[Study on the mechanism of action of total flavonoids of Litsea coreana for reducing blood glucose level in rat with type 2 diabetes mellitus].

To explore the possible mechanism of total flavonoids of Litsea coreana (TFLC) on reducing blood glucose level in rat with type 2 diabetes mellitus (T2DM).Male SD rats of T2DM allocated in two groups were treated with 400 mg/kg TFLC or metformin respectively via gastrogavage for 6 weeks. Blood routine biochemical indices in rats were measured; pathology of rats' liver was examined with HE stain under transmission electron microscopy; levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in liver homogenate were determined, and the expression of protein tyrosine phosphatase 1B (PTP1B) in liver was detected using RT-PCR at the terminal of the experiment.Biochemical measuring showed that the glucose tolerance of rats after treatment was markedly improved in both groups. Meantime, levels of fast blood glucose (FBG), glycohemoglobin (HbA1c), fast blood insulin (FINS), free fatty acid (FFA), total cholesterol (TC), triglyceride (TG) and low density lipoprotein-cholesterol (LDL-C), as well as MDA level in liver were decreased, while levels of high density lipoprotein-cholesterol (HDL-C) in blood and SOD in liver were significantly increased in both groups after treatment, showing insignificant difference between two treatment groups. Light microscopic examination showed markedly fatty degeneration of liver, and electron microscopic examination found mitochondria swelling and endoplasmic reticulum breakage in liver of T2DM rats, but these changes were ameliorated to some extent after treatment. The elevated PTP1B expression in liver of T2DM rats was decreased in the TFLC treated group, but unchanged in the metformin treated group.TFLC can significantly decrease the blood levels of glucose and lipid and ameliorate oxidation stress in liver; its mechanism of action in improving insulin resistance might be related with its suppression on PTP1B expression in rat's liver to enhance the insulin signaling pathway.