Evidence map›Paper›PMID 40500698›Full record

ArticleMolecular medicine (Cambridge, Mass.)2025

Bavachin ameliorates cisplatin-induced nephrotoxicity by enhancing mitochondrial β-oxidation and lipid metabolism through MFN2.

Shilu Luo, Ming Yang, Na Jiang, Chenrui Li, Yan Liu, Lin Sun

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Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
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3citing papers in PubMed, 1 pooled it
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Shilu LuoDepartment of Nephrology, the Second Xiangya Hospital, Central South University, No. 139 Renmin Middle Road, Changsha, Hunan, 410011, China.
Ming YangDepartment of Nephrology, the Second Xiangya Hospital, Central South University, No. 139 Renmin Middle Road, Changsha, Hunan, 410011, China.
Na JiangDepartment of Nephrology, the Second Xiangya Hospital, Central South University, No. 139 Renmin Middle Road, Changsha, Hunan, 410011, China.
Chenrui LiDepartment of Nephrology, the Second Xiangya Hospital, Central South University, No. 139 Renmin Middle Road, Changsha, Hunan, 410011, China.
Yan LiuDepartment of Nephrology, the Second Xiangya Hospital, Central South University, No. 139 Renmin Middle Road, Changsha, Hunan, 410011, China.
Lin SunDepartment of Nephrology, the Second Xiangya Hospital, Central South University, No. 139 Renmin Middle Road, Changsha, Hunan, 410011, China. sunlin@csu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCisplatin-induced nephrotoxicity is a critical adverse reaction that restricts the clinical utilization of cisplatin. Alterations in fatty acid metabolism have been associated with the pathogenesis of cisplatin-induced nephrotoxicity, yet the precise mechanisms remain unclear. Bavachin, a natural flavonoid, exhibits anti-inflammatory, antioxidant, and lipid metabolism-regulating properties, yet its role in mitigating cisplatin-induced nephrotoxicity via mitochondrial β-oxidation remains unexplored. Mitofusin-2 (MFN2), a mitochondrial fusion protein, has emerged as a critical regulator of fatty acid oxidation (FAO) and lipid homeostasis. However, its role in cisplatin-induced nephrotoxicity has not been fully explored.

methodsC57/6L mice were randomly divided into control, DMSO, cisplatin, and cisplatin + Bavachin groups. Blood urea nitrogen (BUN), serum creatinine (SCr), reactive-oxygen-species (ROS), lipid accumulation, and apoptosis were assessed. In vitro, the human proximal tubule epithelial cell line (HK-2) cells were treated with 20 µM cisplatin with or without bavachin. ROS production was detected by the DCFH-DA, lipid deposition was detected by oil red O staining, and MFN2, carnitine palmitoyltransferase 1a (CPT1a) were detected by Western blot (WB).

resultsCompared with the cisplatin group, bavachin treatment reduced BUN (21.8%) and SCr (78.7%) in the cisplatin group, accompanied by improvements in renal pathological changes, lipid deposition, and apoptosis. In addition, bavachin up-regulated the expression of MFN2 and CPT1a, while decreasing the cisplatin-induced ROS overproduction. Similar results were found in vitro. Notably, the mitochondrial FAO has been increased in HK-2 cells treated with bavachin. Further, MFN2 siRNA partially reversed these protective effects, accompanied by decreased CPT1a expression and exacerbated lipid deposition.

conclusionsThis study is the first to confirm MFN2 as a target for renal protection by bavachin. Mechanistically, Bavachin alleviated cisplatin-induced lipid accumulation and apoptosis by upregulating MFN2 expression, which activated CPT1a to promote mitochondrial FAO. These results will provide a new strategy for cisplatin-based cancer therapy and the reduction of its nephrotoxicity.

Indexed as

CisplatinFlavonoidsGTP PhosphohydrolasesLipid MetabolismMitochondriaAnimalsApoptosisCell LineHumansKidneyMaleMiceMice, Inbred C57BLOxidation-ReductionReactive Oxygen SpeciesCisplatinFlavonoidsGTP PhosphohydrolasesMfn2 protein, mouseReactive Oxygen SpeciesAcute kidney injuryBavachinLipid accumulationMFN2Mitochondrial dynamicsOxidative stressRenal protection

Identifiers

PMID40500698
PMCPMC12160371

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