PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35462098-5 2022 This study found that in HK-2 cells, with the prolongation of high concentration glucose stimulation, the expression level of TFEB showed a trend of first increasing and then decreasing; and nuclear translocation of TFEB expression occurred within 24 h. In high-glucose environment, the expression of pyroptosis-related proteins gradually increased over time, while the expression of anti-oxidative stress proteins superoxide dismutase2(SOD2)and NAD(P)H: quinone oxidoreductase 1(NQO1) showed a trend of first increasing and then decreasing. Glucose 81-88 superoxide dismutase 2 Homo sapiens 437-441 35462098-5 2022 This study found that in HK-2 cells, with the prolongation of high concentration glucose stimulation, the expression level of TFEB showed a trend of first increasing and then decreasing; and nuclear translocation of TFEB expression occurred within 24 h. In high-glucose environment, the expression of pyroptosis-related proteins gradually increased over time, while the expression of anti-oxidative stress proteins superoxide dismutase2(SOD2)and NAD(P)H: quinone oxidoreductase 1(NQO1) showed a trend of first increasing and then decreasing. Glucose 262-269 superoxide dismutase 2 Homo sapiens 437-441 35462098-9 2022 The research results suggested that in HK-2 cells in the high glucose environment, TFEB may affect the pyroptosis by regulating the expression of antioxidant enzymes SOD2 and NQO1, which provides a new therapeutic idea for the treatment of diabetic nephropathy. Glucose 62-69 superoxide dismutase 2 Homo sapiens 166-170 31820335-12 2020 Further, lutein protected high glucose-mediated down-regulation of a redox-sensitive transcription factor, Nrf2, and antioxidant enzymes, SOD2, HO-1, and catalase. Glucose 31-38 superoxide dismutase 2 Homo sapiens 138-142 35631465-8 2022 PDGF-C diminished the oxidative stress induced by high glucose, increasing SOD2 expression and SOD activity, and modulating the Keap1 expression gene. Glucose 55-62 superoxide dismutase 2 Homo sapiens 75-79 33090591-4 2020 Cells exposed to high glucose showed lower NF-kappaB and SOD2 methylation levels, increased NF-kappaB and reduced SOD2 expression compared to normal glucose cells. Glucose 22-29 superoxide dismutase 2 Homo sapiens 114-118 35204196-5 2022 SOD2 overexpression increases glucose transporter GLUT-1 and glucose uptake. Glucose 30-37 superoxide dismutase 2 Homo sapiens 0-4 35204196-5 2022 SOD2 overexpression increases glucose transporter GLUT-1 and glucose uptake. Glucose 61-68 superoxide dismutase 2 Homo sapiens 0-4 33090591-4 2020 Cells exposed to high glucose showed lower NF-kappaB and SOD2 methylation levels, increased NF-kappaB and reduced SOD2 expression compared to normal glucose cells. Glucose 22-29 superoxide dismutase 2 Homo sapiens 57-61 26052839-3 2016 Here, we reported that high glucose elevated the level of p-Akt to attenuate endogenous FoxO1 bioactivities in MCs, accompanied with decreases in the mRNA expressions of catalase (CAT) and superoxide dismutase 2 (SOD2). Glucose 28-35 superoxide dismutase 2 Homo sapiens 189-211 32271403-13 2020 Besides, high glucose promoted the expression of 8-OH, and inhibited SOD1, SOD2, and CAT mRNA expressions, resulting in the up-regulated ROS level of CHs. Glucose 14-21 superoxide dismutase 2 Homo sapiens 75-79 31018749-4 2019 Methods and Results Cord-blood-derived CD 34+ stem cells exposed to high glucose displayed increased reactive oxygen species production, overexpression of p66shc gene, and downregulation of antioxidant genes catalase and manganese superoxide dismutase when compared with normoglycemic cells. Glucose 73-80 superoxide dismutase 2 Homo sapiens 221-251 30628023-10 2019 High-glucose treatment for 24 h down-regulated the protein expression of redox-specific transcription factors Nrf-2, XBP-1 and NF-kappaB, and subsequently decreased