- 70, p = 0.034) levels on day 6 compared with the conventional treatment group. 3-n-butylphthalide 4-18 matrix metallopeptidase 9 Homo sapiens 38-43 34987460-9 2021 The changes in MMP-9 and VEGF were significant, starting on day 3 in the butylphthalide group but on day 6 in the conventional treatment group. 3-n-butylphthalide 73-87 matrix metallopeptidase 9 Homo sapiens 15-20 34987460-9 2021 The changes in MMP-9 and VEGF were significant, starting on day 3 in the butylphthalide group but on day 6 in the conventional treatment group. 3-n-butylphthalide 73-87 vascular endothelial growth factor A Homo sapiens 25-29 34987460-12 2021 Conclusion: Butylphthalide combined with conventional treatment can decrease MMP-9 levels and increase VEGF levels. 3-n-butylphthalide 12-26 matrix metallopeptidase 9 Homo sapiens 77-82 34987460-12 2021 Conclusion: Butylphthalide combined with conventional treatment can decrease MMP-9 levels and increase VEGF levels. 3-n-butylphthalide 12-26 vascular endothelial growth factor A Homo sapiens 103-107 34571087-0 2021 DL-3-n-butylphthalide suppressed autophagy and promoted angiogenesis in rats with vascular dementia by activating the Shh/Ptch1 signaling pathway. 3-n-butylphthalide 0-21 sonic hedgehog signaling molecule Rattus norvegicus 118-121 34762904-9 2021 Furthermore, we found that CYP3A4 induction by rifampicin augmented NBP-induced cell toxicity and supplementing with GSH or NAC alleviated the oxidative stresses and reactive metabolites caused by 3-OH-NBP. 3-n-butylphthalide 68-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 34762904-10 2021 SIGNIFICANCE: Our work suggests that glutathione depletion, mitochondrial injury and covalent protein modification are the main causes of NBP-induced hepatotoxicity, which may be prevented by exogenous GSH or NAC supplementation and avoiding concomitant use of CYP3A4 inducers. 3-n-butylphthalide 138-141 synuclein alpha Homo sapiens 209-212 34925379-0 2021 Dl-3-n-Butylphthalide Rescues Dopaminergic Neurons in Parkinson"s Disease Models by Inhibiting the NLRP3 Inflammasome and Ameliorating Mitochondrial Impairment. 3-n-butylphthalide 0-21 NLR family, pyrin domain containing 3 Mus musculus 99-104 34591732-0 2021 Combination of tetrandrine and 3-n-butylphthalide protects against cerebral ischemia-reperfusion injury via ATF2/TLR4 pathway. 3-n-butylphthalide 31-49 activating transcription factor 2 Homo sapiens 108-112 34591732-0 2021 Combination of tetrandrine and 3-n-butylphthalide protects against cerebral ischemia-reperfusion injury via ATF2/TLR4 pathway. 3-n-butylphthalide 31-49 toll like receptor 4 Homo sapiens 113-117 34571087-0 2021 DL-3-n-butylphthalide suppressed autophagy and promoted angiogenesis in rats with vascular dementia by activating the Shh/Ptch1 signaling pathway. 3-n-butylphthalide 0-21 patched 1 Rattus norvegicus 122-127 34571087-7 2021 Furthermore, NBP treatment also reduced the expression of autophagy marker proteins B-cell lymphoma-2 interacting protein 1 (Beclin 1) and microtubule-associated protein 1 light chain 3 (LC3), which were further enhanced by Shh silencing. 3-n-butylphthalide 13-16 beclin 1 Rattus norvegicus 125-133 34571087-7 2021 Furthermore, NBP treatment also reduced the expression of autophagy marker proteins B-cell lymphoma-2 interacting protein 1 (Beclin 1) and microtubule-associated protein 1 light chain 3 (LC3), which were further enhanced by Shh silencing. 3-n-butylphthalide 13-16 sonic hedgehog signaling molecule Rattus norvegicus 224-227 34571087-10 2021 Altogether, our results established that NBP treatment suppressed autophagy and improved angiogenesis and neurobehavioral recovery in VD rats partly by activating the Shh/Ptch1 signaling pathway. 3-n-butylphthalide 41-44 sonic hedgehog signaling molecule Rattus norvegicus 167-170 34571087-10 2021 Altogether, our results established that NBP treatment suppressed autophagy and improved angiogenesis and neurobehavioral recovery in VD rats partly by activating the Shh/Ptch1 signaling pathway. 3-n-butylphthalide 41-44 patched 1 Rattus norvegicus 171-176 34658892-15 2021 NBP treatment increased the number of CD31+ microvessels and perfused microvessels after TIA. 3-n-butylphthalide 0-3 platelet/endothelial cell adhesion molecule 1 Mus musculus 38-42 34374900-0 2021 Antidepressant-like Effect of 3-n-Butylphthalide in Rats Exposed to Chronic Unpredictable Mild Stress: Modulation of Brain-Derived Neurotrophic Factor Level and mTOR Activation in Cortex. 3-n-butylphthalide 30-48 mechanistic target of rapamycin kinase Rattus norvegicus 161-165 34374900-11 2021 In conclusion, these findings indicate that NBP treatment attenuated the depression-like behaviors through the modulation of serotonergic system and BDNF-ERK-mTOR signaling in rat. 3-n-butylphthalide 44-47 brain-derived neurotrophic factor Rattus norvegicus 149-153 34374900-11 2021 In conclusion, these findings indicate that NBP treatment attenuated the depression-like behaviors through the modulation of serotonergic system and BDNF-ERK-mTOR signaling in rat. 3-n-butylphthalide 44-47 Eph receptor B1 Rattus norvegicus 154-157 34374900-11 2021 In conclusion, these findings indicate that NBP treatment attenuated the depression-like behaviors through the modulation of serotonergic system and BDNF-ERK-mTOR signaling in rat. 3-n-butylphthalide 44-47 mechanistic target of rapamycin kinase Rattus norvegicus 158-162 34631224-10 2021 Western blotting of peri-infarct tissue detected increased expressions of VEGF, Ang-1 and reduced nNOS level in NBP-treated mice. 3-n-butylphthalide 112-115 vascular endothelial growth factor A Mus musculus 74-78 34631224-10 2021 Western blotting of peri-infarct tissue detected increased expressions of VEGF, Ang-1 and reduced nNOS level in NBP-treated mice. 3-n-butylphthalide 112-115 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 80-85 34631224-10 2021 Western blotting of peri-infarct tissue detected increased expressions of VEGF, Ang-1 and reduced nNOS level in NBP-treated mice. 3-n-butylphthalide 112-115 nitric oxide synthase 1, neuronal Mus musculus 98-102 34795530-0 2021 Dl-3-N-Butylphthalide Presents Anti-Cancer Activity in Lung Cancer by Targeting PD-1/PD-L1 Signaling. 3-n-butylphthalide 0-21 CD274 antigen Mus musculus 85-90 34795530-8 2021 Meanwhile, the levels of Ki-67 and PD-L1 were reduced by the treatment of NBP in the tumor tissues of the mice. 3-n-butylphthalide 74-77 antigen identified by monoclonal antibody Ki 67 Mus musculus 25-30 34795530-8 2021 Meanwhile, the levels of Ki-67 and PD-L1 were reduced by the treatment of NBP in the tumor tissues of the mice. 3-n-butylphthalide 74-77 CD274 antigen Mus musculus 35-40 34795530-9 2021 NBP suppressed IFN-gamma-induced PD-L1 enhancement in lung cancer cells. 3-n-butylphthalide 0-3 interferon gamma Mus musculus 15-24 34795530-9 2021 NBP suppressed IFN-gamma-induced PD-L1 enhancement in lung cancer cells. 3-n-butylphthalide 0-3 CD274 antigen Mus musculus 33-38 34345290-0 2021 DL-3-n-butylphthalide protects H9c2 cardiomyoblasts from ischemia/reperfusion injury by regulating HSP70 expression via PI3K/AKT pathway activation. 3-n-butylphthalide 0-21 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 99-104 34345290-0 2021 DL-3-n-butylphthalide protects H9c2 cardiomyoblasts from ischemia/reperfusion injury by regulating HSP70 expression via PI3K/AKT pathway activation. 3-n-butylphthalide 0-21 AKT serine/threonine kinase 1 Rattus norvegicus 125-128 34086144-7 2021 The protective effect of NBP on BSCB destruction is related to the regulation of MMP-2/9 induced by SCI. 3-n-butylphthalide 25-28 matrix metallopeptidase 2 Mus musculus 81-88 34658345-9 2021 The results of molecular docking showed that myricetone, butylphthalide, 4-hydroxy-3 butylphthalide, (Z)-ligustilide, and ligustalide-E, among others, had strong affinities to 7 cores targets including BDNF, FOS, PTGS2, and MAPK14. 3-n-butylphthalide 57-71 brain derived neurotrophic factor Homo sapiens 202-206 34658345-9 2021 The results of molecular docking showed that myricetone, butylphthalide, 4-hydroxy-3 butylphthalide, (Z)-ligustilide, and ligustalide-E, among others, had strong affinities to 7 cores targets including BDNF, FOS, PTGS2, and MAPK14. 3-n-butylphthalide 57-71 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 208-211 34452888-1 2021 OBJECTIVE: To compare the e!cacy and functional outcomes of dl-3-n-Butylphthalide (NBP) and human urinary kallidinogenase (HUK) on ischemic stroke patients and to determine their effects on serum tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF). 3-n-butylphthalide 60-81 tumor necrosis factor Homo sapiens 196-223 34497508-6 2021 Additionally, the elevated expressions of collagen and alpha-smooth muscle actin (alpha-SMA) in the kidney from db/db mice were found to be significantly suppressed after DL-NBP treatment. 