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首页> 外文期刊>Cell biology international. >Insulin secretion impairment induced by rosuvastatin partly though autophagy in INS‐1E cells
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Insulin secretion impairment induced by rosuvastatin partly though autophagy in INS‐1E cells

机译：罗苏伐他汀诱导的胰岛素分泌损伤部分虽然在INS-1E细胞中的自噬

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摘要

Abstract Statins are used extensively for the clinical treatment of cardiovascular diseases. Recent studies suggest that statins increase the risk of new‐onset diabetes mellitus (NODM). However, the mechanisms of statin‐induced NODM remain unclear. The present study investigated the effects of autophagy on insulin secretion impairment induced by rosuvastatin (RS) in rat insulinoma cells (INS‐1E) cells. INS‐1E cells were cultured and treated with RS at different concentrations (0.2–20?μM) for 24?h. Insulin secretion in INS‐1E cells was detected by enzyme‐linked immunosorbent assay, and the co‐localization of microtubule‐associated protein light chain 3 (LC3) and lysosome‐associated membrane protein 2 (LAMP‐2) was observed by immunofluorescence staining. Western blotting was used to assess the conversion of LC3 and p62. The results showed that the insulin secretion and cell viability decrease?induced by RS treatment for 24?h occurred in a dose‐dependent manner in INS‐1E cells. RS significantly inhibited the expression of LC3‐II but increased the protein expression of p62. Simultaneously, RS diminished the co‐localization of LC3‐II and LAMP‐2 fluorescence signals. These results suggested that RS‐inhibited autophagy in INS‐1E cells. Rapamycin, an autophagy agonist, reversed the insulin secretion and cell viability suppression induced by RS in INS‐1E cells. RS also decreased the phosphorylation of the mammalian target of rapamycin (mTOR). The results indicated that RS impairs insulin secretion in INS‐1E cells, which may be partly due to the inhibition of autophagy via an mTOR‐dependent pathway.
机译：摘要他汀类药物广泛用于心血管疾病的临床治疗。最近的研究表明他汀类药物增加了新发糖尿病（NODM）的风险。然而，他汀类药物诱导NODM的机制尚不清楚。本研究探讨了自噬对瑞舒伐他汀（RS）诱导的大鼠胰岛素瘤细胞（INS-1E）胰岛素分泌损伤的影响。培养INS-1E细胞，并用不同浓度（0.2–20μM）的RS处理24小时？h、 通过酶联免疫吸附试验检测INS-1E细胞中的胰岛素分泌，并通过免疫荧光染色观察微管相关蛋白轻链3（LC3）和溶酶体相关膜蛋白2（LAMP-2）的共定位。Western blotting用于评估LC3和p62的转化率。结果表明，胰岛素分泌和细胞活力降低？RS治疗诱导24小时？h在INS-1E细胞中呈剂量依赖性。RS显著抑制LC3-II的表达，但增加p62的蛋白表达。同时，RS减少了LC3-II和LAMP-2荧光信号的共定位。这些结果表明RS抑制INS-1E细胞的自噬。雷帕霉素是一种自噬激动剂，可逆转RS在INS-1E细胞中诱导的胰岛素分泌和细胞活力抑制。RS还降低了雷帕霉素（mTOR）哺乳动物靶点的磷酸化。结果表明，RS会损害INS-1E细胞的胰岛素分泌，部分原因可能是通过mTOR依赖性途径抑制自噬。

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  • 来源
    《Cell biology international.》 |2020年第1期|共10页
  • 作者

    Qian Linglin; Zhu Kongbo; Lin Yanshan; An Li; Huang Feiyang; Yao Yuyu; Ren Liqun;

  • 作者单位

    Department of Cardiology Zhongda HospitalMedical School of Southeast UniversityNanjing 210009;

    Department of Cardiology Zhongda HospitalMedical School of Southeast UniversityNanjing 210009;

    Department of Cardiology Zhongda HospitalMedical School of Southeast UniversityNanjing 210009;

    Department of Cardiology Zhongda HospitalMedical School of Southeast UniversityNanjing 210009;

    Department of Cardiology Zhongda HospitalMedical School of Southeast UniversityNanjing 210009;

    Department of Cardiology Zhongda HospitalMedical School of Southeast UniversityNanjing 210009;

    Department of Cardiology Zhongda HospitalMedical School of Southeast UniversityNanjing 210009;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    autophagy; insulin secretion; mTOR; rosuvastatin;

    机译：自噬;胰岛素分泌;mtor;roosuvastatin;

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