Abstract

Lead (Pb) is a kind of widespread toxic environmental pollutant which can cause harm to organisms. Selenium (Se) has the property of mitigating Pb toxicity through decreasing oxidative stress and inflammation caused by Pb. Nucleotide-binding domain, leucine-rich-containing family, and pyrin-domain containing-3 (NLRP3) inflammasome involve in inflammation process. However, the effect of NLRP3 inflammasome in heavy metal-caused animal damage remains unknown. This research aimed to explore the mechanism of mitigative role of Se on Pb-caused renal inflammatory injury in chickens. One-week-old male chickens were provided a standard diet and drinking water, a standard diet added with 1 mg kg-1 of Se and drinking water, a standard diet and drinking water added with 350 mg L-1 Pb, and a standard diet added with 1 mg kg-1 Se and drinking water added with 350 mg L-1 Pb. On the 4th, 8th, and 12th weeks, serum was used to measure creatinine (CREA) and uric acid (UA) contents, and kidneys were used to measure Se and Pb concentrations, histological structure, oxidative stress indicators, relative expressions of cytokines, and inflammatory factors. The results showed that Pb accumulated, Se concentration decreased, CREA and UA contents increased, and renal injury occurred in Pb-treated chicken kidneys. Excess Pb increased MDA content and the expressions of IL-1β, IL-6, IL-17, NLRP3, caspase-1, NF-κB, COX-2, TNF-α, and PTGEs and decreased GSH content, GPx and SOD activities, and IFN-γ expression in the chicken kidneys. Se administration alleviated the aforementioned changes. In addition, toxic effect of Pb on the chicken kidneys was time-dependent. NLRP3 inflammasome, caspase-1, and IL-1β may be sensitive indicators in Pb-induced chicken kidney inflammatory damage. In conclusion, NLRP3 inflammasome took part in antagonistic role of Se against Pb-caused inflammation via changing oxidative stress indicators, cytokines, and inflammation-related genes in the chicken kidneys.

Full Text
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