3-n-butylphthalide 171-177 actin alpha 2, smooth muscle, aorta Mus musculus 82-91 34497508-8 2021 Moreover, we found that DL-NBP could not only reduce the endoplasmic reticulum stress (ERS), but also suppress activation of the renin-angiotensin system to inhibit vascular endothelial growth factor (VEGF) level, which subsequently reduces the podocyte apoptosis in kidney of db/db mice. 3-n-butylphthalide 24-30 vascular endothelial growth factor A Mus musculus 165-199 34497508-8 2021 Moreover, we found that DL-NBP could not only reduce the endoplasmic reticulum stress (ERS), but also suppress activation of the renin-angiotensin system to inhibit vascular endothelial growth factor (VEGF) level, which subsequently reduces the podocyte apoptosis in kidney of db/db mice. 3-n-butylphthalide 24-30 vascular endothelial growth factor A Mus musculus 201-205 34540081-0 2021 The effect of butylphthalide injection on the cognitive function and the TLRs/NF-kappaB pathway in hypertensive intracerebral hemorrhage. 3-n-butylphthalide 14-28 nuclear factor kappa B subunit 1 Homo sapiens 78-87 34540081-1 2021 OBJECTIVE: This study explored and analyzed the effects of butylphthalide injection on the cognitive function and on the TLRs/NF-kappaB pathway in hypertensive intracerebral hemorrhage patients. 3-n-butylphthalide 59-73 nuclear factor kappa B subunit 1 Homo sapiens 126-135 34658345-9 2021 The results of molecular docking showed that myricetone, butylphthalide, 4-hydroxy-3 butylphthalide, (Z)-ligustilide, and ligustalide-E, among others, had strong affinities to 7 cores targets including BDNF, FOS, PTGS2, and MAPK14. 3-n-butylphthalide 57-71 prostaglandin-endoperoxide synthase 2 Homo sapiens 213-218 34658345-9 2021 The results of molecular docking showed that myricetone, butylphthalide, 4-hydroxy-3 butylphthalide, (Z)-ligustilide, and ligustalide-E, among others, had strong affinities to 7 cores targets including BDNF, FOS, PTGS2, and MAPK14. 3-n-butylphthalide 57-71 mitogen-activated protein kinase 14 Homo sapiens 224-230 34452888-1 2021 OBJECTIVE: To compare the e!cacy and functional outcomes of dl-3-n-Butylphthalide (NBP) and human urinary kallidinogenase (HUK) on ischemic stroke patients and to determine their effects on serum tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF). 3-n-butylphthalide 60-81 tumor necrosis factor Homo sapiens 225-234 34452888-1 2021 OBJECTIVE: To compare the e!cacy and functional outcomes of dl-3-n-Butylphthalide (NBP) and human urinary kallidinogenase (HUK) on ischemic stroke patients and to determine their effects on serum tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF). 3-n-butylphthalide 60-81 vascular endothelial growth factor A Homo sapiens 240-274 34452888-1 2021 OBJECTIVE: To compare the e!cacy and functional outcomes of dl-3-n-Butylphthalide (NBP) and human urinary kallidinogenase (HUK) on ischemic stroke patients and to determine their effects on serum tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF). 3-n-butylphthalide 60-81 vascular endothelial growth factor A Homo sapiens 276-280 34452888-1 2021 OBJECTIVE: To compare the e!cacy and functional outcomes of dl-3-n-Butylphthalide (NBP) and human urinary kallidinogenase (HUK) on ischemic stroke patients and to determine their effects on serum tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF). 3-n-butylphthalide 83-86 tumor necrosis factor Homo sapiens 196-223 34452888-1 2021 OBJECTIVE: To compare the e!cacy and functional outcomes of dl-3-n-Butylphthalide (NBP) and human urinary kallidinogenase (HUK) on ischemic stroke patients and to determine their effects on serum tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF). 3-n-butylphthalide 83-86 tumor necrosis factor Homo sapiens 225-234 34452888-1 2021 OBJECTIVE: To compare the e!cacy and functional outcomes of dl-3-n-Butylphthalide (NBP) and human urinary kallidinogenase (HUK) on ischemic stroke patients and to determine their effects on serum tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF). 3-n-butylphthalide 83-86 vascular endothelial growth factor A Homo sapiens 240-274 34452888-1 2021 OBJECTIVE: To compare the e!cacy and functional outcomes of dl-3-n-Butylphthalide (NBP) and human urinary kallidinogenase (HUK) on ischemic stroke patients and to determine their effects on serum tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF). 3-n-butylphthalide 83-86 vascular endothelial growth factor A Homo sapiens 276-280 33850537-0 2021 Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway. 3-n-butylphthalide 0-14 mitogen-activated protein kinase 8 Rattus norvegicus 81-84 34168567-0 2021 DL-3-n-Butylphthalide Attenuates Myocardial Hypertrophy by Targeting Gasdermin D and Inhibiting Gasdermin D Mediated Inflammation. 3-n-butylphthalide 0-21 gasdermin D Mus musculus 69-80 34168567-0 2021 DL-3-n-Butylphthalide Attenuates Myocardial Hypertrophy by Targeting Gasdermin D and Inhibiting Gasdermin D Mediated Inflammation. 3-n-butylphthalide 0-21 gasdermin D Mus musculus 96-107 34168567-7 2021 Furthermore, overexpression of GSDMD-N reduced the protective effects of NBP against Ang II-induced changes. 3-n-butylphthalide 73-76 gasdermin D Mus musculus 31-36 34121985-0 2021 Dl-3-n-Butylphthalide Alleviates Behavioral and Cognitive Symptoms Via Modulating Mitochondrial Dynamics in the A53T-alpha-Synuclein Mouse Model of Parkinson"s Disease. 3-n-butylphthalide 0-21 synuclein, alpha Mus musculus 117-132 35615581-0 2022 Dl-3-n-Butylphthalide Improves Neuroinflammation in Mice with Repeated Cerebral Ischemia-Reperfusion Injury through the Nrf2-Mediated Antioxidant Response and TLR4/MyD88/NF-kappaB Signaling Pathway. 3-n-butylphthalide 0-21 nuclear factor, erythroid derived 2, like 2 Mus musculus 120-124 35615581-0 2022 Dl-3-n-Butylphthalide Improves Neuroinflammation in Mice with Repeated Cerebral Ischemia-Reperfusion Injury through the Nrf2-Mediated Antioxidant Response and TLR4/MyD88/NF-kappaB Signaling Pathway. 3-n-butylphthalide 0-21 toll-like receptor 4 Mus musculus 159-163 35615581-0 2022 Dl-3-n-Butylphthalide Improves Neuroinflammation in Mice with Repeated Cerebral Ischemia-Reperfusion Injury through the Nrf2-Mediated Antioxidant Response and TLR4/MyD88/NF-kappaB Signaling Pathway. 3-n-butylphthalide 0-21 myeloid differentiation primary response gene 88 Mus musculus 164-169 35615581-0 2022 Dl-3-n-Butylphthalide Improves Neuroinflammation in Mice with Repeated Cerebral Ischemia-Reperfusion Injury through the Nrf2-Mediated Antioxidant Response and TLR4/MyD88/NF-kappaB Signaling Pathway. 3-n-butylphthalide 0-21 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 170-179 35615581-8 2022 Importantly, the antioxidant, antineuroinflammatory, and neuroprotective effects of NBP above were abolished by Nrf2 knockout. 3-n-butylphthalide 84-87 nuclear factor, erythroid derived 2, like 2 Mus musculus 112-116 35615581-10 2022 Modulation of TLR4/MyD88/NF-kappaB pathway by Nrf2 is involved in the neuroprotective effect of NBP against VD induced by RCIR injury. 3-n-butylphthalide 96-99 toll-like receptor 4 Mus musculus 14-18 35615581-10 2022 Modulation of TLR4/MyD88/NF-kappaB pathway by Nrf2 is involved in the neuroprotective effect of NBP against VD induced by RCIR injury. 3-n-butylphthalide 96-99 myeloid differentiation primary response gene 88 Mus musculus 19-24 35615581-10 2022 Modulation of TLR4/MyD88/NF-kappaB pathway by Nrf2 is involved in the neuroprotective effect of NBP against VD induced by RCIR injury. 3-n-butylphthalide 96-99 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 25-34 35615581-10 2022 Modulation of TLR4/MyD88/NF-kappaB pathway by Nrf2 is involved in the neuroprotective effect of NBP against VD induced by RCIR injury. 3-n-butylphthalide 96-99 nuclear factor, erythroid derived 2, like 2 Mus musculus 46-50 35259495-0 2022 DL-3-n-butylphthalide prevents oxidative stress and atherosclerosis by targeting Keap-1 and inhibiting Keap-1/Nrf-2 interaction. 3-n-butylphthalide 0-21 kelch-like ECH-associated protein 1 Mus musculus 81-87 35259495-0 2022 DL-3-n-butylphthalide prevents oxidative stress and atherosclerosis by targeting Keap-1 and inhibiting Keap-1/Nrf-2 interaction. 3-n-butylphthalide 0-21 kelch-like ECH-associated protein 1 Mus musculus 103-109 35259495-0 2022 DL-3-n-butylphthalide prevents oxidative stress and atherosclerosis by targeting Keap-1 and inhibiting Keap-1/Nrf-2 interaction. 3-n-butylphthalide 0-21 nuclear factor, erythroid derived 2, like 2 Mus musculus 110-115 35350668-0 2022 Dl-3-n-butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal-enriched protein tyrosine phosphatase/ERK/cAMP-response element-binding protein signaling pathway. 3-n-butylphthalide 0-21 amyloid beta (A4) precursor protein Mus musculus 57-82 35350668-0 2022 Dl-3-n-butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal-enriched protein tyrosine phosphatase/ERK/cAMP-response element-binding protein signaling pathway. 3-n-butylphthalide 0-21 presenilin 1 Mus musculus 83-95 35350668-0 2022 Dl-3-n-butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal-enriched protein tyrosine phosphatase/ERK/cAMP-response element-binding protein signaling pathway. 3-n-butylphthalide 0-21 mitogen-activated protein kinase 1 Mus musculus 177-180 35350668-6 2022 The present study further explored the mechanism of NBP therapy in amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic mice, and the involvement of the STEP/ERK/CREB signaling pathway. 