the expression of HO-1, catalase, and SOD-2. Glucose 5-12 superoxide dismutase 2 Homo sapiens 203-208 27411103-5 2016 Diabetic Glc also promoted beta-catenin nuclear localization and the formation of a complex with FOXO3a that localized to the promoters of Sod2, p21(cip1), and potentially p27(kip1). Glucose 9-12 superoxide dismutase 2 Homo sapiens 139-143 30217947-9 2018 Mechanism study revealed that HDAC2 bound to the promoter of MnSOD and repressed the expression of MnSOD by regulating the level of acetylated H3K9 and H3K27, which led to the promotion of oxidative stress and contributed to the function of HDAC2 in ECs under high glucose condition. Glucose 265-272 superoxide dismutase 2 Homo sapiens 61-66 30217947-9 2018 Mechanism study revealed that HDAC2 bound to the promoter of MnSOD and repressed the expression of MnSOD by regulating the level of acetylated H3K9 and H3K27, which led to the promotion of oxidative stress and contributed to the function of HDAC2 in ECs under high glucose condition. Glucose 265-272 superoxide dismutase 2 Homo sapiens 99-104 30217947-10 2018 Altogether, our evidence demonstrated that HDAC2-MnSOD signaling was critical in oxidative stress and proliferation as well as the survival of ECs under high glucose condition. Glucose 158-165 superoxide dismutase 2 Homo sapiens 49-54 30037352-4 2018 We sought to explore the mechanism underlying defective SOD2 antioxidant response in HUVECs during exposures to constant high glucose and oscillating glucose (as glucose variability model, GV) and the role of miR-21 in increasing the susceptibility to oxidative stress by disrupting reactive oxygen species (ROS) homeostasis. Glucose 150-157 superoxide dismutase 2 Homo sapiens 56-60 30037352-4 2018 We sought to explore the mechanism underlying defective SOD2 antioxidant response in HUVECs during exposures to constant high glucose and oscillating glucose (as glucose variability model, GV) and the role of miR-21 in increasing the susceptibility to oxidative stress by disrupting reactive oxygen species (ROS) homeostasis. Glucose 150-157 superoxide dismutase 2 Homo sapiens 56-60 28552711-0 2017 ALA16VAL-MnSOD gene polymorphism and stroke: Association with dyslipidemia and glucose levels. Glucose 79-86 superoxide dismutase 2 Homo sapiens 9-14 28552711-2 2017 The ALA16VAL-MnSOD gene single nucleotide polymorphism (SNP) has shown to modulate risk factors of several metabolic and vascular diseases, such as blood glucose (GLU) and lipid levels. Glucose 163-166 superoxide dismutase 2 Homo sapiens 13-18 28552711-9 2017 Furthermore, we propose that the Ala16Val-MnSOD SNPs may contribute to hypercholesterolemia and higher GLU levels, increasing the risk to neurovascular events that may lead to stroke. Glucose 103-106 superoxide dismutase 2 Homo sapiens 42-47 27258818-9 2016 Minor allele frequencies (C allele) of the MnSOD Val16Ala polymorphism (rs4880) in the normal glucose tolerance (NGT) and the T2D groups were 13.57% and 14.50%, respectively. Glucose 94-101 superoxide dismutase 2 Homo sapiens 43-48 27137793-1 2016 BACKGROUND: Intracellular antioxidant response to high glucose is mediated by Cu/Mn-superoxide dismutases (SOD-1/SOD-2), catalase (CAT) and glutathione peroxidases (GPx), particularly glutathione peroxidase-1 (GPx-1). Glucose 55-62 superoxide dismutase 2 Homo sapiens 113-118 26052839-3 2016 Here, we reported that high glucose elevated the level of p-Akt to attenuate endogenous FoxO1 bioactivities in MCs, accompanied with decreases in the mRNA expressions of catalase (CAT) and superoxide dismutase 2 (SOD2). Glucose 28-35 superoxide dismutase 2 Homo sapiens 213-217 25755722-8 2015 Further, mechanistic study showed that SIRT3 repression results in SOD2 acetylation, leading to SOD2 inactivation, which enhanced high glucose-induced oxidative stress in endothelial cells. Glucose 135-142 superoxide dismutase 2 Homo sapiens 67-71 26652025-16 