| 王丽艳,宋淑亮.岩藻多聚糖在阿托伐他汀诱导HepG2细胞损伤中的作用的研究[J].中国海洋药物,2027,():-. |
| 岩藻多聚糖在阿托伐他汀诱导HepG2细胞损伤中的作用的研究 |
| Study on the role of fucoidan in atorvastatin-induced HepG2 cell injury |
| 投稿时间：2026-01-16 修订日期：2026-03-22 |
| DOI： |
| 中文关键词: 岩藻多聚糖 阿托伐他汀 药物性肝损伤 氧化应激 HepG2细胞 |
| English Keywords:fucoidan atorvastatin drug-induced liver injury oxidative stress HepG2 cells |
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| 中文摘要: |
| 摘要：目的 探讨岩藻多糖（Fucoidan）对阿托伐他汀（ATO）诱导的HepG2细胞损伤的保护作用。方法 将细胞分为空白对照组、阿托伐他汀模型组（150 μmol/L）以及岩藻多聚糖低、中、高剂量组（100, 200, 400 μg/mL）和双环醇（Bicyclol）组（?2 μg/mL）。HepG2细胞传代培养后，在其细胞培养液中加入岩藻多聚糖和双环醇，作用24h后，再加入阿托伐他汀和岩藻多聚糖或双环醇的混合液，继续培养48h，检测各细胞存活率，丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）含量，丙二醛（MDA）、活性氧（ROS）水平及线粒体膜电位（MMP）。结果 与空白对照组相比，阿托伐他汀（150 μmol/L）处理48小时可显著抑制HepG2细胞活力（P＜0.0001），提高细胞凋亡率至（47.15±5.11）%（P<0.0001）。与模型组相比，不同浓度的岩藻多聚糖和双环醇均能明显提高细胞存活率，抑制ALT、AST水平的升高，减少MDA、ROS的形成，并减少线粒体膜电位的降低，从而缓解了阿托伐他汀诱导的HepG2细胞损伤。结论 岩藻多糖可减轻阿托伐他汀诱导的氧化应激和炎症反应，并为临床防治他汀类药物肝毒性提供新策略。 |
| English Summary: |
| Abstract: Aim: To investigate the protective effect of fucoidan on atorvastatin (ATO)-induced HepG2 cell injury. Methods: Cells were divided into a blank control group, an atorvastatin model group (150 μmol/L), and low, medium, and high-dose fucoidan groups (100, 200, 400 μg/mL) as well as a bicyclol group (2 μg/mL). After subculturing HepG2 cells, fucoidan and bicyclol were added to the cell culture medium. After 24 hours, a mixture of atorvastatin and fucoidan or bicyclol was added, and the cells were further cultured for 48 hours. Measurements were conducted to assess the cell survival rate, alongside the quantification of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, malondialdehyde (MDA) content, reactive oxygen species (ROS) concentration, and mitochondrial membrane potential (MMP). Results: Compared with the blank control group, atorvastatin (150 μmol/L) treatment for 48 hours significantly inhibited HepG2 cell viability (P < 0.0001) and increased the apoptosis rate to (47.15±5.11) % (P < 0.0001). Compared with the model group, fucoidan and bicyclol at different concentrations significantly improved cell survival rate, inhibited the increase in ALT and AST levels, reduced the formation of MDA and ROS, and mitigated the decrease in MMP, thereby alleviating atorvastatin-induced HepG2 cell injury. Conclusion: Fucoidan can alleviate atorvastatin-induced oxidative stress and inflammatory response, providing a new strategy for the clinical prevention and treatment of statin-induced hepatotoxicity. |
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