Wang Xiaoxiao, Zhao Guangshan, Zhao Qiuyan, Hu Mei, Wang Yinping, Li Qian, Wang Shiqiong, Qiao Mingwu, Shen Yue, Li Ning, Huang Xianqing, Wang Dongxu, Gan Ren-You, Song Lianjun
Henan Engineering Technology Research Center of Food Processing and Circulation Safety Control, College of Food Science and Technology, Henan Agricultural University, Zhengzhou, China.
School of Grain Science and Technology, Jiangsu University of Science and Technology, Zhenjiang, China.
J Food Sci. 2025 Mar;90(3):e70163. doi: 10.1111/1750-3841.70163.
Cadmium (Cd) is a widely distributed environmental heavy metal pollutant. It is extremely toxic to the kidney. This study investigated the potential mechanisms of action of lentinan (LNT), a fungal polysaccharide, on protecting against Cd-induced kidney injury in mice. Male Kunming mice were administered with CdCl (2.5 mg/kg/b.w.) by intragastric gavage and LNT in drinking water (1 mg/mL) for 10 weeks. Histological examination revealed that LNT reduced the glomerular atrophy, lymphocyte infiltration, tubular congestion, and collagen accumulation caused by Cd exposure. However, oral administration of LNT decreased Cd levels in kidney by promoting the excretion of Cd in feces and increasing the production of metallothionein (MT) in the kidney. In addition, LNT treatment alleviated Cd-induced kidney excessive mitophagy by upregulating silencing information regulator1 (SIRT1) and prevented subsequent oxidative stress and inflammatory responses by upregulating nuclear factor erythroid 2-related factor 2 (Nrf2) and downregulating nuclear factor kappa-B (NF-κB) signaling pathways. Further, the protein expression levels of profibrotic factors, including Tgf-β1, alpha smooth muscle actin, and collagen type I alpha 1 chain, and the progression of fibrosis, were significantly reduced in the kidneys of mice treated with LNT. Collectively, our findings suggest that LNT can relieve the nephrotoxicity of Cd by decreasing its accumulation via promoting Cd excretion and MT synthesis and regulating the SIRT1/Nrf2/NF-κB signaling pathway.
镉（Cd）是一种广泛分布的环境重金属污染物。它对肾脏具有极高的毒性。本研究调查了真菌多糖香菇多糖（LNT）对预防小鼠镉诱导的肾损伤的潜在作用机制。将雄性昆明小鼠通过灌胃给予CdCl（2.5毫克/千克/体重），并在饮用水中给予LNT（1毫克/毫升），持续10周。组织学检查显示，LNT减轻了镉暴露引起的肾小球萎缩、淋巴细胞浸润、肾小管充血和胶原积累。然而，口服LNT通过促进粪便中镉的排泄和增加肾脏中金属硫蛋白（MT）的产生，降低了肾脏中的镉水平。此外，LNT处理通过上调沉默信息调节因子1（SIRT1）减轻了镉诱导的肾脏过度线粒体自噬，并通过上调核因子红细胞2相关因子2（Nrf2）和下调核因子κB（NF-κB）信号通路，预防了随后的氧化应激和炎症反应。此外，在接受LNT治疗的小鼠肾脏中，包括转化生长因子-β1、α平滑肌肌动蛋白和I型胶原α1链在内的促纤维化因子的蛋白表达水平以及纤维化进程均显著降低。总的来说，我们的研究结果表明，LNT可以通过促进镉排泄和MT合成来减少镉的积累，并调节SIRT1/Nrf2/NF-κB信号通路，从而减轻镉的肾毒性。
