College of Food Science and Technology, Henan Agriculture University, 450002, China.
College of Food Science and Technology, Henan Agriculture University, 450002, China.
Ecotoxicol Environ Saf. 2021 Mar 15;211:111917. doi: 10.1016/j.ecoenv.2021.111917. Epub 2021 Jan 25.
Lead (Pb) is a heavy metal environmental pollutant that can cause functional damage and anemia of immune organs. More and more evidence indicate that the toxicity of lead was related to apoptosis driven by oxidative stress and endoplasmic reticulum stress. This article mainly discusses the protective effect and mechanism of folic acid intervention on lead-induced spleen injury and apoptosis. In this study, Sprague-Dawley rats were randomly divided into control group, lead exposure group (0.2% lead acetate), folic acid + lead group (0.4 mg/kg folic acid and 0.2% lead acetate), and folic acid group (0.4 mg/kg folic acid). By recording and calculating the rat's initial body weight, final body weight, net weight gain, daily weight gain, and spleen index, observe the rat's weight change and spleen weight. And adopt the immunofluorescence staining method to determine the expression level of NrF2, HO-1, GRP78, CHOP protein in the spleen. The results showed that The 0.4 mg/kg folic acid diet did not significantly improve in the body weight and spleen index of lead-exposed rats (P > 0.05). While compared with the control group, the expression levels of HO-1 and CHOP protein were significantly increased in the lead exposure group (P < 0.05), and the expression levels of HO-1 and CHOP protein were significantly reduced in the folic acid intervention group (P < 0.05). In conclusion, lead exposure increased the expression levels of HO-1 and CHOP in the spleen of rats, and caused damage to the spleen. Folic acid down-regulated the expression levels of HO-1 and CHOP proteins through the two pathways of NrF2/HO-1 and GRP78/CHOP, thereby exerting a certain protective effect and alleviating the spleen caused by lead-induced oxidative stress and endoplasmic reticulum stress damage.
铅（Pb）是一种重金属环境污染物，可导致免疫器官功能损伤和贫血。越来越多的证据表明，铅的毒性与氧化应激和内质网应激驱动的细胞凋亡有关。本文主要探讨了叶酸干预对铅诱导的脾损伤和细胞凋亡的保护作用及机制。本研究将 Sprague-Dawley 大鼠随机分为对照组、铅暴露组（0.2%醋酸铅）、叶酸+铅组（0.4mg/kg 叶酸和 0.2%醋酸铅）和叶酸组（0.4mg/kg 叶酸）。通过记录和计算大鼠的初始体重、最终体重、净体重增加、日体重增加和脾指数，观察大鼠体重变化和脾重。并采用免疫荧光染色法测定脾组织中 NrF2、HO-1、GRP78、CHOP 蛋白的表达水平。结果表明，0.4mg/kg 叶酸饮食并未显著改善铅暴露大鼠的体重和脾指数（P＞0.05）。与对照组相比，铅暴露组 HO-1 和 CHOP 蛋白的表达水平显著升高（P＜0.05），而叶酸干预组 HO-1 和 CHOP 蛋白的表达水平显著降低（P＜0.05）。结论：铅暴露增加了大鼠脾组织中 HO-1 和 CHOP 的表达水平，导致脾损伤。叶酸通过 NrF2/HO-1 和 GRP78/CHOP 两条途径下调 HO-1 和 CHOP 蛋白的表达水平，从而发挥一定的保护作用，缓解铅诱导的氧化应激和内质网应激损伤所致的脾损伤。
