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Jin-Xia Y.,Fuzhou University | Jin-Xia Y.,Fujian Provincial Key Laboratory of Integrative Medicine on Geriatrics | Guang-Wen W.,Fuzhou University | Guang-Wen W.,Fujian Provincial Key Laboratory of Integrative Medicine on Geriatrics | And 10 more authors.
Chinese Journal of Tissue Engineering Research | Year: 2014

BACKGROUND: Tougu Xiaotong Capsule has pretty good clinical therapeutic effect on osteoarthritis of early and middle periods. However, the mechanism of Tougu Xiaotong Capsule is not fully clarified. The RhoA GTPases can regulate chondrocyte apoptosis and hypertrophy. OBJECTIVE: To observe the Tougu Xiaotong Capsule on the expression of Rac1and Cdc42 in tumor necrosis factor-α-induced in vitro cultured rat articular chondrocytes, and to explore its mechanism of action for combating osteoarthritis. METHODS: Knee cartilage of the 4-week-old Sprague-Dawley rats was used to stably establish in vitro culture system of chondrocytes. Passage 3 chondrocytes were identified by toluidine blue staining. Chondrocyte apoptosis was successfully induced by 20 μg/L tumor necrosis factor-α and then Tougu Xiaotong Capsule at different dosage (500, 100, 20 mg/L) was given after 24-hour incubation. MTT assay was used to detect cell survival, flow cytrometry to measure mitochondrial membrane potential, and western blot assay to determine the protein expression of Rac1, Cdc42, Bax and Bcl-2. RESULTS AND CONCLUSION: Tougu Xiaotong Capsule could reduce tumor necrosis factor-α-induced apoptosis of chondrocytes to improve the survival rate of the cells, and at the same time, could down-regulate the protein expression of Rac1, Cdc42 and Bax and increase the protein expression of Bcl-2 significantly (P < 0.05). Tougu Xiaotong Capsule possibly plays a therapeutic efficacy on osteoarthritis by reducing promote apoptosis Rac1, Cdc42 and Bax expression and increasing apoptosis inhibiting gene Bcl-2 expression, thereby to inhibit apoptosis of chondrocytes. © 2014 Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved. Source

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