PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32388247-6 2020 Significant reduction in ROS and inflammatory cytokine production (i.e., IL-6, IL-1beta) was observed, including a reduction in ERK1/2 phosphorylation in neutrophils stimulated with LPS and fMLP in the presence of Fbln7-C compared to untreated controls. ros 25-28 interleukin 6 Homo sapiens 73-77 33388592-0 2021 SO2 derivatives induce dysfunction in human trophoblasts via inhibiting ROS/IL-6/STAT3 pathway. ros 72-75 interleukin 6 Homo sapiens 76-80 33388592-15 2021 Decreased ROS/IL-6/STAT3 levels play a role in inhibited cell viability, cell cycle arrest, apoptosis and defective motility. ros 10-13 interleukin 6 Homo sapiens 14-18 33146789-10 2021 In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy. ros 23-26 interleukin 6 Homo sapiens 171-175 32463794-2 2020 Metformin is capable of suppressing one of the molecular triggers of the proinflammatory and prothrombotic processes of urban PM air pollution, namely the mitochondrial ROS/Ca2+ release-activated Ca2+ channels (CRAC)/IL-6 cascade. ros 169-172 interleukin 6 Homo sapiens 217-221 32463794-3 2020 Given the linkage between mitochondrial functionality, ion channels, and inflamm-aging, the ability of metformin to target mitochondrial electron transport and prevent ROS/CRAC-mediated IL-6 release might illuminate new therapeutic avenues to quell the raging of the cytokine and thrombotic-like storms that are the leading causes of COVID-19 morbidity and mortality in older people. ros 168-171 interleukin 6 Homo sapiens 186-190 30262241-0 2020 Corrigendum to "CO-releasing molecules CORM2 attenuates angiotensin II-induced human aortic smooth muscle cell migration through inhibition of ROS/IL-6 generation and matrix metalloproteinases-9 expression" [Redox Biol. ros 143-146 interleukin 6 Homo sapiens 147-151 30240585-5 2019 IL-6 trans-signaling activation caused a significant increase in STAT3 phosphorylation, expression of adhesion molecules, ROS production and apoptosis in HRECs whereas a significant decrease in mitochondrial membrane potential and NO production was observed in IL-6 trans-signaling activated cells. ros 122-125 interleukin 6 Homo sapiens 0-4 31252067-0 2019 Cadmium exposure induces interleukin-6 production via ROS-dependent activation of the ERK1/2 but independent of JNK signaling pathway in human placental JEG-3 trophoblast cells. ros 54-57 interleukin 6 Homo sapiens 25-38 31252067-10 2019 These data indicate that Cd induces IL-6 production in trophoblast cells through a ROS-dependent activation of ERK1/2. ros 83-86 interleukin 6 Homo sapiens 36-40 31171361-0 2019 miR-374a/Myc axis modulates iron overload-induced production of ROS and the activation of hepatic stellate cells via TGF-beta1 and IL-6. ros 64-67 interleukin 6 Homo sapiens 131-135 31171361-4 2019 miR-374a could target Myc, a co-transcription factor of both TGF-beta1 and IL-6, to negatively regulate Myc expression; FAC stimulation significantly suppressed miR-374a expression, whereas the suppressive effect of FAC stimulation on miR-374a expression could be reversed by ROS inhibitor NAC, indicating that miR-374a could be modulated by iron overload-induced ROS. ros 276-279 interleukin 6 Homo sapiens 75-79 31171361-4 2019 miR-374a could target Myc, a co-transcription factor of both TGF-beta1 and IL-6, to negatively regulate Myc expression; FAC stimulation significantly suppressed miR-374a expression, whereas the suppressive effect of FAC stimulation on miR-374a expression could be reversed by ROS inhibitor NAC, indicating that miR-374a could be modulated by iron overload-induced ROS. ros 364-367 interleukin 6 Homo sapiens 75-79 31171361-7 2019 In conclusion, we demonstrate a novel mechanism of miR-374a/Myc axis modulating iron overload-induced production of ROS and the activation of HSCs via TGF-beta1 and IL-6. ros 116-119 interleukin 6 Homo sapiens 165-169 30718954-13 2019 The PSDT mediated by TOI_HNPs induced generation of intracellular ROS and downregulated the expression of HIF-1alpha and IL-6 in SKOV3 cells. ros 66-69 interleukin 6 Homo sapiens 121-125 28478304-3 2018 In turn, increased amounts of ROS/RNS and pro-inflammatory cytokines