Cd^(2+)对克氏原螯虾肝胰腺NF-κB p65表达的影响

Effects of Cd^(2+) on the Expression of NF-κB p65 in Hepatopancreas of Procambarus clarkii

NF-κB既是氧化还原敏感的转录因子,也是重要的免疫通路分子,参与细胞的基因表达、应激响应和感染防御,但其功能在甲壳动物还鲜见报道。研究以亚致死浓度(1.0,5.0 mg/L,96 h LC50≈42 mg/L)的Cd^(2+)为胁迫因子,免疫器官肝胰腺为靶组织,采用免疫组化方法研究了96 h急性Cd^(2+)胁迫对克氏原螯虾NF-κB p65表达的影响。结果表明,与未染毒的对照组相比,Cd^(2+)胁迫导致肝胰腺呈现出典型的病理损伤,NF-κB p65的表达水平分别是对照的6倍和12倍,且染毒组间差异显著,其可能是重金属Cd的免疫毒性效应之一。

NF-κB is not only a redox-sensitive transcription factor, but also an important immune pathway molecule which participates in the gene expression, stress response and infection defense of cells. However, crustaceans is rarely reported. This study evaluated the expression of NF-κB p65 in hepatopancreas via IHC method, by exposing the crayfish Procambarus clarkii to sub-lethal concentrations of Cd^2+(1.0, 5.0 mg/L, 96 h LC50≈42 mg/L). The results showed that compared with the control group, Cd^2+ stress caused typical pathological damage on hepatopancreas. The expression levels of NF-κB p65 were 6, 12 times higher than that of the control, respectively, and the difference between the two stress groups was significant, which may be one of immunotoxicity effects of Cd.