| 摘要: |
| 目的研究牛膝多糖（ABPS）对硝普钠诱导的兔软骨细胞凋亡的影响及可能机制。方法取新西兰白兔膝关节软骨建立兔软骨细胞体系，分别用白芦藜醇、尼克酰胺及不同浓度ABPS（200、300、400滋g/ml）处理经硝普钠诱导凋亡后的P3代软骨细胞。采用流式细胞仪检测细胞凋亡率。采用RT-PCR法检测烟酰胺磷酸核糖转移酶（NAMPT）、信息沉默因子1（Sirt1）、p53和BaxmRNA表达水平。结果与硝普钠组比较，白芦藜醇组、ABPS各组软骨细胞凋亡率均明显下降（均P＜0.05），而尼克酰胺组软骨细胞凋亡率明显上升（P＞0.05）。与ABPS200滋g/ml组比较，ABPS300滋g/ml组及ABPS400滋g/ml组软骨细胞凋亡率明显下降（均P＜0.05）。ABPS可上调抗凋亡基因NAMPT、Sirt1mRNA表达，同时使凋亡基因p53、BaxmRNA表达下调，并且浓度300滋g/ml时效果最明显。结论ABPS可能通过激活NAMPT、Sirt1来抑制p38信号通路下游的关键基因p53，对软骨细胞凋亡起保护作用。 |
| 关键词: 软骨细胞 硝普钠 凋亡 牛膝多糖 信息沉默因子 1 |
| DOI：10.12056/j.issn.1006-2785.2018.40.7.2017-2911 |
| 分类号: |
| 基金项目:浙江省中医药科技计划项目（2014ZB079） |
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| Effect of achyranthes bidentata polysaccharides on apoptosis of articular chondrocytes induced by sodium nitroprusside and its mechanism |
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Hangzhou First People's Hospital
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| Abstract: |
| Objective To investigate the effect of achyranthes bidentata polysaccharides (ABPS) on apoptosis induced by sodium nitroprusside in rabbit chondrocytes and its mechanism. Methods Rabbit chondrocytes were isolated from the articular cartilage of New Zealand white rabbits, and the apoptosis model of P3 chondrocytes was induced by intervention with sodium
nitroprusside. The chondrocytes of induced apoptosis were treated with resveratrol, nianamide, and ABPS (200, 300, 400滋g/ml).
The effects of ABPS on Sirt1-p53 signaling pathway and apoptosis were analyzed by RT-PCR and flow cytometry, respectively. Results Compared with the sodium nitroprusside group, the apoptosis rates of notroprusside-treated chondrocytes in veratrol group and ABPS groups were decreased significantly (both P ＜0.05), however, it was significantly increased in nicotinamide
group (P＜0.05). Compared with the ABPS 200滋g/ml group, the apoptosis rate of notroprusside-treated chondrocytes in ABPS
300滋g/ml group and ABPS 400滋g/ml group decreased significantly (both P＜0.05). ABPS up-regulated the expression of NAMPT and Sirt1, and reduced the expression of apoptosis-related genes p53 and Bax, and the effect was most markedly when the concentration was 300滋g/ml. Conclusion ABPS may protect chondrocyte from apoptosis by activating p38 signaling pathway NAMPT and Sirt1 genes to inhibit p53 expression. |
| Key words: Chondrocytes Sodium nitroprusside Apoptosis Achyranthes bidentata polysaccharides Sirt1 |
