Kangxianling Decoction, a traditional Chinese medicine formula used clinically to attenuate renal fibrosis, appears to protect against the condition by inhibiting ferroptosis, an iron-dependent form of regulated cell death, according to a preclinical study published in Biological Procedures Online. The research, led by Weiguo Yao and colleagues, combined chemical profiling, network pharmacology and laboratory models to map how the multi-herb formula may act at the molecular level.
The team first characterised the chemical composition of Kangxianling Decoction using ultra-performance liquid chromatography coupled with high-resolution mass spectrometry. This analysis identified eight major bioactive components in the formula.
That computational analysis pointed to ferroptosis and the p53 signalling pathway as candidate mechanisms. To test these predictions experimentally, the researchers established a rat model of 5/6 nephrectomy, in which each animal had five-sixths of its kidney tissue surgically removed, to assess the anti-fibrotic effects of Kangxianling Decoction. They evaluated tissue morphology using haematoxylin and eosin staining and Masson’s trichrome staining, techniques that reveal structural damage and collagen deposition associated with fibrosis.
According to the study, the anti-fibrotic effect of Kangxianling Decoction was associated with inhibition of ferroptosis through downregulation of the expression level of P53 and enhancement of antioxidant capacity. The formula also reversed the downregulation of GPX4 that had been caused by ferroptosis.
To validate the predicted signalling pathways and targets at the cellular level, the researchers established a ferroptosis model in HK-2 cells and examined the predicted targets using immunofluorescence and western blotting. The authors conclude that the protective effect of Kangxianling Decoction against renal fibrosis is associated with inhibition of ferroptosis via regulation of the p53/GPX4 pathway, suggesting that the formula may reduce fibrotic damage by preventing ferroptotic injury to kidney tubule cells.
The findings are limited by their preclinical scope. The animal work relied on a surgical nephrectomy model in rats, and the cellular validation used a single kidney cell line, so the results do not establish clinical efficacy in patients with kidney disease. The study was published as a peer-reviewed, accepted manuscript shared ahead of final production, and the published version of record may differ after further edits. The authors note that the formula is already used clinically to attenuate renal fibrosis, but the present study was designed to investigate potential targets and molecular mechanisms rather than to test therapeutic outcomes in humans.
Within those limits, the work offers a mechanistic account of how a multi-component herbal formula might act on a defined cell death pathway. By linking chemical constituents identified by mass spectrometry to predicted targets, and those targets to measured changes in ferroptosis markers, p53 expression and GPX4 levels in rat kidney tissue and cultured kidney cells, the study provides a testable framework for future research into ferroptosis-directed approaches to renal fibrosis.
Subject of Research: Mechanisms of Kangxianling Decoction in attenuating renal fibrosis through inhibition of ferroptosis
Article Title: Kangxianling Decoction Attenuates Renal Fibrosis by Inhibiting Ferroptosis
Article References: Yao, W., Tao, P., Yan, X., Liu, K., & Ji, J. (2026). Kangxianling Decoction Attenuates Renal Fibrosis by Inhibiting Ferroptosis. Biological Procedures Online. https://doi.org/10.1186/s12575-026-00362-0
Image Credits: AI Generated
DOI: 10.1186/s12575-026-00362-0
Keywords: renal fibrosis, ferroptosis, Kangxianling Decoction, traditional Chinese medicine, p53/GPX4 pathway, network pharmacology, UPLC-HRMS, 5/6 nephrectomy, HK-2 cells, oxidative stress, kidney disease, preclinical study
News Source: Drew Townsend. (October 29, 2026). Traditional Chinese Medicine Formula Kangxianling Shows Anti-Fibrosis Effects in Rats by Suppressing Ferroptosis. Scienmag.
