CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Laboratory for Marine Drugs and Bioproducts, Pilot National Laboratory for Marine Science and Technology (Qingdao), Qingdao, China.
Bioengineered. 2021 Dec;12(1):7235-7247. doi: 10.1080/21655979.2021.1973875.
Kidney damages caused by cadmium are considered to be one of the most dangerous consequences for the human body. This study aimed to investigate the protective effects of fucoxanthin supplementation on mice models subjected to cadmium-induced kidney damage. The mice treated with cadmium chloride (CdCl) were observed to have significantly reduced the cross-section area of glomeruli. Cadmium exposure has also caused the damage of the structural integrity of mitochondria and increased blood urea nitrogen (BUN), kidney injury molecule 1 (KIM1), and neutrophil gelatinase associated lipocalin (NGAL) levels. Peroxidase (POD), superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) levels in cadmium-exposed mice were markedly declined. Caspase3, caspase8, and caspase9 gene expressions in association with apoptosis were dramatically elevated in renal tissues. The CdCl treated mice were orally administered with 50 mg/kg Shenfukang, 10 mg/kg, 25 mg/kg, and 50 mg/kg fucoxanthin for 14 days. The results revealed that high doses of fucoxanthin administration significantly decreased BUN, KIM1, NGAL levels, increasing POD, SOD, CAT, and ascorbate APX levels. Fucoxanthin administration also promoted recovery of the renal functions, micro-structural organization, and ultra-structural organization in the renal cells. In summary, the ameliorative effects of fucoxanthin supplementation against cadmium-induced kidney damage were mediated via inhibiting oxidative stress and apoptosis, promoting the recovery of structural integrity of mitochondria.
镉引起的肾脏损伤被认为是对人体最危险的后果之一。本研究旨在探讨岩藻黄质补充对镉诱导的肾损伤小鼠模型的保护作用。用氯化镉 (CdCl) 处理的小鼠观察到肾小球横截面积明显减小。镉暴露还导致了线粒体结构完整性的损伤，并增加了血尿素氮 (BUN)、肾损伤分子 1 (KIM1) 和中性粒细胞明胶酶相关脂质运载蛋白 (NGAL) 的水平。暴露于镉的小鼠的过氧化物酶 (POD)、超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT) 和抗坏血酸过氧化物酶 (APX) 水平明显下降。与细胞凋亡相关的 caspase3、caspase8 和 caspase9 基因表达在肾组织中显著升高。用 50mg/kg 肾福康、10mg/kg、25mg/kg 和 50mg/kg 岩藻黄质对 CdCl 处理的小鼠进行 14 天的口服给药。结果表明，高剂量岩藻黄质给药显著降低了 BUN、KIM1 和 NGAL 水平，增加了 POD、SOD、CAT 和抗坏血酸 APX 水平。岩藻黄质给药还促进了肾脏功能、肾细胞的微观结构和超微结构的恢复。总之，岩藻黄质补充对镉诱导的肾脏损伤的改善作用是通过抑制氧化应激和细胞凋亡，促进线粒体结构完整性的恢复来介导的。
