高级检索
    朱心瑶, 刘治国, 杨雪, 阚荣生, 魏叶. 牛蒡子苷对胰岛素抵抗型小鼠的糖脂代谢调节及心肌保护研究[J]. 徐州医科大学学报, 2021, 41(2): 102-106. DOI: 10.3969/j.issn.2096-3882.2021.02.005
    引用本文: 朱心瑶, 刘治国, 杨雪, 阚荣生, 魏叶. 牛蒡子苷对胰岛素抵抗型小鼠的糖脂代谢调节及心肌保护研究[J]. 徐州医科大学学报, 2021, 41(2): 102-106. DOI: 10.3969/j.issn.2096-3882.2021.02.005
    The mechanism of arctiin improves glucolipid metabolism and protects myocardial in insulin-resistant obese mice[J]. Journal of Xuzhou Medical University, 2021, 41(2): 102-106. DOI: 10.3969/j.issn.2096-3882.2021.02.005
    Citation: The mechanism of arctiin improves glucolipid metabolism and protects myocardial in insulin-resistant obese mice[J]. Journal of Xuzhou Medical University, 2021, 41(2): 102-106. DOI: 10.3969/j.issn.2096-3882.2021.02.005

    牛蒡子苷对胰岛素抵抗型小鼠的糖脂代谢调节及心肌保护研究

    The mechanism of arctiin improves glucolipid metabolism and protects myocardial in insulin-resistant obese mice

    • 摘要: 目的: 研究牛蒡子苷(Arctiin,ARC)对高脂饮食诱导胰岛素抵抗型(Insulin resistance,IR)肥胖小鼠的糖脂代谢调节及对心肌纤维化的改善作用。方法: 45只C57BL/6J雄性小鼠,随机分为正常饲料组(ND,10 kcal% Fat)和高脂饲料组(HFD,60 k cal% Fat)。建立IR模型后HFD组随机分为:高脂组(HFD)、高脂+溶剂组(HFD+CMC-Na)、高脂+牛蒡子苷组(HFD+ARC100mg/kg, HFD+ARC200mg/kg)。ARC灌胃10周后,血清学检测小鼠血脂,血糖水平;HE和Masson染色检测心肌形态和纤维化程度;实时荧光定量PCR(RT-qPCR)和蛋白质印迹法(Western blot,WB)检测心肌Collagen I、Collagen III、AUF1、TGF-β1/Smad3的mRNA和蛋白表达。结果: 与ND组比较,HFD组低密度脂蛋白(LDL-C)、总胆固醇(TC)、甘油三酯(TG)显著升高;空腹血糖(FBG)、空腹胰岛素(FIN)、胰岛素抵抗指数(HOMA-IR)升高;心肌胶原分泌增加,AUF1上调,TGF-β1/Smad3信号通道明显激活;与HFD组比较,HFD+CMC-Na组结果无统计学差异;ARC干预后,TC、TG下降;FBG、FIN、HOMA-IR降低;心肌胶原分泌降低,AUF1和TGF-β1/Smad3信号通道表达明显抑制。结论: ARC能调节糖脂代谢减轻胰岛素抵抗,减少心肌胶原分泌改善心肌纤维化,可能与AUF1表达下调,抑制TGF-β1/Smad3信号通道激活有关。

       

      Abstract: AIM: To explore the effects of arctiin ameliorates glucolipid metabolism and myocardial fibrosis in high-fat diet-induced insulin-resistant obese mice. METHODS: 45 male C57BL/6J mice were randomly divided into normal diet group(ND,10 kcal% Fat), high-fat diet group(HFD,60 kcal% Fat).The HFD group that established insulin-resistant was randomly divided into: HFD group, HFD+CMC-Na group, HFD+Arctiin group. Arctiin treatment with 100, 200mg/(kg·d) for 10 weeks, oral gavage, CMC-Na was used as the vehicle. After 10 weeks, blood lipid and glucose levels were measured. HE and Masson staining were used to detect the morphology and fibrosis of myocardial. RT-qPCR and WB were used to detect the expression of Collagen I, Collagen III, AUF1, TGF-β1/Smad3 signaling Pathway. RESULTS: Compared with ND group, the levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and triglycerides (TG) in HFD group were significantly increased; Fasting blood glucose (FBG) ,Fasting insulin ( FIN), and HOMA-IR were increased; Collagen I, Collagen III, AUF1,TGF-β1/Smad3 signaling Pathway expression were significantly increased. Compared with HFD group, the indicators in HFD+CMC-Na group were shown no statistical significance; the levels of TC and TG in HFD+ARC group were decreased; FBG, FIN and HOMA-IR were decreased, especially in high dose. The expression levels of Collagen I, Collagen III, AUF1, TGF-β1/Smad3 signaling Pathway were reduced. CONCLUSION: Arctiin can regulate glucolipid metabolism, ameliorate insulin resistance, reduce myocardial collagen secretion, and improve myocardial fibrosis. Its mechanism may be connected with the inhibition of AUF1 and TGF-β1/Smad3 pathway.

       

    /

    返回文章
    返回