ArticleBMC nephrology2025
Verbenalin attenuates renal tubular epithelial ferroptosis in ischemia-reperfusion injury induced AKI by regulating the HIF-1α/HO-1 signaling pathway.
Article in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAcute kidney injury (AKI) is a common critical disease. Ferroptosis, which is caused by unrestricted iron-dependent lipid peroxidation, is closely related to AKI progression. Verbena officinalis exhibits antioxidant activity. This study aimed to examine the therapeutic effect and mechanism of verbenalin (an active constituent of Verbena officinalis) on AKI.
methodsAn IRI-AKI mouse model was established. Verbenalin (10 or 20 mg/kg) was administered daily from 2 days before until 2 days after IRI induction. Renal function was evaluated by measuring SCr and BUN levels, while histological damage was assessed via HE and PAS staining. Ferroptosis was quantified by TUNEL assay, iron/MDA levels, and GPX4/xCT protein expression. Bioinformatic and Western blot analyses were employed to explore the mechanism, revealing the involvement of HIF-1α and HO-1. Finally, an H/R model in HK-2 cells was used for further validation.
resultsVerbenalin administration significantly improved renal dysfunction and histological damage in IRI mice. Verbenalin inhibited IRI-induced renal tubular epithelial ferroptosis. HIF-1α and HO-1 expression was upregulated in the verbenalin treatment groups. H/R-induced HK-2 cell ferroptosis was inhibited by verbenalin treatment and worsened by HIF-1α knockdown. Inhibiting HIF-1α expression abrogated the protective effect of verbenalin, and HO-1 and GPX4 expression decreased.
conclusionsVerbenalin plays a renoprotective role in IRI-AKI by inhibiting renal tubular epithelial ferroptosis, partly via the HIF-1α/HO-1 pathway.
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