ZHANG Rong, YANG Xinquan, XIONG Ting, TANG Shan, AI Keqing, ZHONG Hongyan, MAO Yongqing, WANG Daxin. GKT137831 alleviates atorvastatin-induced decreased glucose uptake of skeletal muscle by suppressing reactive oxygen species level[J]. Journal of Clinical Medicine in Practice, 2019, 23(10): 53-57. DOI: 10.7619/jcmp.201910015
Citation: ZHANG Rong, YANG Xinquan, XIONG Ting, TANG Shan, AI Keqing, ZHONG Hongyan, MAO Yongqing, WANG Daxin. GKT137831 alleviates atorvastatin-induced decreased glucose uptake of skeletal muscle by suppressing reactive oxygen species level[J]. Journal of Clinical Medicine in Practice, 2019, 23(10): 53-57. DOI: 10.7619/jcmp.201910015

GKT137831 alleviates atorvastatin-induced decreased glucose uptake of skeletal muscle by suppressing reactive oxygen species level

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  • Received Date: March 15, 2019
  • Accepted Date: April 16, 2019
  • Available Online: February 22, 2021
  • Published Date: May 27, 2019
  •   Objective  To explore the mechanism of GKT137831 on protecting skeletal muscle cells by atorvastatin intervention.
      Methods  Atorvastatin was used to intervene C2C12 cells in skeletal muscle for 48 hours. CCK-8 method was used to analyze the effect of atorvastatin on survival rate of skeletal muscle cells. Western blot was used to detect the expression of NADPH Oxidase 4 (Nox4) after atorvastatin intervention. Flow cytometry was used to detect the effect of atorvastatin on glucose uptake and reactive oxygen species (ROS) in skeletal muscle cells. Co-culture of Nox4 inhibitor GKT137831 was used to analyze the effect of atorvastatin on cellular glucose uptake and ROS level.
      Results  After intervention with atorvastatin on skeletal muscle cells for 48 hours, the glucose uptake ability of C2C12 cells decreased and ROS increased. GKT137831 could alleviate the decrease of glucose uptake and the increase of ROS. CCK-8 results showed that atorvastatin had no effect on cell viability after 48 hours of intervention. Nox4 expression increased after atorvastatin intervention on C2C12 skeletal muscle cells.
      Conclusion  GKT137831 can alleviate atorvastatin-induced decreased glucose uptake of skeletal muscle by suppressing reactive oxygen species level.
  • [1]
    ]Betteridge D J, Carmena R. The diabetogenic action of statins-mechanisms and clinical implications[J]. Nat Rev Endocrinol, 2016, 12(2): 99-110. https://www.cnki.com.cn/Article/CJFDTOTAL-ZHAY201401013.htm
    [2]
    Coleman C I, Reinhart K, Kluger J, et al. The effect of statins on the development of new-onset type 2 diabetes: a meta-analysis of randomized controlled trials[J]. Curr Med Res Opin, 2008, 24(5): 1359-1362. doi: 10.1185/030079908X292029
    [3]
    Sattar N, Preiss D, Murray H M, et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials[J]. Lancet, 2010, 375(9716): 735-742. doi: 10.1016/S0140-6736(09)61965-6
    [4]
    Preiss D, Seshasai S R, Welsh P, et al. Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: a meta-analysis[J]. JAMA, 2011, 305(24): 2556-2264. doi: 10.1001/jama.2011.860
    [5]
    Dormuth C R, Filion K B, Paterson J M, et al. Higher potency statins and the risk of new diabetes: multicentre, observational study of administrative databases[J]. BMJ, 2014, 348: g3244-g3256. doi: 10.1136/bmj.g3244
    [6]
    Sun Q A, Hess D T, Nogueira L, et al. Oxygen-coupled redox regulation of the skeletal muscle ryanodine receptor-Ca2+ release channel by NADPH oxidase 4[J]. Proc Natl Acad Sci, 2011, 108(38): 16098-16103. doi: 10.1073/pnas.1109546108
