Duhuo Jisheng decoction treatment inhibits the sodium nitroprussiate-induced apoptosis of chondrocytes through the mitochondrial-dependent signaling pathway

被引:58
作者
Liu, Fayuan [1 ]
Liu, Guozhong [2 ]
Liang, Wenna [3 ]
Ye, Hongzhi [1 ]
Weng, Xiaping [1 ]
Lin, Pingdong [1 ]
Li, Huiting [4 ]
Chen, Jiashou [4 ]
Liu, Xianxiang [1 ]
Li, Xihai [1 ]
机构
[1] Fujian Univ Tradit Chinese Med, Acad Integrat Med, Fuzhou 350122, Peoples R China
[2] Fujian Med Univ, Affiliated Hosp 1, Fuzhou 350002, Fujian, Peoples R China
[3] Fujian Univ Tradit Chinese Med, Res Base Tradit Chinese Med Syndrome, Fuzhou 350122, Peoples R China
[4] Fujian Univ Tradit Chinese Med, Fujian Key Lab Integrat Med Geriatr, Fuzhou 350122, Peoples R China
关键词
osteoarthritis; Duhuo Jisheng decoction; chondrocyte; apoptosis; NO-INDUCED APOPTOSIS; NITRIC-OXIDE; BCL-2; FAMILY; OSTEOARTHRITIS; BAX; PROLIFERATION; THERAPY; MEMBERS; DEATH;
D O I
10.3892/ijmm.2014.1962
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
Chondrocyte apoptosis activated by the mitochondrial-dependent signaling pathway plays a crucial role in the cartilage degeneration of osteoarthritis. Duhuo Jisheng decoction (DHJSD), a herbal formula from traditional Chinese medicine, has been widely used for treating osteoarthritis (OA). However, the molecular mechanisms behind the therapeutic effect of DHJSD remain to be elucidated. In the present study, the effects of DHJSD on the mitochondrial-dependent signaling pathway in sodium nitroprussiate (SNP)-induced chondrocyte apoptosis were investigated. Chondrocytes, from the knee articular cartilage of Sprague Dawley rats, were identified by type II collagen immunohistochemistry. The chondrocytes, stimulated with or without SNP to induce apoptosis, were treated by DHJSD for various concentrations and times. The viability of SNP-induced chondrocytes treated with DHJSD was enhanced compared to SNP-induced chondrocytes in a dose- and time-dependent manner, as assessed by the MTT assay. The apoptosis of SNP-induced chondrocytes treated by DHJSD was significantly decreased compared to SNP-induced chondrocyte, as shown by 4',6-diamidino-2-phenylindole and A nnexin V/propidium iodide staining. The mitochondrial membrane potential (Delta Psi m) of SNP-induced chondrocytes treated by DHJSD was significantly decreased compared to SNP-induced chondrocyte, as shown by JC-1 staining. To understand the mechanism, the mRNA and protein levels of Bax, B-cell lymphoma 2 (Bcl-2), caspase-9 and caspase-3 were detected by reverse transcription-polymerase chain reaction and western blot analysis, respectively. In SNP-induced chondrocyte treated by DHJSD, the Bcl-2 expression was increased, whereas the expression of Bax, caspase-9 and caspase-3 was decreased compared to SNP-induced chondrocyte. Taken together, these results indicated that DHJSD inhibits the apoptosis of SNP-induced chondrocyte by the mitochondrial-dependent apoptotic pathway, and this may partly explain its therapeutic efficacy for OA.
引用
收藏
页码:1573 / 1580
页数:8
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