PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32840726-7 2021 The expression of caspase-3 gene was significantly increased in the presence of the combination high Zn/high glucose with and without the presence of insulin and IL6 in the culture medium Fas expression instead, showed uneven responses. Glucose 109-116 caspase 3 Mus musculus 18-27 34278483-7 2021 The effects of tacrolimus on the insulin secretion and the activity of caspase-3 of Min6 cells stimulated by glucose exposure were measured by ELISA. Glucose 109-116 caspase 3 Mus musculus 71-80 33027757-11 2020 In SV40 cells, the effect of liraglutide on reversing the upregulation of cleaved caspase-3 induced by high glucose (30 mM) was hampered when SIRT1 was knocked down; also, the downregulation of TXNIP by liraglutide was blocked. Glucose 108-115 caspase 3 Mus musculus 82-91 32942336-8 2021 High glucose led to suppressed viability, enhanced apoptosis, reduced Bcl-2 expression, elevated Bax expression and cleavage of Caspase-3/-9 in GC-1 spg cells, and these effects were abrogated by Clusterin overexpression. Glucose 5-12 caspase 3 Mus musculus 128-140 32104028-14 2020 Here we showed that caspase-3 inhibition prevented GSDME activation and cell death in glucose-treated tubular cells. Glucose 86-93 caspase 3 Mus musculus 20-29 28285015-10 2017 The effect of TNF, high glucose and an AGE was mediated by the transcription factor FOXO1, which increased expression of p21 and caspase-3. Glucose 24-31 caspase 3 Mus musculus 129-138 31217790-5 2019 Moreover, LMP prevented high glucose-induced apoptosis by decreasing the expression of Bax and the activation of caspase-1 and caspase-3. Glucose 29-36 caspase 3 Mus musculus 127-136 30862678-7 2019 The overexpression of DUSP4 prevented the activation of p38, JNK, caspase 3/7 activity, and NADPH oxidase 4 expression induced by high glucose level exposure. Glucose 135-142 caspase 3 Mus musculus 66-77 30548130-7 2018 Apelin-13 decreased activity of Caspase-3 in podocytes after high glucose treatment reflecting an antiapoptotic effect of APJ stimulation. Glucose 66-73 caspase 3 Mus musculus 32-41 29207476-10 2017 Hesperidin inhibited high glucose-induced cell apoptosis by attenuating the downregulation of caspase-9, caspase-3, and Bax/Bcl-2. Glucose 26-33 caspase 3 Mus musculus 105-114 31032949-9 2019 High glucose inhibited p-AKT production and B-Cell CLL/Lymphoma 2 expression, and promoted BAX and caspase-3 expression. Glucose 5-12 caspase 3 Mus musculus 99-108 27698723-7 2016 Compared with the control group, downregulation NOM1 and high glucose concentration of 25 mM significantly increased the cleaved caspase-3 level in MIN6 cells (P<0.05). Glucose 62-69 caspase 3 Mus musculus 129-138 24474649-6 2014 In a glucose dose-dependent manner, severe mitochondrial damage leads to loss of mitochondrial membrane potential and platelet apoptosis (cytochrome c release, caspase 3 activation, and phosphatidylserine exposure). Glucose 5-12 caspase 3 Mus musculus 160-169 27401903-5 2016 In addition, inhibiting the mTOR signal suppressed DRP1 translocation to the mitochondria, pro-apoptotic mitochondrial protein release, and caspase 3 activation when glucose was deprived. Glucose 166-173 caspase 3 Mus musculus 140-149 26832955-6 2016 In vitro, increased levels of markers of inflammasome activation (Nlrp3, caspase-1 cleavage) preceded those of markers of apoptosis activation (caspase-3 and -7, PARP1 cleavage) in glucose-stressed podocytes. Glucose 181-188 caspase 3 Mus musculus 144-160 26918849-4 2016 Ex vivo experiments in 661W photoreceptor cells confirmed the low-glucose induction of death via superoxide production and activation of caspase 3, which was concomitant with a decrease of GSH content. Glucose 66-73 caspase 3 Mus musculus 137-146 25333616-5 2014 We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels. Glucose 59-66 caspase 3 Mus musculus 131-140 25400823-0 2014 MiR-378 overexpression attenuates high glucose-suppressed osteogenic differentiation through targeting CASP3 and activating PI3K/Akt signaling pathway. Glucose 39-46 caspase 3 Mus musculus 103-108 25400823-4 2014 We identified caspase-3 (CASP3) as a target of miR-378 and showed that miR-378 repressed CASP3 mRNA and protein expression under high glucose condition. Glucose 134-141 caspase 3 Mus musculus 14-23 25400823-4 2014 We identified caspase-3 (CASP3) as a target of miR-378 and showed that miR-378 repressed CASP3 mRNA and protein expression under high glucose condition. Glucose 134-141 caspase 3 Mus musculus 25-30 25400823-4 2014 We identified caspase-3 (CASP3) as a target of miR-378 and showed that miR-378 repressed CASP3 mRNA and protein expression under high glucose condition. Glucose 134-141 caspase 3 Mus musculus 89-94 25400823-7 2014 Collectively, these results suggest that miR-378 overexpression attenuates high glucose-suppressed osteogenic differentiation through targeting CASP3 and