【摘 要】
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Objective:To investigate the protective effects of modified Linggui Zhugan Decoction(MLZD),a traditional Chinese medicine formula,on obese type 2 diabetes mellitus (T2DM) rats.Methods:Fifty Sprague-Dawley rats were randomly divided into 5 groups by a rand
【机 构】
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Department of Traditional Chinese Medicine,the First Affiliated Hospital,Sun Yat-sen University,Guan
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Objective:To investigate the protective effects of modified Linggui Zhugan Decoction(MLZD),a traditional Chinese medicine formula,on obese type 2 diabetes mellitus (T2DM) rats.Methods:Fifty Sprague-Dawley rats were randomly divided into 5 groups by a random number table,including normal,obese T2DM (ob-T2DM),MLZD low-dose[MLDZ-L,4.625 g/(kg·d)],MLZD middle-dose[MLD-M,9.25 g/(kg·d)]and MLZD high-dose[MLD-H,18.5 g/(kg·d)]groups,10 rats in each group.After 4-week intervention,blood samples and liver,pancreas,muscle tissues were collected to assess the insulin resistance(IR),blood lipid,adipokines and inflammation cytokines.The alteration of phosphatidylinositol 3 kinase (PI3K)-protein kinase B (PKB or Akt)/the mammalian target of rapamycin (mTOR)-ribosome protein subunit 6 kinase 1(S6K1)/AMP-activated protein kinase (AMPK)-peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 o) pathways were also studied.Results:MLZD dose-dependently reduced fasting blood glucose,fasting insulin,homeostasis model of assessment for IR index and increased insulin sensitive index compared with ob-T2DM rats (P<0.05).Similarly,total cholesterol,triglyceride,low-density lipoprotein cholesterol and free fatty acids were also decreased compared with ob-T2DM rats after 4-week treatment (P<0.05 or P<0.01).Improvements in adipokines and inflammatory cytokines were observed with a raised level of adiponectin and a reduced level of leptin,resistin,tumor necrosis factor-α and interleukin-6 (P<0.05 or P<0.01).MLZD regulated the PI3K-Akt/mTOR-S6K1/AMPK-PGC-1α pathways and restored the tissue structure of liver and pancreas(P<0.05 or P<0.01).Conclusions;MLZD ameliorated glycolipid metabolism and inflammation,which may be attributed to the regulation of PI3K-Akt/mTOR-S6K1/AMPK-PGC-1α pathways.
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