Protective role of α-lipoic acid against microcystin-LR-induced grass carp ovary cell damage
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.