| 王辉,何丽,阮记明,梁惜梅,李福贵,隗黎丽.α-硫辛酸在微囊藻毒素-LR诱导草鱼卵巢细胞损伤中的作用[J].农业环境科学学报,2024,43(3):527-534. |
| α-硫辛酸在微囊藻毒素-LR诱导草鱼卵巢细胞损伤中的作用 |
| Protective role of α-lipoic acid against microcystin-LR-induced grass carp ovary cell damage |
| 投稿时间：2023-03-30 |
| DOI：10.11654/jaes.2023-0241 |
| 中文关键词: 草鱼卵巢细胞 α-硫辛酸 微囊藻毒素-LR 氧化应激 炎症反应 |
| 英文关键词: grass carp ovary cell α-lipoic acid microcystin-LR oxidative stress inflammation |
| 基金项目:国家自然科学基金项目（31760764，31460146） |
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| 摘要点击次数: 281 |
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| 中文摘要: |
| 为研究α-硫辛酸（Alpha lipoic acid，α-LA）在微囊藻毒素-LR（Microcystin-LR，MC-LR）诱导水生动物毒性效应中的保护作用，本研究以草鱼卵巢（Grass carp ovary，GCO）细胞为研究对象，检测分析了不同浓度α-LA以及α-LA与MC-LR共同暴露对GCO细胞活力的影响，随后根据测定的结果设置对照组（不添加MC-LR和α-LA）、125 μmol·L-1α-LA组、24 μmol·L-1 MC-LR组及125 μmol·L-1α-LA+24 μmol·L-1MC-LR组，检测分析了α-LA在缓解MC-LR对GCO细胞活性、氧化应激以及炎症方面的影响。结果表明：与对照组相比，24 μmol·L-1 MC-LR可诱导乳酸脱氢酶（LDH）活性和丙二醛（MDA）含量显著上升，同时显著抑制谷胱甘肽（GSH）活性（P<0.05），当MC-LR处理组中加入125 μmol·L-1 α-LA后，与MC-LR单独暴露组相比，LDH活性和MDA含量均显著下降（P<0.05），但GSH活性却显著上升（P<0.05）。对氧化相关基因分析发现，与对照组相比，24 μmol·L-1 MC-LR可显著降低SOD1、CAT和GST基因的表达量（P<0.05），当125 μmol·L-1 α-LA与24 μmol·L-1 MC-LR共同作用于GCO细胞后，与MC-LR单独暴露组相比，联合暴露组的GST基因的表达量显著上升（P<0.05），但SOD1和CAT两个基因的表达变化不显著（P>0.05）。此外，对炎症因子进行分析发现，MC-LR单独暴露组TNFα和IL11基因的相对表达水平显著高于对照组（P<0.05），但联合暴露组中的TNFα和IL11基因的相对表达水平却显著低于MC-LR单独暴露组（P<0.05）。研究结果表明，α-LA可缓解MC-LR诱导的氧化应激，提高细胞活力，抑制GCO细胞炎症的发生，从而减弱MC-LR对GCO细胞的损伤。 |
| 英文摘要: |
| To evaluate the protective effects of alpha lipoic acid(α-LA) on microcystin-LR(MC-LR)-induced toxicity in aquatic animals, grass carp ovary(GCO) cells were used in this study. The viability of GCO cells across different concentrations of α-LA treatment and the joint exposure of α-LA with MC-LR were analyzed. Then, the control(without adding MC-LR and α-LA), 125 μmol·L-1 α-LA, 24 μmol·L-1 MC-LR, and 125 μmol·L-1 α-LA+24 μmol·L-1 MC-LR groups were set according to these cell viability results; finally, the effects of α-LA on the cell viability, oxidative stress, and inflammation of MC-LR-induced GCO cells were analyzed. The results showed that 24 μmol·L-1 MC-LR treatment significantly increased lactic dehydrogenase(LDH) activity and malondialdehyde(MDA) content, and significantly inhibited the glutathione(GSH) activity of the GCO cells compared to that of the control group(P<0.05). When 125 μmol·L-1 α-LA was added to the MC-LR treated group, LDH activity and MDA content were significantly reduced compared to those of the MC-LR exposed group(P<0.05); however, GSH activity was significantly increased(P<0.05). Compared with the control group, the 24 μmol·L-1 MC-LR group exhibited a significant lower SOD1, CAT, and GST gene expression(P<0.05). In the 125 μmol·L-1 α-LA+24 μmol·L-1 MC-LR group, GST gene expression was significantly increased(P<0.05); however, the expressions of SOD1 and CAT genes were not significantly changed compared with those of the MC-LR exposure group(P>0.05). In addition, analysis of inflammatory factors demonstrated that the relative expression levels of TNFα and IL11 genes in the MC-LR exposure group were significantly higher than those in the control group(P<0.05); nonetheless, the relative expression levels of TNFα and IL11 genes in the combined exposure group were significantly lower than those in the MC-LR exposure group(P<0.05). These results indicate that α-LA can alleviate MC-LR-induced oxidated stress, improve cell viability, and inhibit inflammation of GCO cells, and thus reduce MC-LR-mediated damage to GCO cells. |
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