2015 Delivery of superoxide dismutase (SOD2) using MSCs as a gene delivery vehicle reduces inflammation and improves glucose tolerance in vivo. Glucose 112-119 superoxide dismutase 2 Homo sapiens 34-38 25755722-8 2015 Further, mechanistic study showed that SIRT3 repression results in SOD2 acetylation, leading to SOD2 inactivation, which enhanced high glucose-induced oxidative stress in endothelial cells. Glucose 135-142 superoxide dismutase 2 Homo sapiens 96-100 23590434-7 2014 The periodic fluctuation in MnSOD activity during the cell cycle inversely correlates with cellular superoxide levels as well as glucose and oxygen consumption. Glucose 129-136 superoxide dismutase 2 Homo sapiens 28-33 23590434-8 2014 Based on an inverse correlation between MnSOD activity and glucose consumption during the cell cycle, it is proposed that MnSOD is a central molecular player for the "Warburg effect." Glucose 59-66 superoxide dismutase 2 Homo sapiens 40-45 23590434-8 2014 Based on an inverse correlation between MnSOD activity and glucose consumption during the cell cycle, it is proposed that MnSOD is a central molecular player for the "Warburg effect." Glucose 59-66 superoxide dismutase 2 Homo sapiens 122-127 23494737-7 2013 We have demonstrated that overexpression of SIRT3 under high glucose conditions reduces FOXO1 acetylation, suggesting that deacetylation of FOXO1 by SIRT3 elevates the expression of the FOXO1 target genes, catalase, and manganese superoxide dismutase (MnSOD) while decreasing senescence phenotypes. Glucose 61-68 superoxide dismutase 2 Homo sapiens 220-250 24275138-8 2014 Downregulation of MnSOD and LDHA accompanied the toxicity induced by hypoxia and CoCl2 in 5mM glucose, and these changes were enhanced by oxamate or 2-deoxyglucose. Glucose 94-101 superoxide dismutase 2 Homo sapiens 18-23 24732311-8 2014 The MnSOD expression was positively correlated with fasting plasma glucose and total cholesterol levels both at the transcript level (r = 0.4, P <0.05 for both correlations) and at the protein level (r = 0.3 and r = 0.4, respectively, P <0.05). Glucose 67-74 superoxide dismutase 2 Homo sapiens 4-9 23494737-7 2013 We have demonstrated that overexpression of SIRT3 under high glucose conditions reduces FOXO1 acetylation, suggesting that deacetylation of FOXO1 by SIRT3 elevates the expression of the FOXO1 target genes, catalase, and manganese superoxide dismutase (MnSOD) while decreasing senescence phenotypes. Glucose 61-68 superoxide dismutase 2 Homo sapiens 252-257 23384600-8 2013 High glucose also enhanced podocyte expression of MnSOD and catalase. Glucose 5-12 superoxide dismutase 2 Homo sapiens 50-55 23805295-8 2013 Anti-oxidant defense mechanisms of the lens epithelial cells were diminished as evidenced from loss of mitochondrial membrane integrity and lowered MnSOD after 72 h treatment with high glucose. Glucose 185-192 superoxide dismutase 2 Homo sapiens 148-153 22710435-2 2012 This study investigates the hypothesis that manganese superoxide dismutase (MnSOD) regulates cellular redox flux and glucose consumption during the cell cycle. Glucose 117-124 superoxide dismutase 2 Homo sapiens 44-74 22710435-2 2012 This study investigates the hypothesis that manganese superoxide dismutase (MnSOD) regulates cellular redox flux and glucose consumption during the cell cycle. Glucose 117-124 superoxide dismutase 2 Homo sapiens 76-81 22710435-3 2012 A direct correlation was observed between glucose consumption and percentage of S-phase cells in MnSOD wild-type fibroblasts, which was absent in MnSOD homozygous knockout fibroblasts. Glucose 42-49 superoxide dismutase 2 Homo sapiens 97-102 21053390-0 2011 Glabridin, a phytoestrogen from licorice root, up-regulates manganese superoxide dismutase, catalase and paraoxonase 2 under glucose stress. Glucose 125-132 superoxide dismutase 2 Homo sapiens 60-90 21354306-13 2011 Thus, overexpression of both IRS-1 