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Study on the effects of breviscapine on rats with insulin resistance and related mechanism

ZHAO Dong-liang1, WU Li2, LI Jin-ping2, ZHANG Xing-yuan1, FENG Ji-bo2   

  1. 1.Department of Pharmacology, Shanxi Medical University, Taiyuan 030000, China; 2.Department of Pharmacology, Fenyang College Shanxi Medical University, Fenyang 032200, China
  • Online:2016-06-28 Published:2016-07-25
  • Supported by:

    Key Science and Technology of Shanxi Province, 20051903; Major Program of Scientific Research Fund of Fenyang College Shanxi Medical University, 1418


Objective To investigate the effects of breviscapine on rats with insulin resistance (IR) and possible mechanism. Methods Fifty SD male rats were randomly assigned to the normal control group (NC group, n=10, fed with a normal diet) and IR model group (n=40, fed with a high fat and high sugar diet for 12 weeks for establishment of IR model). Thirty rats in IR model group were selected and randomly assigned to blank control model group (HFD group), high-dose breviscapine group (High group), and low-dose breviscapine group (Low group) with 10 rats in each group. The serum fasting insulin (FINS) and fasting blood glucose (FBG) were measured and the homeostasis model assessment of insulin resistance (HOMA-IR) index was calculated. The protein expression of ribosomal protein S6 kinase 1 (S6K1) and phosphorylation of insulin receptor substract-1 (IRS-1) tyrosine in liver tissues of IR rats after breviscapine treatment were detected with Western blotting and immunohistochemistry (IHC). Results The HOMA-IR index in HFD group was significantly higher as compared with NC group (P=0.000). The HOMA-IR indexes in High group and Low group were significantly lower as compared with HFD group (P=0.000). The results of Western blotting and IHC showed that the expression of S6K1 protein in High group and Low group were lower (P<0.01) and the phosphorylation of IRS-1 tyrosine was higher as compared with HFD group (P<0.01, P<0.05). Conclusion Breviscapine can significantly ameliorate insulin resistance in IR rats. The mechanism may be related to the decreased expression of S6K1 and increased phosphorylation of IRS-1 tyrosine in rat liver tissues.

Key words: breviscapine, insulin resistance, ribosomal protein S6 kinase 1, insulin receptor substract-1, tyrosine phosphorylation