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

Liu,Fayuan; Liu,Guozhong; Liang,Wenna; Ye,Hongzhi; Weng,Xiaping; Lin,Pingdong; Li,Huiting; Chen,Jiashou; Liu,Xianxiang; Li,Xihai

doi:10.3892/ijmm.2014.1962

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

Authors:
- Fayuan Liu
- Guozhong Liu
- Wenna Liang
- Hongzhi Ye
- Xiaping Weng
- Pingdong Lin
- Huiting Li
- Jiashou Chen
- Xianxiang Liu
- Xihai Li
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Affiliations: Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, P.R. China, The First Affiliated Hospital of Fujian Medical University, Fujian 350002, P.R. China, Research Base of Traditional Chinese Medicine Syndrome, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, P.R. China, Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, P.R. China
Published online on: October 10, 2014 https://doi.org/10.3892/ijmm.2014.1962
Pages: 1573-1580

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Abstract

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 Annexin V/propidium iodide staining. The mitochondrial membrane potential (∆Ψm) 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.

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