紫草酸通过抑制凋亡及磷酸化P65改善脂多糖对H9c2细胞的损伤 |
投稿时间:2015-01-23 修订日期:2015-01-27 点此下载全文 |
引用本文:朱小琴,华晓芳,李磊,李小艳.紫草酸通过抑制凋亡及磷酸化P65改善脂多糖对H9c2细胞的损伤[J].医学研究杂志,2016,45(1):143-146 |
DOI:
10.11969/j.issn.1673-548X.2016.01.037 |
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中文摘要:目的 探讨紫草酸对脂多糖(lipopolysaccharides,LPS)诱导的H9C2细胞损伤的保护作用。方法 本实验分组为5组:对照组、LPS组、LPS加紫草酸组(低、中、高剂量)。LPS浓度为2mg/ml,紫草酸浓度分别为5、10、20μmol/L。药物干预时间为12h。用CCK8检测药物对细胞存活率影响,用TUNEL、RT-PCR及Western blot法检测凋亡蛋白及信号通路蛋白的变化。结果 紫草酸对H9C2细胞具有低毒性,它可以降低胞内凋亡的水平,降低炎性反应,且具有浓度依赖性以及时间依赖性。结论 紫草酸可以改善LPS诱导H9C2细胞损伤。 |
中文关键词:紫草酸 H9C2细胞 凋亡 P65 |
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Lithospermic Acid Protects H9c2 Cardiomyocyte Induced by Lipopolysaccharides via Attenuates Apoptosis and Phosphorylation of P65 |
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Abstract:Objective To investigate the effect of lithospermic acid on H9C2 cell injury by LPS. Methods The study had 5 groups:control, LPS, LPS and lithospermic acid (high, middle, low). Concentration of LPS was 2mg/ml, and concentration of lithospermic acid were 5,10 and 20μmol/L. The intervention time of lithospermic acid was 12h. The cell survival rate detected by CCK8. The signal pathy way, inflammatory cytokines and apoptosis makers detected by TUNEL, RT-PCR and westernblot after dealing with experimental factors designed. Results Lithospermic acid on H9C2 cells had low toxicity. It can reduce the level of inflammatory cytokines, apoptosis makers in the concentration-depended and time-depended. Conclusion Lithospermic acid attenuated apoptosis in H9C2 cell by induced by LPS. |
keywords:Lithospermic acid H9C2 cells Apoptosis P65 |
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