3-n-butylphthalide 52-55 presenilin 1 Mus musculus 99-111 35350668-7 2022 The results suggested that NBP treatment effectively ameliorated the spatial learning and memory impairment of the APP/PS1 transgenic mice, which was assessed using a Morris water maze. 3-n-butylphthalide 27-30 presenilin 1 Mus musculus 119-122 35559381-0 2022 Keap1-Nrf2/ARE signal pathway activated by butylphthalide in the treatment of ischemic stroke. 3-n-butylphthalide 43-57 kelch like ECH associated protein 1 Homo sapiens 0-5 35559381-0 2022 Keap1-Nrf2/ARE signal pathway activated by butylphthalide in the treatment of ischemic stroke. 3-n-butylphthalide 43-57 NFE2 like bZIP transcription factor 2 Homo sapiens 6-10 35559381-14 2022 The mechanism may be that butylphthalide improves the CVR of patients, enhances the establishment of collateral compensatory vessels, and changes the expression of the Keap1-Nrf2/ARE signaling pathway, thereby exerting the neuroprotective effect. 3-n-butylphthalide 26-40 kelch like ECH associated protein 1 Homo sapiens 168-173 35559381-14 2022 The mechanism may be that butylphthalide improves the CVR of patients, enhances the establishment of collateral compensatory vessels, and changes the expression of the Keap1-Nrf2/ARE signaling pathway, thereby exerting the neuroprotective effect. 3-n-butylphthalide 26-40 NFE2 like bZIP transcription factor 2 Homo sapiens 174-178 35236646-0 2022 Effects of butylphthalide on the levels of serum C-reactive protein, Parkinson disease protein 7 and neurotrophin-3 and neurological function in patients with acute cerebral infarction. 3-n-butylphthalide 11-25 C-reactive protein Homo sapiens 49-67 35236646-0 2022 Effects of butylphthalide on the levels of serum C-reactive protein, Parkinson disease protein 7 and neurotrophin-3 and neurological function in patients with acute cerebral infarction. 3-n-butylphthalide 11-25 neurotrophin 3 Homo sapiens 101-115 35236646-1 2022 To explore the effects of butylphthalide on the levels of serum CRP, PAPK7, NT-3 and neurological function in patients with acute cerebral infarction (ACI). 3-n-butylphthalide 26-40 C-reactive protein Homo sapiens 64-67 35236646-1 2022 To explore the effects of butylphthalide on the levels of serum CRP, PAPK7, NT-3 and neurological function in patients with acute cerebral infarction (ACI). 3-n-butylphthalide 26-40 3'-nucleotidase Homo sapiens 76-80 6536162-0 1984 [The anticonvulsant action of 3-n-butylphthalide (Ag-1) and 3-n-butyl-4, 5-dihydrophthalide (Ag-2)]. 3-n-butylphthalide 30-48 NBPF member 10 Homo sapiens 50-54 33850537-5 2021 The positive expression of Bax was markedly higher (P<0.05), while that of Bcl-2 was notably lower in the model group and the butylphthalide group (P<0.05), compared with those in the sham-operation group. 3-n-butylphthalide 126-140 BCL2, apoptosis regulator Rattus norvegicus 75-80 33850537-6 2021 Furthermore, the positive expression of Bax was notably decreased (P<0.05), while that of Bcl-2 was markedly increased in the butylphthalide group in comparison with those in model group (P<0.05). 3-n-butylphthalide 126-140 BCL2 associated X, apoptosis regulator Rattus norvegicus 40-43 33850537-6 2021 Furthermore, the positive expression of Bax was notably decreased (P<0.05), while that of Bcl-2 was markedly increased in the butylphthalide group in comparison with those in model group (P<0.05). 3-n-butylphthalide 126-140 BCL2, apoptosis regulator Rattus norvegicus 90-95 33850537-7 2021 The model group and the butylphthalide group had markedly higher relative protein expression levels of p-JNK and p-p38 MAPK than the sham-operation group (P<0.05), and the butylphthalide group displayed notably lower relative protein expression levels of p-JNK and p-p38 MAPK than the model group (P<0.05). 3-n-butylphthalide 24-38 mitogen-activated protein kinase 8 Rattus norvegicus 105-108 33850537-7 2021 The model group and the butylphthalide group had markedly higher relative protein expression levels of p-JNK and p-p38 MAPK than the sham-operation group (P<0.05), and the butylphthalide group displayed notably lower relative protein expression levels of p-JNK and p-p38 MAPK than the model group (P<0.05). 3-n-butylphthalide 24-38 mitogen-activated protein kinase 8 Rattus norvegicus 257-260 33850537-7 2021 The model group and the butylphthalide group had markedly higher relative protein expression levels of p-JNK and p-p38 MAPK than the sham-operation group (P<0.05), and the butylphthalide group displayed notably lower relative protein expression levels of p-JNK and p-p38 MAPK than the model group (P<0.05). 3-n-butylphthalide 172-186 mitogen-activated protein kinase 8 Rattus norvegicus 257-260 33850537-8 2021 The relative mRNA expression level of Bax was markedly increased (P<0.05), while that of Bcl-2 was notably decreased in the model group and the butylphthalide group (P<0.05), compared with those in the sham-operation group. 3-n-butylphthalide 144-158 BCL2 associated X, apoptosis regulator Rattus norvegicus 38-41 33850537-8 2021 The relative mRNA expression level of Bax was markedly increased (P<0.05), while that of Bcl-2 was notably decreased in the model group and the butylphthalide group (P<0.05), compared with those in the sham-operation group. 3-n-butylphthalide 144-158 BCL2, apoptosis regulator Rattus norvegicus 89-94 33850537-9 2021 Compared with those in the model group, the relative mRNA expression level of Bax decreased markedly (P<0.05), and that of Bcl-2 increased notably in the butylphthalide group (P<0.05). 3-n-butylphthalide 154-168 BCL2 associated X, apoptosis regulator Rattus norvegicus 78-81 33850537-9 2021 Compared with those in the model group, the relative mRNA expression level of Bax decreased markedly (P<0.05), and that of Bcl-2 increased notably in the butylphthalide group (P<0.05). 3-n-butylphthalide 154-168 BCL2, apoptosis regulator Rattus norvegicus 123-128 33850537-11 2021 In conclusion, butylphthalide may inhibit nerve cell apoptosis in rats with cerebral infarction to exert a protective effect, which may be associated with the JNK/p38 MAPK signaling pathway. 3-n-butylphthalide 15-29 mitogen-activated protein kinase 8 Rattus norvegicus 159-162 34284541-1 2021 INTRODUCTION: To investigate the neuroprotective effect and mechanism of DL-3-n-butylphthalide (NBP) on the brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) and its downstream signalling pathway after cerebral ischemia/reperfusion injury (CIRI) in rats. 3-n-butylphthalide 73-94 brain-derived neurotrophic factor Rattus norvegicus 108-141 34284541-1 2021 INTRODUCTION: To investigate the neuroprotective effect and mechanism of DL-3-n-butylphthalide (NBP) on the brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) and its downstream signalling pathway after cerebral ischemia/reperfusion injury (CIRI) in rats. 3-n-butylphthalide 73-94 brain-derived neurotrophic factor Rattus norvegicus 143-147 34284541-1 2021 INTRODUCTION: To investigate the neuroprotective effect and mechanism of DL-3-n-butylphthalide (NBP) on the brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) and its downstream signalling pathway after cerebral ischemia/reperfusion injury (CIRI) in rats. 3-n-butylphthalide 73-94 neurotrophic receptor tyrosine kinase 2 Rattus norvegicus 168-172 34284541-1 2021 INTRODUCTION: To investigate the neuroprotective effect and mechanism of DL-3-n-butylphthalide (NBP) on the brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) and its downstream signalling pathway after cerebral ischemia/reperfusion injury (CIRI) in rats. 3-n-butylphthalide 96-99 brain-derived neurotrophic factor Rattus norvegicus 108-141 34284541-1 2021 INTRODUCTION: To investigate the neuroprotective effect and mechanism of DL-3-n-butylphthalide (NBP) on the brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) and its downstream signalling pathway after cerebral ischemia/reperfusion injury (CIRI) in rats. 3-n-butylphthalide 96-99 brain-derived neurotrophic factor Rattus norvegicus 143-147 34284541-1 2021 INTRODUCTION: To investigate the neuroprotective effect and mechanism of DL-3-n-butylphthalide (NBP) on the brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) and its downstream signalling pathway after cerebral ischemia/reperfusion injury (CIRI) in rats. 3-n-butylphthalide 96-99 neurotrophic receptor tyrosine kinase 2 Rattus norvegicus 168-172 35145408-11 2021 The results of this study showed that NBP as monotherapy or combination therapy had better performance in increasing the MoCA (monotherapy: SMDN = 1.05, 95% CI (0.69, 1.42), p < 0.00001; SMDP = 1.06, 95% CI (0.59, 1.52), p < 0.00001. combination: SMDO = 0.81, 95% CI (0.62, 1.01), p < 0.00001; SMDN = 0.90, 95% CI (0.46, 1.33), p < 0.0001; SMDD = 1.04, 95% CI (0.71, 1.38), p < 0.00001), MMSE (monotherapy: MDN = 4.89, 95% CI (4.14, 5.63)), p < 0.00001). 3-n-butylphthalide 38-41 dedicator of cytokinesis 3 Homo sapiens 121-125 33850537-1 2021 The aim of the present study was to investigate the influence of butylphthalide on nerve cell apoptosis in rats with cerebral infarction through the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling pathway. 