and IRS-2 induces complete resistance to glucose-induced caspase-3 activation via PI3-kinase mediated BAD phosphorylation and MnSOD expression independent of FoxO1. Glucose 76-83 superoxide dismutase 2 Homo sapiens 161-166 17916951-2 2007 Manganese (Mn), the key component of the Mitochondrial antioxidant (MnSOD), plays a key role in the superoxide uncoupling protein 2 (UCP-2) pathway in inhibiting of glucose-stimulated insulin secretion (GSIS). Glucose 165-172 superoxide dismutase 2 Homo sapiens 68-73 20514411-5 2010 We observed that CuZnSOD and MnSOD overexpression prevents metabolic stress-induced necrosis and HMGB1 release by inhibiting mitochondrial ROS and intracellular O2- production in response to glucose depletion in two dimensional cell culture. Glucose 191-198 superoxide dismutase 2 Homo sapiens 29-34 20088710-4 2010 The effect of MnSOD mimic, MnTBAP or over-expression of MnSOD on glucose-induced alterations in mtDNA homeostasis and its functional consequence was determined in retinal endothelial cells. Glucose 65-72 superoxide dismutase 2 Homo sapiens 56-61 20088710-8 2010 Thus, the protection of mtDNA from glucose-induced oxidative damage is one of the plausible mechanisms by which MnSOD ameliorates the development of diabetic retinopathy. Glucose 35-42 superoxide dismutase 2 Homo sapiens 112-117 17184177-2 2007 In endothelial cells, high-glucose treatment increases mitochondrial ROS and normalization of the ROS production by inhibitors of mitochondrial metabolism, or by overexpression of UCP-1 or MnSOD, prevents glucose-induced activation of PKC, formation of AGE, and accumulation of sorbitol, all of which are believed to be the main molecular mechanisms of diabetic complications. Glucose 27-34 superoxide dismutase 2 Homo sapiens 189-194 17184177-2 2007 In endothelial cells, high-glucose treatment increases mitochondrial ROS and normalization of the ROS production by inhibitors of mitochondrial metabolism, or by overexpression of UCP-1 or MnSOD, prevents glucose-induced activation of PKC, formation of AGE, and accumulation of sorbitol, all of which are believed to be the main molecular mechanisms of diabetic complications. Glucose 205-212 superoxide dismutase 2 Homo sapiens 189-194 12448827-9 2002 In both cell lines, high glucose resulted in an increase of total SOD activity, as a consequence of the increase in Cu,Zn-SOD activity. Glucose 25-32 superoxide dismutase 2 Homo sapiens 66-69 11555836-2 2001 Manganese (Mn)(2+)-dependent superoxide dismutase (SOD-2) is primarily responsible for metabolism of superoxide produced in mitochondria by respiratory chain activity during aerobic metabolism of glucose and other substrates. Glucose 196-203 superoxide dismutase 2 Homo sapiens 51-56 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 60-67 superoxide dismutase 2 Homo sapiens 23-28 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 60-67 superoxide dismutase 2 Homo sapiens 30-38 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 60-67 superoxide dismutase 2 Homo sapiens 30-35 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 60-67 superoxide dismutase 2 Homo sapiens 30-35 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 222-229 superoxide dismutase 2 Homo sapiens 23-28 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 222-229 superoxide dismutase 2 Homo sapiens 30-38 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 222-229 superoxide dismutase 2 Homo sapiens 30-35 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 222-229 superoxide dismutase 2 Homo sapiens 30-35 11555836-11 2001 These results support a role for increased cellular superoxide production derived from NAD(P)H oxidase activity in the stimulation of collagen accumulation induced in MC by high glucose and demonstrate that an increase in mitochondrial SOD-2 activity suppresses this response. Glucose 178-185 superoxide dismutase 2 Homo sapiens 236-241