TNFalpha, IL-1beta, IL-6 led to the irreversible DNA damage, persistent DDR activation, proliferation inhibition, reduction in cell growth and immune impairment. ros 30-33 interleukin 6 Homo sapiens 89-93 30029111-9 2018 This enhanced ROS inflicted severe inflammation and subsequent fibrosis, evident from increased pro-inflammatory-cum-fibrogenic cytokines generation (IL-1beta, IL-2, IL-6, TNF-alpha and TGF-beta). ros 14-17 interleukin 6 Homo sapiens 166-170 28812210-14 2018 In conclusion, IL-34-stimulated THP-1 can produce higher levels of ROS, which promoted IL-6 secretion and up-regulated Th17 cells. ros 67-70 interleukin 6 Homo sapiens 87-91 28600879-10 2018 After N-acetyl cysteine treatment ROS level was partly abolished providing additional enhancement of IL-6 and suppression of IL-8 and VEGF production. ros 34-37 interleukin 6 Homo sapiens 101-105 28946937-10 2017 Our data also suggest that secreted IL-6 regulates CLB2.0-induced MUC5AC and MUC1 expression via ROS-mediated downregulation of claudin-1 expression to maintain mucus homeostasis in the airway. ros 97-100 interleukin 6 Homo sapiens 36-40 28946937-5 2017 CLB2.0-induced IL-6 secretion was mediated by ROS. ros 46-49 interleukin 6 Homo sapiens 15-19 28292711-0 2017 CO-releasing molecules CORM2 attenuates angiotensin II-induced human aortic smooth muscle cell migration through inhibition of ROS/IL-6 generation and matrix metalloproteinases-9 expression. ros 127-130 interleukin 6 Homo sapiens 131-135 28946937-6 2017 The ROS scavenger N-acetylcysteine inhibited CLB2.0-induced IL-6 secretion, thereby decreasing the CLB2.0-induced MUC5AC expression, whereas CLB2.0-induced MUC1 expression increased. ros 4-7 interleukin 6 Homo sapiens 60-64 27995612-8 2017 IL-15 and IL-6 expression are stimulated by IFN-y and correlate with ROS levels in BM mononuclear cells. ros 69-72 interleukin 6 Homo sapiens 10-14 27543848-7 2016 Inhibition of TLR2 or TLR4 reduced IL-6 production as well as expression of these other factors, and agents inhibiting ROS, MAPKs, NF-kappaB and JAK reduced IL-6 production. ros 119-122 interleukin 6 Homo sapiens 157-161 27427241-7 2016 The most potent metals, Cd(2+), Zn(2+) and As(3+) induced highest levels of oxidative activity, and ROS appeared to be central in their CXCL8 and IL-6 responses. ros 100-103 interleukin 6 Homo sapiens 146-150 27167341-10 2016 Taken together, SDF-1alpha and IL-6 secreted from PSC induced PDAC cell proliferation via Nrf2-activated metabolic reprogramming and ROS detoxification. ros 133-136 interleukin 6 Homo sapiens 31-35 27050175-2 2016 It is based on evidence that a continuous long-term exposure to oral bacteremia and bacterial toxins induces inflammatory immune response after immune evasion releases growth factors such as FGF, EGF, TGF-Beta, free radicals such as ROS and NOS, cytokines such as TNFAlfa, IL-1 Beta, IL-6; and matrix metalloproteinase such as MMP-9. ros 233-236 interleukin 6 Homo sapiens 284-288 26794444-4 2016 Here, we showed that the repression of SOCS3 and sustained activation of IL-6/STAT3 pathway in HBV-producing HCC cells were caused by HBV-induced mitochondrial ROS accumulation. ros 160-163 interleukin 6 Homo sapiens 73-77 26794444-9 2016 Taken together, our data show that HBV-induced mitochondrial ROS production represses SOCS3 expression through Snail-mediated epigenetic silencing, leading to the sustained activation of IL-6/STAT3 pathway and ultimately contributing to hepatocarcinogenesis. ros 61-64 interleukin 6 Homo sapiens 187-191 25857619-13 2015 Exposure to lipopolysaccharide induced a dramatic increase in both NF-kappaB activation and IL-6 expression in both wt and mdx myotubes, suggesting that the altered IL-6 gene expression after electrical stimulation in mdx muscle cells is due to dysregulation of Ca2+ release and ROS production, both of which impinge on NF-kappaB signaling. ros 279-282 interleukin 6 Homo sapiens 165-169 26402162-8 2015 RESULTS: IL6 induced ROS and carbonyl content in all 3 cell lines (all P<0.001). ros 21-24 interleukin 6 Homo sapiens 9-12 26402162-10 2015 Selenite decreases the IL6-induced ROS and carbonyl content, while enhances Gpx and Trx activities. ros 35-38 interleukin 