PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27110686-6 2016 In addition, we show that short-term in vivo treatment with low dosages of two molecularly distinct proteasome inhibitors celastrol and epoxomicin reverse hyperglycemia in mice with beta-cell failure by increasing insulin production and insulin sensitivity. celastrol 122-131 insulin Homo sapiens 214-221 27110686-6 2016 In addition, we show that short-term in vivo treatment with low dosages of two molecularly distinct proteasome inhibitors celastrol and epoxomicin reverse hyperglycemia in mice with beta-cell failure by increasing insulin production and insulin sensitivity. celastrol 122-131 insulin Homo sapiens 237-244 25961164-0 2015 Celastrol Protects against Antimycin A-Induced Insulin Resistance in Human Skeletal Muscle Cells. celastrol 0-9 insulin Homo sapiens 47-54 25961164-2 2015 The aim of the present study was to evaluate the functional roles of an anti-inflammatory compound, celastrol, in mitochondrial dysfunction and insulin resistance induced by antimycin A (AMA) in human skeletal muscle cells. celastrol 100-109 insulin Homo sapiens 144-151 25961164-3 2015 We found that celastrol treatment improved insulin-stimulated glucose uptake activity of AMA-treated cells, apparently via PI3K/Akt pathways, with significant enhancement of mitochondrial activities. celastrol 14-23 insulin Homo sapiens 43-50 25961164-5 2015 Celastrol significantly increased protein phosphorylation of insulin signaling cascades with amplified expression of AMPK protein and attenuated NF-kappaB and PKC theta activation in human skeletal muscle treated with AMA. celastrol 0-9 insulin Homo sapiens 61-68 25961164-6 2015 The improvement of insulin signaling pathways by celastrol was also accompanied by augmented GLUT4 protein expression. celastrol 49-58 insulin Homo sapiens 19-26 25961164-7 2015 Taken together, these results suggest that celastrol may be advocated for use as a potential therapeutic molecule to protect against mitochondrial dysfunction-induced insulin resistance in human skeletal muscle cells. celastrol 43-52 insulin Homo sapiens 167-174 30287053-0 2019 Celastrol Reverses Palmitic Acid-Induced Insulin Resistance in HepG2 Cells via Restoring the miR-223 and GLUT4 Pathway. celastrol 0-9 insulin Homo sapiens 41-48 33753246-5 2021 Celastrol reversed insulin resistance via multiple routes to protect against type 2 diabetes. celastrol 0-9 insulin Homo sapiens 19-26 25474091-3 2014 In the present study, we sought to investigate the direct effects of celastrol (potent NF-kappaB inhibitor) upon mitochondrial dysfunction-induced insulin resistance in 3T3-L1 adipocytes. celastrol 69-78 insulin Homo sapiens 147-154 30287053-1 2019 OBJECTIVES: The natural triterpenoid compound celastrol ameliorates insulin resistance (IR) in animal models, but the underlying molecular mechanism is unclear. celastrol 46-55 insulin Homo sapiens 68-75 30439604-0 2018 Celastrol antagonizes high glucose-evoked podocyte injury, inflammation and insulin resistance by restoring the HO-1-mediated autophagy pathway. celastrol 0-9 insulin Homo sapiens 76-83 30439604-8 2018 Simultaneously, the inhibitory effects of HG on insulin-triggered glucose uptake and nephrin expression were overturned after celastrol exposure. celastrol 126-135 insulin Homo sapiens 48-55 30439604-10 2018 Nevertheless, blocking the autophagy signaling by its antagonist 3-MA muted celastrol-protected against HG-evoked cell injury, inflammation and insulin resistance. celastrol 76-85 insulin Homo sapiens 144-151 30439604-13 2018 These finding suggest that celastrol may protect against HG-induced podocyte injury, inflammation and insulin resistance by restoring HO-1-mediated autophagy pathway, implying a promising therapeutic strategy against DN. celastrol 27-36 insulin Homo sapiens 102-109 29667734-8 2018 Taking together, we proved that celastrol could reverses PA-caused TLR4-MD2 activation-dependent insulin resistance via disrupting PA binding to MD2. celastrol 32-41 insulin Homo sapiens 97-104 28161417-0 2017 Celastrol attenuates mitochondrial dysfunction and inflammation in palmitate-mediated insulin resistance in C3A hepatocytes. celastrol 0-9 insulin Homo sapiens 86-93 28161417-2 2017 Celastrol, an anti-inflammatory compound from the root of Tripterygium Wilfordii has been reported to mitigate insulin resistance and inflammation in animal disease models. celastrol 0-9 insulin Homo sapiens 111-118 28161417-4 2017 The present study sought to explore the mechanistic roles of celastrol upon insulin resistance induced by palmitate in C3A human hepatocytes. celastrol 61-70 insulin Homo sapiens 76-83 28161417-8 2017 However, celastrol at the optimum concentration of 30nM was able to reverse these deleterious occasions and protected the cells from mitochondrial dysfunction and insulin resistance. celastrol 9-18 insulin Homo sapiens 163-170 28161417-9 2017 Importantly, we presented evidence for the first time that celastrol efficiently prevented palmitate-induced insulin resistance in hepatocytes at least, via improved mitochondrial functions and insulin signaling pathways. celastrol 59-68 insulin Homo sapiens 109-116 28161417-9 2017 Importantly, we presented evidence for the first time that celastrol efficiently prevented palmitate-induced insulin resistance in hepatocytes at least, via improved mitochondrial functions and insulin signaling pathways. celastrol 59-68 insulin Homo sapiens 194-201 29667734-0 2018 Celastrol reverses palmitic acid (PA)-caused TLR4-MD2 activation-dependent insulin resistance via disrupting MD2-related cellular binding to PA. celastrol 0-9 insulin Homo sapiens 75-82 29667734-4 2018 As celastrol is reported to directly target MD2, we thought disrupting the binding between FFAs and MD2 might be one of the ways for celastrol to inhibit FFAs-caused inflammation and insulin resistance. celastrol 133-142 insulin Homo sapiens 183-190 29667734-5 2018 In this study, we found evidence to support our hypothesis: celastrol could reverse PA-caused TLR4/MD2 activation-dependent insulin resistance, as determined by glucose-lowering ability, cellular glucose uptake, insulin action-related proteins and TLR4/MD2/NF-kappaB activation. celastrol 60-69 insulin Homo sapiens 124-131 29667734-5 2018 In this study, we found evidence to support our hypothesis: celastrol could reverse PA-caused TLR4/MD2 activation-dependent insulin resistance, as determined by glucose-lowering ability, cellular glucose uptake, insulin action-related proteins and TLR4/MD2/NF-kappaB activation. celastrol 60-69 insulin Homo sapiens 212-219