3-n-butylphthalide 65-79 mitogen-activated protein kinase 8 Rattus norvegicus 149-172 33850537-1 2021 The aim of the present study was to investigate the influence of butylphthalide on nerve cell apoptosis in rats with cerebral infarction through the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling pathway. 3-n-butylphthalide 65-79 mitogen-activated protein kinase 8 Rattus norvegicus 174-177 33850537-1 2021 The aim of the present study was to investigate the influence of butylphthalide on nerve cell apoptosis in rats with cerebral infarction through the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling pathway. 3-n-butylphthalide 65-79 mitogen activated protein kinase 14 Rattus norvegicus 179-215 33850537-5 2021 The positive expression of Bax was markedly higher (P<0.05), while that of Bcl-2 was notably lower in the model group and the butylphthalide group (P<0.05), compared with those in the sham-operation group. 3-n-butylphthalide 126-140 BCL2 associated X, apoptosis regulator Rattus norvegicus 27-30 33888111-15 2021 Both VOC-P188 solid dispersion and VOC-beta-CD inclusion compound could be prospective means for improving oral bioavailability of SA, NBP, NOL, ZL and BP in VOC. 3-n-butylphthalide 135-138 ACD, shelterin complex subunit and telomerase recruitment factor Rattus norvegicus 39-46 33461169-0 2021 Dl-3-n-butylphthalide inhibits neuroinflammation by stimulating foxp3 and Ki-67 in an ischemic stroke model. 3-n-butylphthalide 0-21 forkhead box P3 Rattus norvegicus 64-69 32958696-9 2021 RESULTS: Compared with the vehicle group, NBP treatment significantly increased the VEGF expression in the poststroke brain. 3-n-butylphthalide 42-45 vascular endothelial growth factor A Mus musculus 84-88 33462377-0 2021 DL-3-n-butylphthalide ameliorates diabetes-associated cognitive decline by enhancing PI3K/Akt signaling and suppressing oxidative stress. 3-n-butylphthalide 0-21 thymoma viral proto-oncogene 1 Mus musculus 90-93 33462377-7 2021 Furthermore, DL-NBP administration attenuated diabetes-induced morphological alterations and increased neuronal survival and restored the levels of synaptic protein PSD95, synaptophysin and synapsin-1 as well as dendritic density in the hippocampus, especially at a dose of 60 mg/kg. 3-n-butylphthalide 13-19 discs large MAGUK scaffold protein 4 Mus musculus 165-170 33462377-7 2021 Furthermore, DL-NBP administration attenuated diabetes-induced morphological alterations and increased neuronal survival and restored the levels of synaptic protein PSD95, synaptophysin and synapsin-1 as well as dendritic density in the hippocampus, especially at a dose of 60 mg/kg. 3-n-butylphthalide 13-19 synaptophysin Mus musculus 172-185 33462377-7 2021 Furthermore, DL-NBP administration attenuated diabetes-induced morphological alterations and increased neuronal survival and restored the levels of synaptic protein PSD95, synaptophysin and synapsin-1 as well as dendritic density in the hippocampus, especially at a dose of 60 mg/kg. 3-n-butylphthalide 13-19 synapsin I Mus musculus 190-200 33462377-8 2021 Moreover, we revealed that DL-NBP administration suppressed oxidative stress by upregulating Nrf2/HO-1 signaling, and increased brain-derived neurotrophic factor (BDNF) expression by activating PI3K/Akt/CREB signaling in the hippocampus. 3-n-butylphthalide 27-33 nuclear factor, erythroid derived 2, like 2 Mus musculus 93-97 33462377-8 2021 Moreover, we revealed that DL-NBP administration suppressed oxidative stress by upregulating Nrf2/HO-1 signaling, and increased brain-derived neurotrophic factor (BDNF) expression by activating PI3K/Akt/CREB signaling in the hippocampus. 3-n-butylphthalide 27-33 heme oxygenase 1 Mus musculus 98-102 33462377-8 2021 Moreover, we revealed that DL-NBP administration suppressed oxidative stress by upregulating Nrf2/HO-1 signaling, and increased brain-derived neurotrophic factor (BDNF) expression by activating PI3K/Akt/CREB signaling in the hippocampus. 3-n-butylphthalide 27-33 brain derived neurotrophic factor Mus musculus 128-161 33462377-8 2021 Moreover, we revealed that DL-NBP administration suppressed oxidative stress by upregulating Nrf2/HO-1 signaling, and increased brain-derived neurotrophic factor (BDNF) expression by activating PI3K/Akt/CREB signaling in the hippocampus. 3-n-butylphthalide 27-33 brain derived neurotrophic factor Mus musculus 163-167 33462377-8 2021 Moreover, we revealed that DL-NBP administration suppressed oxidative stress by upregulating Nrf2/HO-1 signaling, and increased brain-derived neurotrophic factor (BDNF) expression by activating PI3K/Akt/CREB signaling in the hippocampus. 3-n-butylphthalide 27-33 thymoma viral proto-oncogene 1 Mus musculus 199-202 33462377-8 2021 Moreover, we revealed that DL-NBP administration suppressed oxidative stress by upregulating Nrf2/HO-1 signaling, and increased brain-derived neurotrophic factor (BDNF) expression by activating PI3K/Akt/CREB signaling in the hippocampus. 3-n-butylphthalide 27-33 cAMP responsive element binding protein 1 Mus musculus 203-207 33296663-0 2021 Dl-3-n-butylphthalide Promotes Neurite Outgrowth of Primary Cortical Neurons by Sonic Hedgehog Signaling via Upregulating Gap43. 3-n-butylphthalide 0-21 sonic hedgehog signaling molecule Homo sapiens 80-94 33296663-0 2021 Dl-3-n-butylphthalide Promotes Neurite Outgrowth of Primary Cortical Neurons by Sonic Hedgehog Signaling via Upregulating Gap43. 3-n-butylphthalide 0-21 growth associated protein 43 Homo sapiens 122-127 33519417-0 2020 Dl-3-n-Butylphthalide Alleviates Hippocampal Neuron Damage in Chronic Cerebral Hypoperfusion via Regulation of the CNTF/CNTFRalpha/JAK2/STAT3 Signaling Pathways. 3-n-butylphthalide 0-21 ciliary neurotrophic factor Rattus norvegicus 115-119 33519417-0 2020 Dl-3-n-Butylphthalide Alleviates Hippocampal Neuron Damage in Chronic Cerebral Hypoperfusion via Regulation of the CNTF/CNTFRalpha/JAK2/STAT3 Signaling Pathways. 3-n-butylphthalide 0-21 ciliary neurotrophic factor receptor Rattus norvegicus 120-130 33519417-0 2020 Dl-3-n-Butylphthalide Alleviates Hippocampal Neuron Damage in Chronic Cerebral Hypoperfusion via Regulation of the CNTF/CNTFRalpha/JAK2/STAT3 Signaling Pathways. 3-n-butylphthalide 0-21 Janus kinase 2 Rattus norvegicus 131-135 33519417-0 2020 Dl-3-n-Butylphthalide Alleviates Hippocampal Neuron Damage in Chronic Cerebral Hypoperfusion via Regulation of the CNTF/CNTFRalpha/JAK2/STAT3 Signaling Pathways. 3-n-butylphthalide 0-21 signal transducer and activator of transcription 3 Rattus norvegicus 136-141 33519417-10 2020 More importantly, D3NB reversed the inhibition of CNTF/CNTFRalpha expression and activated the JAK2/STAT3 pathway. 3-n-butylphthalide 18-22 ciliary neurotrophic factor Rattus norvegicus 50-54 33519417-10 2020 More importantly, D3NB reversed the inhibition of CNTF/CNTFRalpha expression and activated the JAK2/STAT3 pathway. 3-n-butylphthalide 18-22 ciliary neurotrophic factor receptor Rattus norvegicus 55-65 33519417-10 2020 More importantly, D3NB reversed the inhibition of CNTF/CNTFRalpha expression and activated the JAK2/STAT3 pathway. 3-n-butylphthalide 18-22 Janus kinase 2 Rattus norvegicus 95-99 33519417-10 2020 More importantly, D3NB reversed the inhibition of CNTF/CNTFRalpha expression and activated the JAK2/STAT3 pathway. 3-n-butylphthalide 18-22 signal transducer and activator of transcription 3 Rattus norvegicus 100-105 33519417-11 2020 Additionally, JAK2/STAT3 pathway inhibitor AG490 counteracted the protective effects of D3NB in vitro. 3-n-butylphthalide 88-92 Janus kinase 2 Rattus norvegicus 14-18 33519417-11 2020 Additionally, JAK2/STAT3 pathway inhibitor AG490 counteracted the protective effects of D3NB in vitro. 3-n-butylphthalide 88-92 signal transducer and activator of transcription 3 Rattus norvegicus 19-24 33519417-12 2020 Our results suggest that D3NB could improve cognitive function after CCH and that this neuroprotective effect may be associated with reduced hippocampal neuronal apoptosis via modulation of CNTF/CNTFRalpha/JAK2/STAT3 signaling pathways. 3-n-butylphthalide 25-29 ciliary neurotrophic factor Rattus norvegicus 190-194 33519417-12 2020 Our results suggest that D3NB could improve cognitive function after CCH and that this neuroprotective effect may be associated with reduced hippocampal neuronal apoptosis via modulation of CNTF/CNTFRalpha/JAK2/STAT3 signaling pathways. 3-n-butylphthalide 25-29 ciliary neurotrophic factor receptor Rattus norvegicus 195-205 33519417-12 2020 Our results suggest that D3NB could improve cognitive function after CCH and that this neuroprotective effect may be associated with reduced hippocampal neuronal apoptosis via modulation of CNTF/CNTFRalpha/JAK2/STAT3 signaling pathways. 3-n-butylphthalide 25-29 Janus kinase 2 Rattus norvegicus 206-210 33519417-12 2020 Our results suggest that D3NB could improve cognitive function after CCH and that this neuroprotective effect may be associated with reduced hippocampal neuronal apoptosis via modulation of CNTF/CNTFRalpha/JAK2/STAT3 signaling pathways. 3-n-butylphthalide 25-29 signal transducer and activator of transcription 3 Rattus norvegicus 211-216 32644834-11 2020 NBP treatment significantly improved spatial learning and memory in VaD rats, and may enhance cholinergic system function via BDNF-mediated neuroprotection. 