Welcome to Chinese Journal of Clinical Pharmacology and Therapeutics,Today is Share:

Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2013, Vol. 18 ›› Issue (7): 743-748.

Previous Articles     Next Articles

Effects of metformin on intracellular reactive oxygen species and apoptosis induced by advanced glycation end products on rat cranioaural osteoblasts

ZHEN Dong-hu, LIU Li-juan, CHEN Jian-guo, TANG Xu-lei   

  1. Department of Endocrinology, the First Hospital of Lanzhou University, Lanzhou 730000, Gansu, China
  • Received:2012-10-10 Revised:2013-04-08 Online:2013-07-26 Published:2013-06-20

Abstract: AIM: To explore the effects of metformin (MF) on intracellular reactive oxygen species (ROS) and apoptosis in advanced glycation end products (AGEs)-induced rat cranioaural osteoblasts.METHODS: Rat cranioaural osteoblasts were isolated and cultured. The fluorescence of 2′, 7′-dichlorofluorescin (DCF) was measured by flow cytometry as a mean of estimating the formation of ROS, the cell apoptosis was detected by double-staining (Annexin V-FITC/ PI).RESULTS: With 500 μg/mL AGEs, intracellular ROS and the cell apoptosis were markedly increased(both P<0.01), as compared with that observed with bovine serum albumin(BSA) group; MF(100-500 μmol/L) decreased intracellular ROS in both BSA group and AGEs group in a dose-dependent manner, with maximal inhibition attained at a concentration of 500 μmol/L. Introducing different concentrations of metformin (100-500 μmol/L) into the medium significantly lowered the number of apoptotic cells in a dose-dependent manner in both BSA group and AGEs group and maximal inhibition was reached at a concentration of 400 μmol/L.CONCLUSION: AGEs markedly induced intracellular ROS and the cell apoptosis. However, metformin significantly decreased intracellular ROS and apoptosis, which could ameliorate deleterious effects of AGEs on osteoblasts.

Key words: Metformin, Glycation end products, Reactive oxygen species, Apoptosis

CLC Number: