长期砷暴露诱导小鼠肾脏氧化应激和炎性反应OA

Objective:To establish a mouse model exposed to arsenic for 6 months and elucidate the nephrotoxic ef-fects induced by chronic low-dose arsenic exposure.Methods:Sixteen mice were randomly divided into a control group(drinking distilled water)and an arsenic exposure group.The arsenic exposure group received water containing 5 mg/L arse-nic for 6 months.Renal structural changes were evaluated by HE staining.Blood urea nitrogen(BUN),creatinine(CR),total superoxide dismutase(T-SOD)activity,and malondialdehyde(MDA)levels in serum were measured by biochemical meth-ods.The mRNA expression levels of nuclear factor-κB(NF-κB)and the pro-inflammatory cytokine tumor necrosis factor-α(TNF-α)were detected by quantitative real-time PCR.Results:In the arsenic exposure group,the glomerular capillaries showed slight congestion,and the renal tubular structure was largely intact.However,edema was observed in the epithelial cells of the proximal convoluted tubules,and inflammatory cell infiltration was present in the renal interstitium.This indicates that arsenic exposure induced an inflammatory response and caused structural damage to the mouse kidneys.Compared with the control group,the arsenic exposure group showed significantly increased serum levels of BUN,CR,and MDA,signifi-cantly decreased T-SOD activity,and significantly elevated mRNA expression of NF-κB and the pro-inflammatory factor TNF-α.All differences were statistically significant(P<0.01).Conclusion:Long-term arsenic exposure induces oxidative stress and an inflammatory response in mouse kidneys,with NF-κB and TNF-α involved in the renal inflammatory response.