3-n-butylphthalide 0-3 brain-derived neurotrophic factor Rattus norvegicus 126-130 33198448-0 2020 Effects of butylphthalide on cognitive dysfunction and expression of superoxide dismutase and Smac in cortex of rats with chronic cerebral ischemia. 3-n-butylphthalide 11-25 diablo, IAP-binding mitochondrial protein Rattus norvegicus 94-98 32205688-0 2020 Butylphthalide has an Anti-Inflammatory Role in Spinal Cord Injury by Promoting Macrophage/Microglia M2 Polarization via p38 Phosphorylation. 3-n-butylphthalide 0-14 mitogen-activated protein kinase 14 Mus musculus 121-124 32205688-2 2020 OBJECTIVE: This report aims to evaluate the in vivo effects of Butylphthalide NBP) on SCI biology and to explore its potential mechanism. 3-n-butylphthalide 63-77 NUBP iron-sulfur cluster assembly factor 1, cytosolic Homo sapiens 78-81 32205688-6 2020 Butylphthalide (3-n-butylphthalide or NBP) treatment can significantly alleviate ischemic brain damage, and further study has confirmed that central neuroprotective effects can be realized by converting M1 polarized microglia/macrophages to the M2 phenotype. 3-n-butylphthalide 0-14 NUBP iron-sulfur cluster assembly factor 1, cytosolic Homo sapiens 38-41 32377741-9 2020 Molecular examination indicated that SIRT1 and BDNF expression levels in the hippocampus were increased by NBP treatment. 3-n-butylphthalide 107-110 sirtuin 1 Rattus norvegicus 37-42 32377741-9 2020 Molecular examination indicated that SIRT1 and BDNF expression levels in the hippocampus were increased by NBP treatment. 3-n-butylphthalide 107-110 brain-derived neurotrophic factor Rattus norvegicus 47-51 32377741-11 2020 In addition, NBP in combination with a SIRT1 inhibitor suppressed BDNF protein expression, but inhibition of BDNF did not inhibit SIRT1 protein expression in rats with VCI. 3-n-butylphthalide 13-16 brain-derived neurotrophic factor Rattus norvegicus 66-70 32744007-0 2020 [Effects of butylphthalide on H2S/CBS pathway in hippocampal and amygdala and learning and memory ability in chronic alcoholism rats]. 3-n-butylphthalide 12-26 cystathionine beta synthase Rattus norvegicus 34-37 32581761-0 2020 Dl-3-n-Butylphthalide Promotes Remyelination and Suppresses Inflammation by Regulating AMPK/SIRT1 and STAT3/NF-kappaB Signaling in Chronic Cerebral Hypoperfusion. 3-n-butylphthalide 0-21 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 87-91 32581761-0 2020 Dl-3-n-Butylphthalide Promotes Remyelination and Suppresses Inflammation by Regulating AMPK/SIRT1 and STAT3/NF-kappaB Signaling in Chronic Cerebral Hypoperfusion. 3-n-butylphthalide 0-21 sirtuin 1 Rattus norvegicus 92-97 32581761-0 2020 Dl-3-n-Butylphthalide Promotes Remyelination and Suppresses Inflammation by Regulating AMPK/SIRT1 and STAT3/NF-kappaB Signaling in Chronic Cerebral Hypoperfusion. 3-n-butylphthalide 0-21 signal transducer and activator of transcription 3 Rattus norvegicus 102-107 32581761-9 2020 Additionally, NBP induced the activation of AMPK/SIRT1 signaling while inhibiting the STAT3/NF-kappaB pathway. 3-n-butylphthalide 14-17 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 44-48 32581761-9 2020 Additionally, NBP induced the activation of AMPK/SIRT1 signaling while inhibiting the STAT3/NF-kappaB pathway. 3-n-butylphthalide 14-17 sirtuin 1 Rattus norvegicus 49-54 32581761-9 2020 Additionally, NBP induced the activation of AMPK/SIRT1 signaling while inhibiting the STAT3/NF-kappaB pathway. 3-n-butylphthalide 14-17 signal transducer and activator of transcription 3 Rattus norvegicus 86-91 32581761-10 2020 These results indicate that NBP alleviates cognitive impairment following CCH by promoting remyelination and suppressing inflammation via modulation of AMPK/SIRT1 and STAT3/NF-kappaB signaling. 3-n-butylphthalide 28-31 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 152-156 32581761-10 2020 These results indicate that NBP alleviates cognitive impairment following CCH by promoting remyelination and suppressing inflammation via modulation of AMPK/SIRT1 and STAT3/NF-kappaB signaling. 3-n-butylphthalide 28-31 sirtuin 1 Rattus norvegicus 157-162 32581761-10 2020 These results indicate that NBP alleviates cognitive impairment following CCH by promoting remyelination and suppressing inflammation via modulation of AMPK/SIRT1 and STAT3/NF-kappaB signaling. 3-n-butylphthalide 28-31 signal transducer and activator of transcription 3 Rattus norvegicus 167-172 31822157-7 2020 The incidence of cerebral infarction with an ABCD2 score less than 3 points was significantly lower than that with an ABCD2 score of more than 3 points (p < .05), with less adverse reactions.Conclusion: Butylphthalide injection is helpful and safe for preventing stroke following TIA, and treating TIA with positive DWI and progression to infarction. 3-n-butylphthalide 203-217 ATP binding cassette subfamily D member 2 Homo sapiens 45-50 31822157-7 2020 The incidence of cerebral infarction with an ABCD2 score less than 3 points was significantly lower than that with an ABCD2 score of more than 3 points (p < .05), with less adverse reactions.Conclusion: Butylphthalide injection is helpful and safe for preventing stroke following TIA, and treating TIA with positive DWI and progression to infarction. 3-n-butylphthalide 203-217 ATP binding cassette subfamily D member 2 Homo sapiens 118-123 32104252-0 2020 Dl-3n-butylphthalide improves spatial learning and memory in rats with vascular dementia by reducing autophagy via regulation of the mTOR signaling pathway. 3-n-butylphthalide 0-20 mechanistic target of rapamycin kinase Rattus norvegicus 133-137 32066705-0 2020 Dl-3-n-butylphthalide attenuates mouse behavioral deficits to chronic social defeat stress by regulating energy metabolism via AKT/CREB signaling pathway. 3-n-butylphthalide 0-21 thymoma viral proto-oncogene 1 Mus musculus 127-130 32066705-0 2020 Dl-3-n-butylphthalide attenuates mouse behavioral deficits to chronic social defeat stress by regulating energy metabolism via AKT/CREB signaling pathway. 3-n-butylphthalide 0-21 cAMP responsive element binding protein 1 Mus musculus 131-135 32066705-9 2020 NBP affected gene expression of key enzymes of the TCA cycle, as well as protein expression of p-AKT and p-CREB. 3-n-butylphthalide 0-3 cAMP responsive element binding protein 1 Mus musculus 107-111 32066705-10 2020 Our findings provide the first evidence showing that NBP can attenuate stress-induced behavioral deficits by modulating energy metabolism by regulating activation of the AKT/CREB signaling pathway. 3-n-butylphthalide 53-56 thymoma viral proto-oncogene 1 Mus musculus 170-173 32744000-12 2020 The Iba-1 positive cells in butylphthalide intervention group were reduced compared with chronic sleep deprivation group (P<0. 3-n-butylphthalide 28-42 allograft inflammatory factor 1 Rattus norvegicus 4-9 32066705-10 2020 Our findings provide the first evidence showing that NBP can attenuate stress-induced behavioral deficits by modulating energy metabolism by regulating activation of the AKT/CREB signaling pathway. 3-n-butylphthalide 53-56 cAMP responsive element binding protein 1 Mus musculus 174-178 32038259-0 2019 Dl-NBP (Dl-3-N-Butylphthalide) Treatment Promotes Neurological Functional Recovery Accompanied by the Upregulation of White Matter Integrity and HIF-1alpha/VEGF/Notch/Dll4 Expression. 3-n-butylphthalide 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 145-155 32038259-0 2019 Dl-NBP (Dl-3-N-Butylphthalide) Treatment Promotes Neurological Functional Recovery Accompanied by the Upregulation of White Matter Integrity and HIF-1alpha/VEGF/Notch/Dll4 Expression. 3-n-butylphthalide 0-6 vascular endothelial growth factor A Homo sapiens 156-160 32038259-0 2019 Dl-NBP (Dl-3-N-Butylphthalide) Treatment Promotes Neurological Functional Recovery Accompanied by the Upregulation of White Matter Integrity and HIF-1alpha/VEGF/Notch/Dll4 Expression. 3-n-butylphthalide 0-6 delta like canonical Notch ligand 4 Homo sapiens 167-171 32038259-0 2019 Dl-NBP (Dl-3-N-Butylphthalide) Treatment Promotes Neurological Functional Recovery Accompanied by the Upregulation of White Matter Integrity and HIF-1alpha/VEGF/Notch/Dll4 Expression. 3-n-butylphthalide 8-29 hypoxia inducible factor 1 subunit alpha Homo sapiens 145-155 32038259-0 2019 Dl-NBP (Dl-3-N-Butylphthalide) Treatment Promotes Neurological Functional Recovery Accompanied by the Upregulation of White Matter Integrity and HIF-1alpha/VEGF/Notch/Dll4 Expression. 3-n-butylphthalide 8-29 vascular endothelial growth factor A Homo sapiens 156-160 32038259-0 2019 Dl-NBP (Dl-3-N-Butylphthalide) Treatment Promotes Neurological Functional Recovery Accompanied by the Upregulation of White Matter Integrity and HIF-1alpha/VEGF/Notch/Dll4 Expression. 3-n-butylphthalide 8-29 delta like canonical Notch ligand 4 Homo sapiens 167-171 31840938-6 2020 The expressions of autophagy-related proteins, including ATG7, Beclin1 and LC3II, were significantly increased after TBI/OGD, and which were reversed by Dl-NBP treatment both in vivo and in vitro. 