Hypoglycemic activity of puerarin through modulation of oxidative stress and mitochondrial function via AMPK.
10.1016/S1875-5364(20)60022-X
- Author:
Bi-Yu HOU
1
;
Yue-Rong ZHAO
1
;
Peng MA
1
;
Chun-Yang XU
2
;
Ping HE
1
;
Xiu-Ying YANG
1
;
Li ZHANG
1
;
Gui-Fen QIANG
3
;
Guan-Hua DU
4
Author Information
1. State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College and Beijing Key Laboratory of Drug Target and Screening Research, Beijing 100050, China.
2. Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100026, China.
3. State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College and Beijing Key Laboratory of Drug Target and Screening Research, Beijing 100050, China. Electronic address: qianggf@imm.ac.cn.
4. State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College and Beijing Key Laboratory of Drug Target and Screening Research, Beijing 100050, China. Electronic address: dugh@imm.ac.cn.
- Publication Type:Journal Article
- Keywords:
Diabetes;
Hypoglycemic;
Mitochondrial function;
Oxidative stress;
Puerarin
- From:
Chinese Journal of Natural Medicines (English Ed.)
2020;18(11):818-826
- CountryChina
- Language:English
-
Abstract:
Hyperglycemia is the dominant phenotype of diabetes and the main contributor of diabetic complications. Puerarin is widely used in cardiovascular diseases and diabetic vascular complications. However, little is known about its direct effects on diabetes. The aim of our study is to investigate its antidiabetic effect in vivo and in vitro, and explore the underlying mechanism. We used type I diabetic mice induced by streptozotocin to observe the effects of puerarin on glucose metabolism. In addition, oxidative stress and hepatic mitochondrial respiratory activity were evaluated in type I diabetic mice. In vitro, glucose consumption in HepG2 cells was assayed along with the qPCR detection of glucogenesis genes expression. Moreover, ATP production was examined and phosphorylation of AMPK was determined using Western blot. Finally, the molecular docking was performed to predict the potential interaction of puerarin with AMPK utilizing program LibDock of Discovery Studio 2018 software. The results showed that puerarin improved HepG2 glucose consumption and upregulated the glucogenesis related genes expression. Also, puerarin lowered fasting and fed blood glucose with improvement of glucose tolerance in type I diabetic mice. Further mechanism investigation showed that puerarin suppressed oxidative stress and improved hepatic mitochondrial respiratory function with enhancing ATP production and activating phosphorylation of AMPK. Docking study showed that puerarin interacted with AMPK activate site and enhancing phosphorylation. Taken together, these findings indicated that puerarin exhibited the hypoglycemic effect through attenuating oxidative stress and improving mitochondrial function via AMPK regulation, which may serve as a potential therapeutic option for diabetes treatment.
