Abstract：
Mercuric chloride (HgCl2) is a widespread inorganic mercury with digestive toxicity. The pancreas is an important digestive organ in animals, and pancreatic fibrosis (PF) is a major pathological feature of chronic pancreatitis, which can be caused by heavy metals. Selenium (Se) is an essential trace element for the animal organism, performing biological functions in the form of selenoproteins, as well as alleviating the toxicity of heavy metals. In this study, we explored the specific mechanisms underlying the protective effect of Se on HgCl2-induced pancreatic injury in chickens. Morphological observation and serum biochemical analysis showed that Se attenuated HgCl2-caused pancreatic tissue damage and elevated glucose concentration and α-amylase activity. Next, the expression of oxidative stress indicators such as MDA and GSH-Px as well as inflammation-related markers including IL-1β, IL-6, and TNF-α were detected. Results showed that Se had an inhibitory effect on HgCl2-induced oxidative stress and inflammation. Furthermore, we found that Se alleviated HgCl2-induced PF by detecting the expression of markers related to PF including TGF-β1, α-SMA, COL1A1, and FN1. Mechanistically, Se attenuated HgCl2-induced PF via the MAPK signaling pathway. Importantly, several selenoproteins, especially those with antioxidant activity, were involved in the protective effect of Se on HgCl2 toxicity. In conclusion, our findings demonstrated that Se inhibited HgCl2-induced oxidative stress and inflammation and alleviated chicken PF through the MAPK signaling pathway, in which some antioxidant selenoproteins were involved.
摘要：
氯化汞（HgCl2）是一种普遍存在的无机汞，具有消化毒性。胰腺是动物的重要消化器官,胰腺纤维化(PF)是慢性胰腺炎的主要病理特征,这可能是由重金属引起的。硒(Se)是动物机体必需的微量元素,以硒蛋白的形式执行生物学功能，以及减轻重金属的毒性。在这项研究中,我们探讨了硒对HgCl2诱导的鸡胰腺损伤的保护作用的具体机制。形态学观察和血清生化分析表明，硒可以减轻HgCl2引起的胰腺组织损伤，并提高葡萄糖浓度和α-淀粉酶活性。接下来,氧化应激指标如MDA和GSH-Px以及炎症相关标志物如IL-1β的表达,检测IL-6和TNF-α。结果表明，硒对HgCl2诱导的氧化应激和炎症具有抑制作用。此外，我们发现硒通过检测与PF相关的标志物TGF-β1，α-SMA的表达减轻了HgCl2诱导的PF，COL1A1和FN1。机械上,硒通过MAPK信号通路减弱HgCl2诱导的PF。重要的是,几种硒蛋白，尤其是那些有抗氧化活性的，参与了Se对HgCl2毒性的保护作用。总之,我们的研究结果表明，硒通过MAPK信号通路抑制HgCl2诱导的氧化应激和炎症，减轻鸡PF，其中涉及一些抗氧化硒蛋白。
