High glucose promotes apoptosis and autophagy of MC3T3-E1 osteoblasts

作者全名："Zhang, Pei; Liao, Jing; Wang, Xiaoju; Feng, Zhengping"

作者地址："[Zhang, Pei; Liao, Jing; Wang, Xiaoju; Feng, Zhengping] Chongqing Med Univ, Dept Endocrinol, Affiliated Hosp 1, 1 Youyi Rd, Chongqing 400016, Peoples R China"

通信作者："Feng, ZP (通讯作者)，Chongqing Med Univ, Dept Endocrinol, Affiliated Hosp 1, 1 Youyi Rd, Chongqing 400016, Peoples R China."

来源：ARCHIVES OF MEDICAL SCIENCE

ESI学科分类：CLINICAL MEDICINE

WOS号：WOS:000921618400007

JCR分区：Q1

影响因子：3.8

年份：2023

卷号：19

期号：1

开始页：138

结束页：150

文献类型：Article

关键词：autophagy; oxidative stress; apoptosis; osteoblast; glucose fluctuation

摘要："Introduction: Diabetes and osteoporosis are common metabolic diseases. Abnormal high glucose can lead to the apoptosis of osteoblasts. Autophagy is a highly conserved cellular process that degrades proteins or organelles. In the present study, we comparatively analyzed the effects of high glucose and glucose fluctuation on apoptosis and autophagy of MC3T3-E1 osteoblasts. Material and methods: MC3T3-E1 cells were respectively treated with different concentrations of D-glucose: 5.5 mM for the control group, 25 mM for the high glucose group and 5.5/25 mM for the glucose fluctuation group. Results: High glucose and glucose fluctuation decreased MC3T3-E1 proliferation and activated autophagy. Also, high glucose and glucose fluctuation might induce the production of reactive oxygen species, decline the mitochondrial membrane potential and trigger apoptosis. The differences in the glucose fluctuation treatment group were more significant. Moreover, N-acetylcysteine, an antioxidant reagent, dramatically eliminated the intracellular reactive oxygen species induced by high glucose and glucose fluctuation, and significantly inhibited the autophagy and apoptosis in MC3T3-E1 osteoblasts. Furthermore, treatment with chloroquine, an inhibitor of autophagy, significantly increased the apoptosis of MC3T3-E1 osteoblasts. Conclusions: High glucose, especially high glucose fluctuation, inhibits proliferation and promotes apoptosis and autophagy of MC3T3-E1 osteoblasts. This may occur through inducing oxidative stress and mitochondrial damage in the osteoblasts."

基金机构：Chongqing Medical Research Fund [2012-2041]

基金资助正文：This study was supported by the Chongqing Medical Research Fund (grant number 2012-2041).