Effects of metformin on apoptosis induced by advanced glycation end- products and expressions of caspase-3, Bax and Bcl-2 in human dermal fibroblasts in vitro
- VernacularTitle:二甲双胍对糖基化终末产物诱导的成纤维细胞凋亡及相关蛋白caspase-3、Bax及Bcl-2表达的影响
- Author:
Ruoyu PANG
1
;
Meiping GUAN
;
Zongji ZHENG
;
Yaoming XUE
Author Information
1. 南方医科大学南方医院内分泌代谢科
- Keywords:
diabetic foot ulceration;
advanced glycation end products;
fibroblasts;
apoptosis;
metformin
- From:
Journal of Southern Medical University
2015;(6):898-902
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of metformin in protecting against advanced glycation end products (AGEs)-induced apoptosis in human primary dermal fibroblasts. Methods Fibroblasts were exposed to 100, 200, or 300μg/mL AGEs, 300μg/mL bovine serum albumin (BSA), or 300μg/mL AGEs and 1 mmol/L metformin for 24, 48, or 72 h. The exposed cells were examined for cell apoptosis using a cell counting kit. The expressions of caspase-3, Bax and Bcl-2 protein in the fibroblasts treated for 72 h were detected with Western blotting. Results AGEs exposures caused significant dose- and time-dependent apoptosis in the fibroblasts. A 72-h exposure to 300μg/mL AGEs resulted in obviously increased apoptosis of the fibroblasts compared to the control group (0.72 ± 0.02 vs 1 ± 0.04, P<0.05), and metformin significantly decreased AGEs-induced apoptosis (0.98 ± 0.02 vs 0.72 ± 0.02, P<0.05). The expressions of caspase-3 and Bax protein were significantly increased (P<0.05) and Bcl-2 protein expression was decreased (P<0.05) with a lowered Bcl-2/Bax ratio in AGEs-treated fibroblasts (P<0.05), and such changes were significantly reversed by metformin treatment (P<0.05). Conclusion Metformin can antagonize AGEs-induced apoptosis in human dermal fibroblasts by regulating the expressions of caspase-3, Bax and Bcl-2.
