Antidiabetic effect of a flavonoid-rich extract from Sophora alopecuroides L. in HFD- and STZ- induced diabetic mice through PKC/GLUT4 pathway and regulating PPARα and PPARγ expression

J Ethnopharmacol. 2021 Mar 25:268:113654. doi: 10.1016/j.jep.2020.113654. Epub 2020 Nov 30.

Abstract

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 semi-preparative 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 PPARα and PPARγ 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 μg/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 Gö6983, 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 PPARα and PPARγ expression.

Keywords: Diabetes; Dyslipidemia; GLUT4; Insulin resistance; pPKC.

MeSH terms

  • Animals
  • Diabetes Mellitus, Experimental / drug therapy
  • Diabetes Mellitus, Experimental / genetics
  • Diabetes Mellitus, Experimental / metabolism
  • Diet, High-Fat / adverse effects
  • Flavonoids / isolation & purification
  • Flavonoids / pharmacology
  • Flavonoids / therapeutic use
  • Gene Expression
  • Glucose Transporter Type 4 / biosynthesis*
  • Glucose Transporter Type 4 / genetics
  • Hypoglycemic Agents / isolation & purification
  • Hypoglycemic Agents / pharmacology
  • Hypoglycemic Agents / therapeutic use*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • PPAR alpha / biosynthesis*
  • PPAR alpha / genetics
  • PPAR gamma / biosynthesis*
  • PPAR gamma / genetics
  • Plant Extracts / isolation & purification
  • Plant Extracts / pharmacology
  • Plant Extracts / therapeutic use
  • Protein Kinase C / biosynthesis*
  • Protein Kinase C / genetics
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Sophora*
  • Streptozocin

Substances

  • Flavonoids
  • Glucose Transporter Type 4
  • Hypoglycemic Agents
  • PPAR alpha
  • PPAR gamma
  • Plant Extracts
  • Slc2a4 protein, mouse
  • Streptozocin
  • Protein Kinase C