activating the PI3K/Akt pathway. Glucose 80-87 caspase 3 Mus musculus 144-149 26999661-7 2016 UDCA or 4-PBA prevented hyperglycemia-induced or high glucose (HG)-induced apoptosis in podocytes in vivo and in vitro via the inhibition of caspase-3 and caspase-12 activation. Glucose 54-61 caspase 3 Mus musculus 141-150 26653778-7 2015 Exposure of cells to 25mM glucose (diabetic-type conditions) increased cell death in response to all insults as measured by caspase 3/7 activation and Annexin V/PI flow cytometry. Glucose 26-33 caspase 3 Mus musculus 124-133 26081285-11 2015 Caspase-3/7 activity and apoptosis monitored by TUNEL assay were significantly increased in podocytes treated with high glucose. Glucose 120-127 caspase 3 Mus musculus 0-9 23945590-7 2013 Accordingly, TIS lymphomas, unlike senescence models that lack a strong SASP response, were more sensitive to blocking glucose utilization or autophagy, which led to their selective elimination through caspase-12- and caspase-3-mediated endoplasmic-reticulum-related apoptosis. Glucose 119-126 caspase 3 Mus musculus 218-227 21428210-7 2011 The results suggested that p38MAPK mediates high glucose induced osteoblast apoptosis, partly through modulating the expressions of caspase-3, bax and bcl-2. Glucose 49-56 caspase 3 Mus musculus 132-141 21813561-7 2011 We found that apoptosis was increased in both STZ-induced diabetic mice and high-glucose-treated HRVECs, which was due to increased activation of PARP, cleaved caspase3, and reduced expression of Notch1 and p-Akt. Glucose 81-88 caspase 3 Mus musculus 160-168 23531619-7 2013 Cultured podocytes exposed to high glucose concentration (HG; 25 mM) for 96 h exhibited high levels of apoptotic markers and caspase-3/7 enzymatic activity. Glucose 35-42 caspase 3 Mus musculus 125-134 20962117-7 2011 In vitro, high-glucose (25 mM) induced ROS generation and significantly increased MK4 cell apoptosis and caspase-3 activity via activation of NF-kappaB pathway, with p53 phosphorylation and nuclear translocation compared with normal glucose (5 mM). Glucose 15-22 caspase 3 Mus musculus 105-114 18973755-5 2009 High glucose also induced an increased activity of both caspase-3 and -8, which led to activation of PKR, since this was completely attenuated by the specific caspase inhibitors. Glucose 5-12 caspase 3 Mus musculus 56-72 21738719-11 2011 In vitro experiments confirmed the low-glucose induction of 661W cell death via superoxide production and activation of caspase 3, which was concomitant with a decrease of GSH content. Glucose 39-46 caspase 3 Mus musculus 120-129 19550108-3 2009 Quantitative reverse transcriptase (RT) PCR analysis revealed that the expression levels of the pro-apoptotic genes Bax and Casp3 at the blastocyst stage were increased significantly by the addition of either 25 or 55 mM glucose to the culture medium. Glucose 221-228 caspase 3 Mus musculus 124-129 18973755-8 2009 These results suggest that high glucose induces muscle atrophy through the caspase-3/-8 induced activation of PKR, leading to phosphorylation of eIF2alpha and depression of protein synthesis, together with PKR-mediated ROS production, through p38MAPK and increased protein degradation. Glucose 32-39 caspase 3 Mus musculus 75-87 16380497-6 2006 Increased extracellular glucose (30 mmol/l) rapidly stimulated generation of intracellular reactive oxygen species (ROS) through NADPH oxidase and mitochondrial pathways and led to activation of proapoptotic p38 mitogen-activated protein kinase and caspase 3 and to apoptosis of conditionally immortalized podocytes in vitro. Glucose 24-31 caspase 3 Mus musculus 249-258 17888615-7 2007 In addition, high glucose-induced apoptosis in neural progenitor cells was associated with activation of caspase-3. Glucose 18-25 caspase 3 Mus musculus 105-114 16368712-9 2006 Consistent with these results, we found evidence for the activation of unfolded protein response (UPR) marked by elevated levels of phosphorylated translation initiation factor, eIF2alpha, increased expression of chaperone proteins such as glucose-regulated protein-78 and activation of caspase-12, a cysteine proteinase in the ER, mediating caspase-3 activation and apoptosis. Glucose 240-247 caspase 3 Mus musculus 342-351 18378205-7 2008 Results show, for the first time, that high d-Glc inhibits osteoclast formation, ROS production, caspase-3 activity and migration in response to RANKL through a metabolic pathway. Glucose 44-49 caspase 3 Mus musculus 97-106 12031984-13 2002 Inhibition of caspase-3 with a specific inhibitor, Ac-DEVD-cmk, suppressed apoptosis induced by high levels of glucose. Glucose 111-118 caspase 3 Mus musculus 14-23 12031984-16 2002 Hyperglycemia-induced myocardial apoptosis is mediated, at least in part, by activation of the cytochrome c-activated caspase-3 pathway, which may be triggered by ROS derived from high levels of glucose. Glucose 195-202 caspase 3 Mus musculus 118-127