Vitamin C Prevents Hydrocortisone-Induced Injury in HMEC-1 through Promoting Bestrophin-3 Expression

• Published in: Nutrition and cancer Vol. 71; no. 5; pp. 852 - 860
• Main Authors: Wang, Xuexin, Zhang, Guoping, Zhu, Chaohua, Lin, Lei, Zhao, Zhenshuan, Yu, Xiaoguang, Liu, Guobin, Zhang, Haijing, Li, Quanhai, Dong, Wei, Wang, Jian
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 04-07-2019; Taylor & Francis Ltd
• Subjects: Apoptosis; Ascorbic acid; Ascorbic Acid - pharmacology; Bcl-2 protein; Bestrophins - metabolism; Blotting, Western; Cell injury; Cell Survival - drug effects; Cell viability; Cells, Cultured; Cholecystokinin; Endothelial cells; Endothelial Cells - drug effects; Humans; Hydrocortisone; Hydrocortisone - administration & dosage; Injury prevention; Measurement methods; Microvasculature; Microvessels; Muscle Proteins - metabolism; Overexpression; siRNA; Steroids; Synergistic effect; Vitamin C; Vitamins - pharmacology; Western blotting
• ISSN: 0163-5581; 1532-7914
• DOI: 10.1080/01635581.2018.1539184

Objective: To investigate the protective effects and underlying mechanisms of Vitamin C (VC) on hydrocortisone (HC)-induced cell injury in human microvascular endothelial cells (HMEC).
Methods: Cell viability was measured by CCK-8 assay and the expression of Best-3 was detected by Western blotting assay. The experiment was divided into normal control, HC injury group, VC treatment groups, HC + Best-3 siRNA group, HC + VC + Best-3 siRNA group, HC + pcDNA3.1 Best-3 group, and HC + VC + pcDNA3.1 Best-3 group.
Results: HC inhibited HMEC-1 cell viability was balanced with lower expression of Best-3 in a dose-dependent manner. Conversely, VC promoted HMEC-1 cell viability was paralleled to higher expression of Best-3 in a dose-dependent manner. Silencing Best-3 with Best-3 siRNA inhibited HMEC-1 cell viability, however, over-expression of Best-3 with pcDNA3.1 Best-3 promoted HMEC-1 cell viability. Moreover, VC and over-expression of Best-3 prevented HC-induced HMEC-1 cell apoptosis; however, silencing Best-3 further enhanced HC-induced HMEC-1 cell apoptosis. HC reduced Best-3 expression, which was alleviated by VC treatment. HC treatment decreased Bcl-2 expression, facilitated Bax expression. Both of VC and over-expression of Best-3 promoted Bcl-2 expression and decreased Bax expression. Additionally, VC and Best-3 expression have a synergistic effect.
Conclusions: VC can efficiently attenuate HC-induced HMEC-1 cell injury, which may be related to promote Best-3 expression.