期刊
JOURNAL OF ETHNOPHARMACOLOGY
卷 268, 期 -, 页码 -出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2020.113654
关键词
Diabetes; Insulin resistance; GLUT4; pPKC; Dyslipidemia
资金
- National Natural Science Foundation of China [81573561, 81911540487]
- Fundamental Research Funds for the Central Universities, South-Central University for Nationalities [CZY19026]
The study found that the extract from Sophora alopecuroides L. can improve hyperglycemia, dyslipidemia, and insulin resistance by activating the PKC/GLUT4 pathway and regulating PPAR α and PPAR γ expression.
Headings ethnopharmacological relevance: Sophora alopecuroides L. is a traditional ethnopharmacological plant, which is widely used in traditional Chinese medicine and Mongolian and Uighur medicine to ameliorate thirst disease. Aim of the study: This study aimed to investigate the antidiabetic activities and mechanisms of a flavonoid-rich extract from Sophora alopecuroides L. (SA-FRE) both in vivo and vitro. Materials and methods: The main six chemical constituents of SA-FRE were elucidated based on an off-line semipreparative liquid chromatography nuclear magnetic resonance (LC-NMR) protocol. Myc-GLUT4-mOrange-L6 cell models and mouse model with diabetes induced by high-fat diet combined with STZ injection were respectively adopted to investigate the antidiabetic effects of SA-FRE both in vitro and vivo. Results: In vivo, 4-week treatment of SA-FRE ameliorated hyperglycemia, dyslipidemia, and insulin resistance in diabetic mice. Mechanically, SA-FRE regulated PPAR alpha and PPAR gamma expression in white adipose tissue (WAT) and liver, thereby ameliorating dyslipidemia. Moreover, SA-FRE increased the phosphorylation of PKC and further stimulated the GLUT4 expression in WAT and skeletal muscle, thus increasing the glucose utilization in vivo. In vitro, 50 mu g/mL SA-FRE increased GLUT4 translocation to about 1.91-fold and glucose uptake to 1.82-fold in L6-myotubes. SA-FRE treatment increased the GLUT4 expression at both gene and protein levels. Furthermore, only God6983, a PKC inhibitor, reversed the SA-FRE-induced GLUT4 translocation and expression at the gene and protein levels. Conclusions: Generally, SA-FRE ameliorated hyperglycemia, dyslipidemia, and insulin resistance partly through activating PKC/GLUT4 pathway and regulating PPAR alpha and PPAR gamma expression.
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