Effects of Tougu Xiaotong Capsules on the expression of Rac1 and Cdc42 in chondrocytes
10.3969/j.issn.2095-4344.2014.42.005
- VernacularTitle:透骨消痛胶囊对凋亡软骨细胞Rac1和Cdc42表达的影响
- Author:
Jinxia YE
;
Guangwen WU
;
Xihai LI
;
Chunsong ZHENG
;
Huifeng XU
;
Hongzhi YE
;
Xianxiang LIU
- Publication Type:Journal Article
- Keywords:
chondrocytes;
apoptosis;
drugs,Chinese HERBAL;
rac1 GTP-binding protein;
cdc42 GTP-binding protein
- From:
Chinese Journal of Tissue Engineering Research
2014;(42):6747-6751
- CountryChina
- Language:Chinese
-
Abstract:
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 ful y 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 successful y induced by 20μg/L tumor necrosis factor-αand then Tougu Xiaotong Capsule at different dosage (500, 100, 20 mg/L) was given after 24-hour incubation. MTT assay was used to detect cellsurvival, 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.