3-n-butylphthalide 153-159 autophagy related 7 Homo sapiens 57-61 31840938-6 2020 The expressions of autophagy-related proteins, including ATG7, Beclin1 and LC3II, were significantly increased after TBI/OGD, and which were reversed by Dl-NBP treatment both in vivo and in vitro. 3-n-butylphthalide 153-159 beclin 1 Homo sapiens 63-70 31578943-0 2019 DL-3-n-butylphthalide (NBP) ameliorates cognitive deficits and CaMKII-mediated long-term potentiation impairment in the hippocampus of diabetic db/db mice. 3-n-butylphthalide 0-21 calcium/calmodulin-dependent protein kinase II, beta Mus musculus 63-69 31969495-9 2019 The intervention of butylphthalide significantly upregulated the expressions of Cdc42 as well as ZO-1/Occludin (P<0.05), but exerted no effect on GM130 (P<0.05). 3-n-butylphthalide 20-34 cell division cycle 42 Rattus norvegicus 80-85 31969495-9 2019 The intervention of butylphthalide significantly upregulated the expressions of Cdc42 as well as ZO-1/Occludin (P<0.05), but exerted no effect on GM130 (P<0.05). 3-n-butylphthalide 20-34 tight junction protein 1 Rattus norvegicus 97-101 31969495-9 2019 The intervention of butylphthalide significantly upregulated the expressions of Cdc42 as well as ZO-1/Occludin (P<0.05), but exerted no effect on GM130 (P<0.05). 3-n-butylphthalide 20-34 occludin Rattus norvegicus 102-110 31969495-10 2019 Immunofluorescent staining showed that GM130 was co-localized with Cdc42 and administration of butylphthalide improved the expression of Cdc42 around the hematoma without affecting the expression of GM130. 3-n-butylphthalide 95-109 golgin A2 Rattus norvegicus 39-44 31969495-10 2019 Immunofluorescent staining showed that GM130 was co-localized with Cdc42 and administration of butylphthalide improved the expression of Cdc42 around the hematoma without affecting the expression of GM130. 3-n-butylphthalide 95-109 cell division cycle 42 Rattus norvegicus 137-142 31969495-10 2019 Immunofluorescent staining showed that GM130 was co-localized with Cdc42 and administration of butylphthalide improved the expression of Cdc42 around the hematoma without affecting the expression of GM130. 3-n-butylphthalide 95-109 golgin A2 Rattus norvegicus 199-204 31969495-11 2019 IHC showed that expressions of occludin and ZO-1 around the hematoma were significantly decreased in the ICH group (P<0.05), whereas butylphthalide treatment elevated the expressions of ZO-1 and occludin around the hematoma compared with the ICH group (P<0.05). 3-n-butylphthalide 136-150 tight junction protein 1 Rattus norvegicus 189-193 31969495-11 2019 IHC showed that expressions of occludin and ZO-1 around the hematoma were significantly decreased in the ICH group (P<0.05), whereas butylphthalide treatment elevated the expressions of ZO-1 and occludin around the hematoma compared with the ICH group (P<0.05). 3-n-butylphthalide 136-150 occludin Rattus norvegicus 198-206 31969495-13 2019 The application of butylphthalide can alleviate neurological impairment and blood-brain barrier disruption, which is related to the up-regulation of Cdc42, but not GM130. 3-n-butylphthalide 19-33 cell division cycle 42 Rattus norvegicus 149-154 31724337-0 2019 Effects of dl-3-n-butylphthalide on serum lipoprotein-associated phospholipase A2 and hypersensitive C-reactive protein levels in acute cerebral infarction. 3-n-butylphthalide 11-32 phospholipase A2 group VII Homo sapiens 42-81 31724337-1 2019 OBJECTIVE: This study aims to explore the curative effect of dl-3-n-butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on serum lipoprotein-associated phospholipase A2 (Lp-PLA2) and hypersensitive C-reactive protein (hs-CRP) levels. 3-n-butylphthalide 61-82 phospholipase A2 group VII Homo sapiens 163-202 31724337-1 2019 OBJECTIVE: This study aims to explore the curative effect of dl-3-n-butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on serum lipoprotein-associated phospholipase A2 (Lp-PLA2) and hypersensitive C-reactive protein (hs-CRP) levels. 3-n-butylphthalide 61-82 phospholipase A2 group VII Homo sapiens 204-211 31724337-1 2019 OBJECTIVE: This study aims to explore the curative effect of dl-3-n-butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on serum lipoprotein-associated phospholipase A2 (Lp-PLA2) and hypersensitive C-reactive protein (hs-CRP) levels. 3-n-butylphthalide 61-82 C-reactive protein Homo sapiens 232-250 31724337-1 2019 OBJECTIVE: This study aims to explore the curative effect of dl-3-n-butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on serum lipoprotein-associated phospholipase A2 (Lp-PLA2) and hypersensitive C-reactive protein (hs-CRP) levels. 3-n-butylphthalide 84-87 phospholipase A2 group VII Homo sapiens 163-202 31724337-1 2019 OBJECTIVE: This study aims to explore the curative effect of dl-3-n-butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on serum lipoprotein-associated phospholipase A2 (Lp-PLA2) and hypersensitive C-reactive protein (hs-CRP) levels. 3-n-butylphthalide 84-87 phospholipase A2 group VII Homo sapiens 204-211 31724337-1 2019 OBJECTIVE: This study aims to explore the curative effect of dl-3-n-butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on serum lipoprotein-associated phospholipase A2 (Lp-PLA2) and hypersensitive C-reactive protein (hs-CRP) levels. 3-n-butylphthalide 84-87 C-reactive protein Homo sapiens 232-250 31724337-9 2019 CONCLUSION: Dl-3-n-butylphthalide can improve the expression of Lp-PLA2 and hs-CRP in serum in ACI patients. 3-n-butylphthalide 12-33 phospholipase A2 group VII Homo sapiens 64-71 31595195-4 2019 NBP induced downregulation of intercellular adhesion molecule 1 and protease-activated receptor 1 in cerebrovascular endothelial cells after cerebral ischemia and reperfusion. 3-n-butylphthalide 0-3 intercellular adhesion molecule 1 Mus musculus 30-97 31188648-11 2019 Cell immunofluorescence staining indicated that the fluorescence staining intensity of HO-1 in the NBP group was significantly higher than that in the control group. 3-n-butylphthalide 99-102 heme oxygenase 1 Homo sapiens 87-91 31188648-13 2019 The translocation of Nrf2 in nuclei was observed within 2 h and Nrf2 was identified in nuclei for up to 48 h. Conclusions: Our study demonstrated that NBP had a protective effect on H2O2-induced cytotoxicity in retinal Muller cells in vitro and that it was a potent activator of Nrf2 and HO-1signaling. 3-n-butylphthalide 151-154 NFE2 like bZIP transcription factor 2 Homo sapiens 21-25 31188648-13 2019 The translocation of Nrf2 in nuclei was observed within 2 h and Nrf2 was identified in nuclei for up to 48 h. Conclusions: Our study demonstrated that NBP had a protective effect on H2O2-induced cytotoxicity in retinal Muller cells in vitro and that it was a potent activator of Nrf2 and HO-1signaling. 3-n-butylphthalide 151-154 NFE2 like bZIP transcription factor 2 Homo sapiens 64-68 31188648-13 2019 The translocation of Nrf2 in nuclei was observed within 2 h and Nrf2 was identified in nuclei for up to 48 h. Conclusions: Our study demonstrated that NBP had a protective effect on H2O2-induced cytotoxicity in retinal Muller cells in vitro and that it was a potent activator of Nrf2 and HO-1signaling. 3-n-butylphthalide 151-154 NFE2 like bZIP transcription factor 2 Homo sapiens 64-68 31601076-2 2019 Hematoxylin/eosin and Nissl staining showed that, compared to the sham/control group, the Dl-3-n-butylphthalide group had no obvious hippocampal and cerebellar neuron loss, but there was a significant neuron loss in the P1 and P2 groups (P < 0.05), which was more obvious in the P2 group (P < 0.05). 3-n-butylphthalide 90-111 perforin 1 Rattus norvegicus 220-229 31773715-0 2019 Effects of butylphthalide on oxidative stress and inflammatory response in rats with myocardial infarction through Akt/Nrf2 signaling pathway. 3-n-butylphthalide 11-25 AKT serine/threonine kinase 1 Rattus norvegicus 115-118 31773715-0 2019 Effects of butylphthalide on oxidative stress and inflammatory response in rats with myocardial infarction through Akt/Nrf2 signaling pathway. 3-n-butylphthalide 11-25 NFE2 like bZIP transcription factor 2 Rattus norvegicus 119-123 31773715-1 2019 OBJECTIVE: The aim of this study was to investigate the effects of butylphthalide on oxidative stress and inflammatory response in rats with myocardial infarction through the protein kinase B/nuclear factor E2-related factor 2 (Akt/Nrf2) signaling pathway. 3-n-butylphthalide 67-81 AKT serine/threonine kinase 1 Rattus norvegicus 228-231 31773715-1 2019 OBJECTIVE: The aim of this study was to investigate the effects of butylphthalide on oxidative stress and inflammatory response in rats with myocardial infarction through the protein kinase B/nuclear factor E2-related factor 2 (Akt/Nrf2) signaling pathway. 3-n-butylphthalide 67-81 NFE2 like bZIP transcription factor 2 Rattus norvegicus 232-236 31773715-15 2019 The expression level of NOX-1 increased markedly in the model group and butylphthalide group compared with the sham group (p<0.05). 3-n-butylphthalide 72-86 NADPH oxidase 1 Rattus norvegicus 24-29 31773715-17 2019 Meanwhile, the protein expression levels of p-Akt and p-Nrf2 were significantly higher in the model group and butylphthalide group than those of the sham group (p<0.05). 