    [7]
    Handayaningsih A E, Iguchi G, Fukuoka H, et al. Reactive oxygen species play an essential role in IGF-Ⅰ signaling and IGF-Ⅰ-induced myocyte hypertrophy in C2C12 myocytes[J]. Endocrinology, 2011, 152(3): 912-921. doi: 10.1210/en.2010-0981
    [8]
    Li Q, Su J, Jin S J, et al. Argirein alleviates vascular endothelial insulin resistance through suppressing the activation of Nox4-dependent O2-production in diabetic rats[J]. Free Radic Biol Med, 2018, 121: 169-179. doi: 10.1016/j.freeradbiomed.2018.04.573
    [9]
    Gan Z, Fu T, Kelly D P, et al. Skeletal muscle mitochondrial remodeling in exercise and diseases[J]. Cell Res, 2018, 28(10): 969-980. http://qikan.cqvip.com/Qikan/Article/Detail?id=676732339
    [10]
    Godoy J C, Niesman I R, Busija A R, et al. Atorvastatin, but not pravastatin, inhibits cardiac Akt/mTOR signaling and disturbs mitochondrial ultrastructure in cardiac myocytes[J]. FASEB J, 2019, 33(1): 1209-1225. doi: 10.1096/fj.201800876R
    [11]
    Echaniz-Laguna A, Mohr M, Tranchant C. Neuromuscular symptoms and elevated creatine kinase after statin withdrawal[J]. N Engl J Med, 2010, 62(6): 564-575. http://europepmc.org/abstract/med/20147729
    [12]
    Sun B, Zhong Z, Wang F, et al. Atorvastatin impaired glucose metabolism in C2C12 cells partly via inhibiting cholesterol-dependent glucose transporter 4 translocation[J]. Biochem Pharmacol, 2018, 150: 108-119. doi: 10.1016/j.bcp.2018.01.021
    [13]
    王朝阳. 大剂量降脂药物在缺血性卒中患者中的应用效果[J]. 实用临床医药杂志, 2015, 199(3): 117-118. doi: 10.7619/jcmp.201503037
    [14]
    王娜, 祁学章, 舒志刚, 等. 自发性脑出血患者的他汀应用和脑微出血情况分析[J]. 实用临床医药杂志, 2018, 22(7): 19-22. doi: 10.7619/jcmp.201807005
    [15]
    Sasaki J, Iwashita M, Kono S. Statins: beneficial or adverse for glucose metabolism[J]. J Atheroscler Thromb, 2006, 13(3): 123-129. doi: 10.5551/jat.13.123
    [16]
    Banach M, Malodobra-Mazur M, Gluba A, et al. Statin therapy and new-onset diabetes: molecular mechanisms and clinical relevance[J]. Curr Pharm Des, 2013, 19(27): 4904-4912. doi: 10.2174/1381612811319270014
    [17]
    Mita T, Watada H, Nakayama S, et al. Preferable effect of pravastatin compared to atorvastatin on beta cell function in Japanese early-state type 2 diabetes with hypercholesterolemia[J]. Endocr J, 2007, 54(3): 441-447. http://www.ncbi.nlm.nih.gov/pubmed/17457013
    [18]
    Jiang J X, Chen X, Serizawa N, et al. Liver fibrosis and hepatocyte apoptosis are attenuated by GKT137831, a novel NOX4/NOX1 inhibitor in vivo[J]. Free Radic Biol Med, 2012, 53(2): 289-296. http://pubmedcentralcanada.ca/pmcc/articles/PMC3392471/
    [19]
    Watson A M, Li J, Samijono D, et al. Quinapril treatment abolishes diabetes-associated atherosclerosis in RAGE/apolipoprotein E double knockout mice[J]. Atherosclerosis, 2014, 235(2): 444-458. http://www.ncbi.nlm.nih.gov/pubmed/24945577
    [20]
    Petruzzelli L, Herrera R, Rosen O M. Insulin receptor is an insulin-dependent tyrosine protein kinase: copurification of insulin-binding activity and protein kinase activity to homogeneity from human placenta[J]. Proc Natl Acad Sci, 1984, 81(11): 3327-3331.
    [21]
    Gorin Y, Cavaglieri R C, Khazim K, et al. Targeting NADPH oxidase with a novel dual Nox1/Nox4 inhibitor attenuates renal pathology in type 1 diabetes[J]. Am J Physiol Renal Physiol, 2015, 308(11): F1276-F1287. http://europepmc.org/abstract/med/25656366
    [22]
    Ferreira L F, Laitano O. Regulation of NADPH oxidases in skeletal muscle[J]. Free Radic Biol Med, 2016, 98: 18-28.
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