Baicalein protects renal tubular epithelial cells againsthypoxia-reoxygenation injury

被引:16
作者
Chen, Chun [1 ]
Cai, Chudan [2 ]
Lin, Hanfei [2 ]
Zhang, Weidai [2 ]
Peng, Yanqiang [2 ]
Wu, Kefei [2 ]
机构
[1] Shantou Univ, Coll Med, Affiliated Hosp 1, Dept Tradit Chinese Med, Shantou, Peoples R China
[2] Shantou Univ, Coll Med, Affiliated Hosp 1, Dept Nephrol, 57 Changping Rd, Shantou 515021, Guangdong, Peoples R China
关键词
Baicalein; oxidative stress; inflammation; hypoxia-reoxygenation; renal tubular epithelial cell; ACUTE KIDNEY INJURY; ISCHEMIA/REPERFUSION INJURY; INDUCED APOPTOSIS; INHIBITION; PATHWAYS; RAT; EXPRESSION;
D O I
10.1080/0886022X.2018.1532910
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
100201 [内科学]; 100221 [泌尿外科学];
摘要
Background: To investigate the protective effects and mechanism of baicalein (BAI), a naturally occurring flavonoid, against hypoxia-reoxygenation (HR) injury in renal tubular epithelial cells (HK-2). Methods: Cultured human renal proximal tubular cell line HK-2 was exposed to 24 h of hypoxia (5% CO2, 1% O-2, and 94% N-2), followed by 12 h of reoxygenation (5% CO2, 21% O-2, and 74% N-2). HK-2 cells were divided into three groups: control, HR, and HR-BAI (0.3 mu g/ml). Reactive oxygen species (ROS) were measured and cell apoptosis was analyzed by flow cytometry and morphology. ELISAs were performed to determine the levels of IL-1, intercellular adhesion molecule-1 (ICAM-1), and monocyte chemotactic protein-1 (MCP-1). IL-1 beta, ICAM-1, and MCP-1 mRNA levels were determined by real-time quantitative PCR. Results: HK-2 cells that underwent HR exhibited increases in IL-1 beta expression by 0.94%, ROS by 0.59%, ICAM-1 expression by 0.8%, and MCP-1 expression by 1.2%. Moreover, HK-2 cell apoptosis was increased after HR (p < .05). Compared with the HR group, BAI treatment reduced the elevation of oxidative stress (ROS) by 0.76%, as well as HR-mediated induction of IL-1 beta and apoptosis of HK2 cells. Protein and mRNA levels of ICAM-1 and MCP-1 were also reduced. Conclusions: BAI protects renal tubular epithelial cells from HR injury by reducing inflammatory cytokine expression and oxidative stress.
引用
收藏
页码:603 / 610
页数:8
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