Hypoglycemic Mechanism of Polygonum capitatum Extract on Spontaneous Model of Type 2 Diabetic db/db Mice
- Author:
Bo-Yu LIU
1
Author Information
- Publication Type:Journal Article
- Keywords: db/db mice; Mechanism; Polygonum capitatum; Type 2 diabetes mellitus
- From: Chinese Pharmaceutical Journal 2017;52(5):384-390
- CountryChina
- Language:Chinese
- Abstract: OBJECTIVE: To investigate the Polygonum capitatum's influences on the related indicators in db/db mice which is the obesity model of type 2 diabetes mellitus. METHODS: Randomly dividing the mice into 5 groups: model group, rosiglitazone hydrochloride group, low-, moderate-and high-dose groups of Polygonum capitatum (5,10,20 g·kg-1), make the db/m mice as blank control. Give the medicine for four weeks. The body weight, blood sugar were determined every week. At the end of fourth week, measuring the glucose tolerance and INS, IL-6 in serum. After all the mice were killed, testing the cholesterol and triglyceride in liver and skeletal muscle and then collecting the liver tissue for HE staining. At the meantime, the expression level of AMPK and GLUT4 in liver were detected by Q-PCR. RESULTS: Polygonum capitatum can improve the body weight, blood sugar and glucose tolerance of db/db mice as well as the content of INS and IL-6 in serum, but increase the content of SOD and decrease the content of MDA in mice, furthermore, the cholesterol and triglyceride levels in the liver and skeletal muscle were also declined. HE staining showed that Polygonum capitatum could reduce the number of vacuoles in the liver of db/db mice, and make its shape more complete and ordered. What's more, raising the expression of AMPK and GLUT4 in the liver. CONCLUSION: Polygonum capitatum can improve the condition of insulin resistance state, alleviate inflammation and advance the ability of db/db mice, which can also reduce the number of vacuoles in liver, and relieve the tissue lipid metabolic disorder. Meanwhile, Polygonum capitatum can promote the uptake of glucose in liver tissues, which is resulted from upregulation of expression in hepatic AMPK and GLUT4 gene.