6 Homo sapiens 23-26 24992685-5 2014 RESULTS: In response to treatment with either TNF-alpha or IL-6 (0-100 ng/ml, 0-24 hrs), our studies consistently demonstrated significant dose- and time-dependent decreases in the expression of all interendothelial junction proteins examined, in parallel with dose- and time-dependent increases in ROS generation and HBMvEC permeability. ros 299-302 interleukin 6 Homo sapiens 59-63 23087143-10 2012 Meanwhile, EGCG reduced Ang II- and IL-6-stimulated generation of ROS in macrophages. ros 66-69 interleukin 6 Homo sapiens 36-40 23087143-11 2012 CONCLUSION: EGCG is able to inhibit Ang II- and IL-6-stimulated CRP expression in macrophages to produce an anti-inflammation by interfering with ROS generation. ros 146-149 interleukin 6 Homo sapiens 48-52 21732177-6 2011 Further, IL-6 treatment led to decreased mitochondrial membrane potential, decreased cellular ATP production, and increased intracellular ROS levels. ros 138-141 interleukin 6 Homo sapiens 9-13 20145198-6 2010 Moreover, the addition of NAC, a scavenger of ROS, abrogated the rVpr-induced formation of OxPC, the phosphorylation of C/EBP-beta, a substrate of MAPK, and IL-6 production. ros 46-49 interleukin 6 Homo sapiens 157-161 19892012-11 2010 These results demonstrate that CSE-induced ROS generation was mediated through the TLR4/MyD88/TRAF6/c-Src/NADPH oxidase pathway, in turn initiated the activation of MAPKs and NF-kappaB, and ultimately induced COX-2/PGE(2)/IL-6-dependent airway inflammation. ros 43-46 interleukin 6 Homo sapiens 222-226 19815061-7 2010 ROS also triggered pro-inflammatory responses in cultured T98G cells, which were demonstrated by the increased gene expression and protein levels of IL-6 and IL-8. ros 0-3 interleukin 6 Homo sapiens 149-153 10321921-5 1999 Further studies have shown that IL-6, c-fos, and Bcl-2 are all elevated in Paget"s disease--all of these factors can be activated by virally induced ROS. ros 149-152 interleukin 6 Homo sapiens 32-36 17981627-4 2008 Inflammatory response after stroke suggests that cytokines (TNF-alpha, IL-1alpha/beta, IL-6), affect the phospholipid metabolism and subsequent production of eicosanoids, ceramide, and ROS that may potentiate brain injury. ros 185-188 interleukin 6 Homo sapiens 87-91 9788898-5 1998 ROS/RNS appear to play a variety of roles that lead to changes in expression of genes such as interleukin-6 and intercellular adhesion molecule 1. ros 0-3 interleukin 6 Homo sapiens 94-107 34930286-8 2021 Besides, the Lipo-RSV could scavenge ROS and inhibit the NF-kappaB signal and inflammasomes, thereby reducing the pro-inflammatory cytokines IL-1beta, IL-6, and TNF-alpha. ros 37-40 interleukin 6 Homo sapiens 151-155 35218740-0 2022 Carbon monoxide releasing molecule-2 attenuates angiotensin II-induced IL-6/Jak2/Stat3-associated inflammation by inhibiting NADPH oxidase- and mitochondria-derived ROS in human aortic smooth muscle cells. ros 165-168 interleukin 6 Homo sapiens 71-75 35628356-8 2022 These results suggested that inhibiting a vicious cycle of the ROS/STAT3/IL-6 axis by ASC-J9 may represent a potential therapeutic approach to suppress cell proliferation and ECM production in KFs. ros 63-66 interleukin 6 Homo sapiens 73-77 35460571-6 2022 Cytokines, such as TNF-alpha, INF-gamma, IL-6, and IL-13, were upregulated in infected cells sparking mitochondrial ROS production and change in electron transport chain complexes. ros 116-119 interleukin 6 Homo sapiens 41-45 35218740-6 2022 The results showed that Ang II induced inflammatory responses of HASMCs via NADPH oxidase- and mitochondria-derived ROS/NF-kappaB/IL-6/Jak2/Stat3 pathway which was attenuated by the pretreatment with CORM-2. ros 116-119 interleukin 6 Homo sapiens 130-134 35218740-10 2022 Taken together, the present study indicates that CORM-2-induced Nrf2/HO-1 alleviates IL-6/Jak2/Stat3-mediated inflammatory responses to Ang II by inhibiting NADPH oxidase- and mitochondria-derived ROS, suggesting that CORM-2 is a promising pharmacologic candidate to reverse the pathological changes involved in the inflammation of vessel wall for the prevention and treatment of AAA. ros 197-200 interleukin 6 Homo sapiens 85-89