3-n-butylphthalide 110-124 AKT serine/threonine kinase 1 Rattus norvegicus 46-49 31773715-17 2019 Meanwhile, the protein expression levels of p-Akt and p-Nrf2 were significantly higher in the model group and butylphthalide group than those of the sham group (p<0.05). 3-n-butylphthalide 110-124 NFE2 like bZIP transcription factor 2 Rattus norvegicus 56-60 31773715-18 2019 However, the protein expression levels of p-Akt and p-Nrf2 in the butylphthalide group were remarkably lower than the model group (p<0.05). 3-n-butylphthalide 66-80 AKT serine/threonine kinase 1 Rattus norvegicus 44-47 31773715-18 2019 However, the protein expression levels of p-Akt and p-Nrf2 in the butylphthalide group were remarkably lower than the model group (p<0.05). 3-n-butylphthalide 66-80 NFE2 like bZIP transcription factor 2 Rattus norvegicus 54-58 31773715-19 2019 The mRNA expression levels of IL-1beta, TNF-alpha and NOX-1 were markedly higher in the model group and butylphthalide group than those of the sham group (p<0.05). 3-n-butylphthalide 104-118 interleukin 1 beta Rattus norvegicus 30-38 31773715-19 2019 The mRNA expression levels of IL-1beta, TNF-alpha and NOX-1 were markedly higher in the model group and butylphthalide group than those of the sham group (p<0.05). 3-n-butylphthalide 104-118 tumor necrosis factor Rattus norvegicus 40-49 31773715-19 2019 The mRNA expression levels of IL-1beta, TNF-alpha and NOX-1 were markedly higher in the model group and butylphthalide group than those of the sham group (p<0.05). 3-n-butylphthalide 104-118 NADPH oxidase 1 Rattus norvegicus 54-59 31773715-21 2019 In addition, the content of IL-1beta and TNF-alpha increased in the model group and butylphthalide group when compared with the sham group (p<0.05). 3-n-butylphthalide 84-98 interleukin 1 beta Rattus norvegicus 28-36 31773715-21 2019 In addition, the content of IL-1beta and TNF-alpha increased in the model group and butylphthalide group when compared with the sham group (p<0.05). 3-n-butylphthalide 84-98 tumor necrosis factor Rattus norvegicus 41-50 31773715-22 2019 The content of IL-1beta and TNF-alpha in the butylphthalide group was significantly lower than the model group (p<0.05). 3-n-butylphthalide 45-59 interleukin 1 beta Rattus norvegicus 15-23 31773715-22 2019 The content of IL-1beta and TNF-alpha in the butylphthalide group was significantly lower than the model group (p<0.05). 3-n-butylphthalide 45-59 tumor necrosis factor Rattus norvegicus 28-37 31773715-24 2019 CONCLUSIONS: Butylphthalide inhibits inflammatory and oxidative stress responses after AMI by regulating the Akt/Nrf2 signaling pathway, thereby inhibiting myocardial apoptosis and benefiting the morphological repair of myocardial tissues. 3-n-butylphthalide 13-27 AKT serine/threonine kinase 1 Rattus norvegicus 109-112 31773715-24 2019 CONCLUSIONS: Butylphthalide inhibits inflammatory and oxidative stress responses after AMI by regulating the Akt/Nrf2 signaling pathway, thereby inhibiting myocardial apoptosis and benefiting the morphological repair of myocardial tissues. 3-n-butylphthalide 13-27 NFE2 like bZIP transcription factor 2 Rattus norvegicus 113-117 31493665-0 2019 Butylphthalide ameliorates airway inflammation and mucus hypersecretion via NF-kappaB in a murine asthma model. 3-n-butylphthalide 0-14 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 76-85 31578943-0 2019 DL-3-n-butylphthalide (NBP) ameliorates cognitive deficits and CaMKII-mediated long-term potentiation impairment in the hippocampus of diabetic db/db mice. 3-n-butylphthalide 23-26 calcium/calmodulin-dependent protein kinase II, beta Mus musculus 63-69 31578943-4 2019 This study was designed to evaluate the effects of NBP on the cognitive deficits through activating CaMKII-mediated LTP process and protecting neuron structure of hippocampus in diabetic db/db mice. 3-n-butylphthalide 51-54 calcium/calmodulin-dependent protein kinase II, beta Mus musculus 100-106 31177016-0 2019 DL-3-n-butylphthalide attenuates lipopolysaccharide-induced acute lung injury via SIRT1-dependent and -independent regulation of Nrf2. 3-n-butylphthalide 0-21 nuclear factor, erythroid derived 2, like 2 Mus musculus 129-133 29943092-0 2018 Dl-3-n-Butylphthalide improves lipopolysaccharide-induced depressive-like behavior in rats: involvement of Nrf2 and NF-kappaB pathways. 3-n-butylphthalide 0-21 NFE2 like bZIP transcription factor 2 Rattus norvegicus 107-111 31456664-0 2019 Dl-3-n-Butylphthalide Reduces Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion Through GDNF/GFRalpha1/Ret Signaling Preventing Hippocampal Neuron Apoptosis. 3-n-butylphthalide 0-21 glial cell derived neurotrophic factor Rattus norvegicus 101-105 31456664-0 2019 Dl-3-n-Butylphthalide Reduces Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion Through GDNF/GFRalpha1/Ret Signaling Preventing Hippocampal Neuron Apoptosis. 3-n-butylphthalide 0-21 GDNF family receptor alpha 1 Rattus norvegicus 106-119 31389585-0 2019 3-N-butylphthalide inhibits neuronal apoptosis in rats with cerebral infarction via targeting P38/MAPK. 3-n-butylphthalide 0-18 mitogen activated protein kinase 14 Rattus norvegicus 94-97 31389585-0 2019 3-N-butylphthalide inhibits neuronal apoptosis in rats with cerebral infarction via targeting P38/MAPK. 3-n-butylphthalide 0-18 mitogen activated protein kinase 14 Rattus norvegicus 98-102 31389585-1 2019 OBJECTIVE: To study the effect of 3-n-butylphthalide (NBP) on neuronal apoptosis in rats with cerebral infarction (CI) through the p38/mitogen-activated protein kinase (MAPK) pathway. 3-n-butylphthalide 34-52 mitogen activated protein kinase 14 Rattus norvegicus 131-167 31389585-1 2019 OBJECTIVE: To study the effect of 3-n-butylphthalide (NBP) on neuronal apoptosis in rats with cerebral infarction (CI) through the p38/mitogen-activated protein kinase (MAPK) pathway. 3-n-butylphthalide 34-52 mitogen activated protein kinase 14 Rattus norvegicus 169-173 31389585-1 2019 OBJECTIVE: To study the effect of 3-n-butylphthalide (NBP) on neuronal apoptosis in rats with cerebral infarction (CI) through the p38/mitogen-activated protein kinase (MAPK) pathway. 3-n-butylphthalide 54-57 mitogen activated protein kinase 14 Rattus norvegicus 131-167 31389585-1 2019 OBJECTIVE: To study the effect of 3-n-butylphthalide (NBP) on neuronal apoptosis in rats with cerebral infarction (CI) through the p38/mitogen-activated protein kinase (MAPK) pathway. 3-n-butylphthalide 54-57 mitogen activated protein kinase 14 Rattus norvegicus 169-173 30306574-0 2019 DL-3-n-butylphthalide alleviates vascular cognitive impairment by regulating endoplasmic reticulum stress and the Shh/Ptch1 signaling-pathway in rats. 3-n-butylphthalide 0-21 sonic hedgehog signaling molecule Rattus norvegicus 114-117 30306574-0 2019 DL-3-n-butylphthalide alleviates vascular cognitive impairment by regulating endoplasmic reticulum stress and the Shh/Ptch1 signaling-pathway in rats. 3-n-butylphthalide 0-21 patched 1 Rattus norvegicus 118-123 30784219-7 2019 CONCLUSION: NBP treatment promoted the expression of vascular endothelial growth factor and angiopoietin-1, induced angiogenesis, and improved neurobehavioral recovery. 3-n-butylphthalide 12-15 angiopoietin 1 Rattus norvegicus 92-106 30897537-0 2019 Dl-3-n-Butylphthalide regulates the Ang-1/Ang-2/Tie-2 signaling axis to promote neovascularization in chronic cerebral hypoperfusion. 3-n-butylphthalide 0-21 angiopoietin 1 Rattus norvegicus 36-41 30897537-0 2019 Dl-3-n-Butylphthalide regulates the Ang-1/Ang-2/Tie-2 signaling axis to promote neovascularization in chronic cerebral hypoperfusion. 3-n-butylphthalide 0-21 angiogenin, ribonuclease A family, member 2 Rattus norvegicus 42-47 30897537-0 2019 Dl-3-n-Butylphthalide regulates the Ang-1/Ang-2/Tie-2 signaling axis to promote neovascularization in chronic cerebral hypoperfusion. 3-n-butylphthalide 0-21 TEK receptor tyrosine kinase Rattus norvegicus 48-53 30897537-7 2019 The Tie-2 level was significantly decreased and identified in CCH 2 week (W), CCH 4 W and CCH 8 W. In addition, Ang-1 level and Ang-1/Ang-2 ratio were significantly decreased in CCH 2 W and CCH 4 W while Ang-2 level was increased in the CCH, whereas DNB treatment created the inverse effect to some extent. 3-n-butylphthalide 250-253 TEK receptor tyrosine kinase Rattus norvegicus 4-9 30897537-8 2019 Moreover, the expression of VEGF and CD34 in the earlier stage of CCH and the diameters of bilateral vertebral arteries (VAs), were significantly enlarged by DNB treatment. 3-n-butylphthalide 158-161 vascular endothelial growth factor A Rattus norvegicus 28-32 30897537-8 2019 Moreover, the expression of VEGF and CD34 in the earlier stage of CCH and the diameters of bilateral vertebral arteries (VAs), were significantly enlarged by DNB treatment. 3-n-butylphthalide 158-161 CD34 molecule Rattus norvegicus 37-41 31173324-0 2019 3-n-butylphthalide inhibits the apoptosis of nerve cells in rats with cerebral small vessel disease via the PI3K/Akt pathway. 