FUCOXANTHIN PROTECTS AGAINST CISPLATIN-INDUCED KIDNEY INJURY IN MICE AND ITS RELATED MECHANISM

LI Yi-cheng; REN Xiang-yu; YANG Zui-su; LIU Zhong-liang; DING Ya-ping

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Acta Nutrimenta Sinica ›› 2025, Vol. 47 ›› Issue (4) : 374-382.

ORIGINAL ARTICLES

FUCOXANTHIN PROTECTS AGAINST CISPLATIN-INDUCED KIDNEY INJURY IN MICE AND ITS RELATED MECHANISM

LI Yi-cheng¹, REN Xiang-yu², YANG Zui-su², LIU Zhong-liang¹, DING Ya-ping¹

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Abstract

Objective To investigate the protective action and molecular mechanisms of fucoxanthin (Fx) on cisplatin-induced kidney injury in mice. Methods Fifty mice were divided into a control group (n = 10) and an experimental group (n = 40). The experimental group received an intraperitoneal injection of cisplatin (7 mg/kg) once per week for four consecutive weeks to induce kidney injury. The experimental group was then further divided into four subgroups: model group, positive drug amifostine group (10 mg/kg), low-dose Fx group (50 mg/(kg·d)), and high-dose Fx group [100 mg/(kg·d)]. The normal and model groups received a standard diet, while the other three groups underwent respective interventions for another four weeks. At the end of the experiment, the mice were sacrificed to measure serum levels of creatinine (CRE), blood urea nitrogen (BUN), and uric acid (UA). Oxidative enzyme activity, inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), as well as kidney injury markers kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL), were assessed in kidney tissues. Histopathological changes in the kidney were evaluated using hematoxylin and eosin (HE) staining. Western blot analysis was performed to detect the expressions of oxidative stress-related nuclear factor erythroid 2-related factor 2 (Nrf2) family members and ferroptosis-related glutathione peroxidase 4 (GPX4) proteins. Immunohistochemistry was also used to observe Nrf2 and GPX4 protein levels in kidney tissues. Results Fx intervention reduced serum CRE, BUN, and UA levels in mice, decreased TNF-α, IL-1β, and IL-6 levels in the kidney, increased antioxidant enzyme activity, and lowered KIM-1 and NGAL levels. Renal histopathological changes were also improved. Additionally, Fx increased the expressions of Nrf2, heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), and GPX4 proteins. Immunohistochemical analysis showed that Fx treatment led to increased Nrf2 and GPX4 protein expression in kidney tissues. Conclusion Fx protests against cisplatin-induced kidney injury in mice. The mechanism may involve alleviation of inflammation and oxidative stress, and inhibition of ferroptosis via activation of the Nrf2/GPX4 signaling pathway.

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fucoxanthin / kidney injury / cisplatin / ferroptosis

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LI Yi-cheng, REN Xiang-yu, YANG Zui-su, LIU Zhong-liang, DING Ya-ping. FUCOXANTHIN PROTECTS AGAINST CISPLATIN-INDUCED KIDNEY INJURY IN MICE AND ITS RELATED MECHANISM[J]. Acta Nutrimenta Sinica. 2025, 47(4): 374-382

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