Li Ning, Wen Liuding, Yu Zengli, Li Tiange, Wang Tianlin, Qiao Mingwu, Song Lianjun, Huang Xianqing
Henan Engineering Technology Research Center of Food Processing and Circulation Safety Control, College of Food Science and Technology, Henan Agricultural University, Zhengzhou, China.
College of Public Health, Zhengzhou University, Zhengzhou, China.
Front Nutr. 2022 Nov 15;9:1035162. doi: 10.3389/fnut.2022.1035162. eCollection 2022.
Lead (Pb) has many applications in daily life, but in recent years, various problems caused by lead exposure have aroused people's concern. Folic acid is widely found in fruits and has received more attention for its antioxidant function. However, the role of folic acid in lead-induced kidney injury in rats is unclear. This study was designed to investigate the effects of folic acid on oxidative stress and endoplasmic reticulum stress in the kidney of rats caused by lead exposure.
Forty specific pathogen-free male rats were randomly divided into control, lead, intervention, and folic acid groups. The levels of SOD, GSH-Px, GSH, and MDA were measured by biochemical kits. The protein levels of Nrf2, HO-1, CHOP, and GRP78 were measured by immunofluorescence.
This study showed that lead exposure increased the blood levels of lead in mice. However, the intervention of folic acid decreased the levels of lead, but the difference was not statistically significant. Lead exposure causes oxidative stress by decreasing kidney SOD, GSH-Px, and GSH levels and increasing MDA levels. However, folic acid alleviated the oxidative damage caused by lead exposure by increasing the levels of GSH-Px and GSH and decreasing the levels of MDA. Immunofluorescence results showed that folic acid intervention downregulated the upregulation of kidney Nrf2, HO-1, GRP78, and CHOP expression caused by lead exposure.
Overall, folic acid alleviates kidney oxidative stress induced by lead exposure by regulating Nrf2 and HO-1, while regulating CHOP and GRP78 to mitigate apoptosis caused by excessive endoplasmic reticulum stress.
铅(Pb)在日常生活中有许多应用,但近年来,铅暴露引起的各种问题已引起人们的关注。叶酸广泛存在于水果中,并因其抗氧化功能而受到更多关注。然而,叶酸在铅诱导的大鼠肾损伤中的作用尚不清楚。本研究旨在探讨叶酸对铅暴露所致大鼠肾脏氧化应激和内质网应激的影响。
将40只无特定病原体雄性大鼠随机分为对照组、铅组、干预组和叶酸组。采用生化试剂盒检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽(GSH)和丙二醛(MDA)水平。采用免疫荧光法检测核因子E2相关因子2(Nrf2)、血红素加氧酶-1(HO-1)、C/EBP同源蛋白(CHOP)和葡萄糖调节蛋白78(GRP78)的蛋白水平。
本研究表明,铅暴露会增加小鼠血液中的铅水平。然而,叶酸干预可降低铅水平,但差异无统计学意义。铅暴露通过降低肾脏SOD、GSH-Px和GSH水平以及增加MDA水平而导致氧化应激。然而,叶酸通过增加GSH-Px和GSH水平并降低MDA水平,减轻了铅暴露引起的氧化损伤。免疫荧光结果显示,叶酸干预下调了铅暴露所致肾脏Nrf2、HO-1、GRP78和CHOP表达的上调。
总体而言,叶酸通过调节Nrf2和HO-1减轻铅暴露诱导的肾脏氧化应激,同时调节CHOP和GRP78减轻内质网应激过度引起的细胞凋亡。