3-n-butylphthalide 0-18 AKT serine/threonine kinase 1 Rattus norvegicus 113-116 31173324-13 2019 The levels of Bax and Caspase-3 in rat serum were significantly down-regulated, and the apoptosis rate of nerve cells in brain tissues of rats were reduced in the NBP group. 3-n-butylphthalide 163-166 BCL2 associated X, apoptosis regulator Rattus norvegicus 14-17 31173324-14 2019 Furthermore, the protein levels of phosphorylated PI3K and phosphorylated Akt were remarkably elevated in the NBP group. 3-n-butylphthalide 110-113 AKT serine/threonine kinase 1 Rattus norvegicus 74-77 31173325-0 2019 dl-3n-butylphthalide reduces oxygen-glucose deprivation-induced endothelial cell damage by increasing PGC-1alpha. 3-n-butylphthalide 0-20 PPARG coactivator 1 alpha Rattus norvegicus 102-112 29634349-8 2019 In our study, we elucidated for new mechanisms by which Dl-NBP enhanced TrX activity, suppressed TXNIP, and ameliorated neuronal apoptosis in the APP/PS1 mouse brains. 3-n-butylphthalide 56-62 thioredoxin 1 Mus musculus 72-75 29634349-8 2019 In our study, we elucidated for new mechanisms by which Dl-NBP enhanced TrX activity, suppressed TXNIP, and ameliorated neuronal apoptosis in the APP/PS1 mouse brains. 3-n-butylphthalide 56-62 thioredoxin interacting protein Mus musculus 97-102 29634349-8 2019 In our study, we elucidated for new mechanisms by which Dl-NBP enhanced TrX activity, suppressed TXNIP, and ameliorated neuronal apoptosis in the APP/PS1 mouse brains. 3-n-butylphthalide 56-62 presenilin 1 Mus musculus 150-153 29634349-9 2019 In human glioblastoma A172 cells and neuroblastoma SH-SY5Y cells, we delineated the Dl-NBP-mediated signaling pathways by which Dl-NBP-dependent upregulation of Nrf2 mediated the reciprocal regulation of reducing proinflammatory cytokine and inhibiting Abeta production in the glial and neuronal cells overexpressing APPswe. 3-n-butylphthalide 84-90 NFE2 like bZIP transcription factor 2 Homo sapiens 161-165 29634349-9 2019 In human glioblastoma A172 cells and neuroblastoma SH-SY5Y cells, we delineated the Dl-NBP-mediated signaling pathways by which Dl-NBP-dependent upregulation of Nrf2 mediated the reciprocal regulation of reducing proinflammatory cytokine and inhibiting Abeta production in the glial and neuronal cells overexpressing APPswe. 3-n-butylphthalide 84-90 amyloid beta precursor protein Homo sapiens 253-258 29634349-9 2019 In human glioblastoma A172 cells and neuroblastoma SH-SY5Y cells, we delineated the Dl-NBP-mediated signaling pathways by which Dl-NBP-dependent upregulation of Nrf2 mediated the reciprocal regulation of reducing proinflammatory cytokine and inhibiting Abeta production in the glial and neuronal cells overexpressing APPswe. 3-n-butylphthalide 128-134 NFE2 like bZIP transcription factor 2 Homo sapiens 161-165 29634349-9 2019 In human glioblastoma A172 cells and neuroblastoma SH-SY5Y cells, we delineated the Dl-NBP-mediated signaling pathways by which Dl-NBP-dependent upregulation of Nrf2 mediated the reciprocal regulation of reducing proinflammatory cytokine and inhibiting Abeta production in the glial and neuronal cells overexpressing APPswe. 3-n-butylphthalide 128-134 amyloid beta precursor protein Homo sapiens 253-258 29634349-11 2019 CONCLUSION: Dl-NBP treatment could suppress TXNIP-NLRP3 interaction and inhibit NLRP3 inflammasome activation via upregulating Nrf2. 3-n-butylphthalide 12-18 thioredoxin interacting protein Homo sapiens 44-49 29634349-11 2019 CONCLUSION: Dl-NBP treatment could suppress TXNIP-NLRP3 interaction and inhibit NLRP3 inflammasome activation via upregulating Nrf2. 3-n-butylphthalide 12-18 NLR family pyrin domain containing 3 Homo sapiens 50-55 29634349-11 2019 CONCLUSION: Dl-NBP treatment could suppress TXNIP-NLRP3 interaction and inhibit NLRP3 inflammasome activation via upregulating Nrf2. 3-n-butylphthalide 12-18 NLR family pyrin domain containing 3 Homo sapiens 80-85 29634349-11 2019 CONCLUSION: Dl-NBP treatment could suppress TXNIP-NLRP3 interaction and inhibit NLRP3 inflammasome activation via upregulating Nrf2. 3-n-butylphthalide 12-18 NFE2 like bZIP transcription factor 2 Homo sapiens 127-131 30813694-0 2019 [Effects of butylphthalide on plasma nitric oxide and endothelin-1 in severe elderly OSAHS patients]. 3-n-butylphthalide 12-26 endothelin 1 Homo sapiens 54-66 30813694-1 2019 Objective:To investigate the effect of butylphthalide on plasma nitric oxide(NO) and endothelin-1(ET-1) in severe elderly OSAHS patients. 3-n-butylphthalide 39-53 endothelin 1 Homo sapiens 85-97 30813694-1 2019 Objective:To investigate the effect of butylphthalide on plasma nitric oxide(NO) and endothelin-1(ET-1) in severe elderly OSAHS patients. 3-n-butylphthalide 39-53 endothelin 1 Homo sapiens 98-102 30813694-9 2019 Compared with non-invasive ventilation control group, the level of plasma NO increased and the level of plasma ET-1 decreased after 3 and 6 months of treatment in butylphthalide combined with non-invasive ventilation group (P<0.05). 3-n-butylphthalide 163-177 endothelin 1 Homo sapiens 111-115 30813694-10 2019 Conclusion:Butylphthalide may improve the vascular endothelial function of severe elderly OSAHS patients by increasing the level of NO and decreasing the level of ET-1 in plasma. 3-n-butylphthalide 11-25 endothelin 1 Homo sapiens 163-167 30550176-7 2018 Compared with treatment group of butylphthalide after treatment, the level of SOD increased and the level of MDA decreased in butylphthalide with non-invasive ventilator group (P<0.05); The scores of MoCA on cognitive function before treatment in the three groups was not statistically significant (P>0.05). 3-n-butylphthalide 33-47 superoxide dismutase 1 Homo sapiens 78-81 30154935-0 2018 Inhibiting of GRASP65 Phosphorylation by DL-3-N-Butylphthalide Protects against Cerebral Ischemia-Reperfusion Injury via ERK Signaling. 3-n-butylphthalide 41-62 golgi reassembly stacking protein 1 Mus musculus 14-21 30026693-8 2018 In addition, brain-derived neurotrophic factor/tropomyosin receptor kinase B signaling, previously shown to promote synaptic plasticity, was significantly enhanced by the DL-NBP administration. 3-n-butylphthalide 171-177 brain derived neurotrophic factor Mus musculus 13-46 30154935-0 2018 Inhibiting of GRASP65 Phosphorylation by DL-3-N-Butylphthalide Protects against Cerebral Ischemia-Reperfusion Injury via ERK Signaling. 3-n-butylphthalide 41-62 mitogen-activated protein kinase 1 Mus musculus 121-124 29687870-0 2018 Dl-3-n-butylphthalide protects the blood brain barrier of cerebral infarction by activating the Nrf-2/HO-1 signaling pathway in mice. 3-n-butylphthalide 0-21 nuclear factor, erythroid derived 2, like 2 Mus musculus 96-101 29764545-0 2018 [Effects of N-butylphthalide on the expressions of ZO-1 and claudin-5 in blood-brain barrier of rats with acute carbon monoxide poisoning]. 3-n-butylphthalide 12-28 tight junction protein 1 Rattus norvegicus 51-55 29764545-0 2018 [Effects of N-butylphthalide on the expressions of ZO-1 and claudin-5 in blood-brain barrier of rats with acute carbon monoxide poisoning]. 3-n-butylphthalide 12-28 claudin 5 Rattus norvegicus 60-69 29764545-1 2018 OBJECTIVE: To explore the effects of N-butylphthalide on the expressions of ZO-1 and claudin-5 in blood-brain barrier (BBB) in rats with acute carbon monoxide (CO) poisoning. 3-n-butylphthalide 37-53 tight junction protein 1 Rattus norvegicus 76-80 29764545-1 2018 OBJECTIVE: To explore the effects of N-butylphthalide on the expressions of ZO-1 and claudin-5 in blood-brain barrier (BBB) in rats with acute carbon monoxide (CO) poisoning. 3-n-butylphthalide 37-53 claudin 5 Rattus norvegicus 85-94 29687870-0 2018 Dl-3-n-butylphthalide protects the blood brain barrier of cerebral infarction by activating the Nrf-2/HO-1 signaling pathway in mice. 3-n-butylphthalide 0-21 heme oxygenase 1 Mus musculus 102-106 29687870-14 2018 DBT improved the ultrastructure in capillary endothelial cells of BBBs and increased the expressions of Nrf-2 and HO-1. 3-n-butylphthalide 0-3 nuclear factor, erythroid derived 2, like 2 Mus musculus 104-109 29687870-14 2018 DBT improved the ultrastructure in capillary endothelial cells of BBBs and increased the expressions of Nrf-2 and HO-1. 3-n-butylphthalide 0-3 heme oxygenase 1 Mus musculus 114-118 29687870-15 2018 CONCLUSIONS: DBT may protect BBB by activating the Nrf-2/HO-1 signaling pathway, thus achieving its protective effect on the brain. 3-n-butylphthalide 13-16 nuclear factor, erythroid derived 2, like 2 Mus musculus 51-56 29687870-15 2018 CONCLUSIONS: DBT may protect BBB by activating the Nrf-2/HO-1 signaling pathway, thus achieving its protective effect on the brain. 3-n-butylphthalide 13-16 heme oxygenase 1 Mus musculus 57-61 29175633-0 2018 DL-3-n-butylphthalide alleviates vascular cognitive impairment induced by chronic cerebral hypoperfusion by activating the Akt/Nrf2 signaling pathway in the hippocampus of rats. 3-n-butylphthalide 0-21 AKT serine/threonine kinase 1 Rattus norvegicus 123-126 29175633-0 2018 DL-3-n-butylphthalide alleviates vascular cognitive impairment induced by chronic cerebral hypoperfusion by activating the Akt/Nrf2 signaling pathway in the hippocampus of rats. 3-n-butylphthalide 0-21 NFE2 like bZIP transcription factor 2 Rattus norvegicus 127-131