Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei Province, People's Republic of China.
Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, People's Republic of China.
Iran J Basic Med Sci. 2013 Dec;16(12):1276-81.
OBJECTIVE(S): Protein kinase C (PKCα) is involved in modulating articular chondrocytes apoptosis induced by nitric oxide (NO). Hyaluronic acid (HA) inhibits nitric oxide-induced apoptosis of articular chondrocytes by protecting PKCα, but the mechanism remains unclear. The present study was performed to investigate the effects and mechanisms of PKCα regulate protective effect of hyaluronic acid. Materials and Methods The ratio of apoptotic cell and cell viability was surveyed by PCNA and MTT assay. The expression of caspase-3 was determined by real-time PCR and western blot.
It was showed that HA was able to reduce the nuclei fragment and PCNA expression, and NO-induced articular apoptosis blocked by HA, pretreated chondrocytes with PMA, HA significantly inhibits the activation of caspase-3 induced by NO, but pretrement with CHR, HA significantly incresed the expression of caspase-3.
The results may be showed that PKCa regulate the expresion of caspase-3, which contribute to the apoptosis of chondrocytes induced by NO. PKC α agonists enhance the protective effect of hyaluronic acid on nitric oxide-induced articular chondrocytes apoptosis.
蛋白激酶 C(PKCα)参与调节一氧化氮(NO)诱导的关节软骨细胞凋亡。透明质酸(HA)通过保护 PKCα 抑制一氧化氮诱导的关节软骨细胞凋亡,但机制尚不清楚。本研究旨在探讨 PKCα 调节透明质酸保护作用的机制。
通过 PCNA 和 MTT 检测细胞凋亡率和细胞活力。实时 PCR 和 Western blot 检测 caspase-3 的表达。
HA 可减少细胞核片段和 PCNA 表达,阻断 HA 对 NO 诱导的关节软骨细胞凋亡,PKCα 激动剂 PMA 预处理软骨细胞后,HA 显著抑制 NO 诱导的 caspase-3 激活,但 CHR 预处理后,HA 显著增加 caspase-3 的表达。
结果表明 PKCα 调节 caspase-3 的表达,促进 NO 诱导的软骨细胞凋亡。PKCα 激动剂增强了透明质酸对一氧化氮诱导的关节软骨细胞凋亡的保护作用。