Evidence map›Paper›PMID 40826372›Full record

ArticleBiological research2025

Effect of sodium thiosulfate on preventing renal ischemia-reperfusion injury in high-fat diet-fed rats: the role of renal mitochondrial quality.

Priyanka N Prem, Gino A Kurian

Abstract read
In one paragraph

Article in Biological research, 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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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Priyanka N PremSchool of Chemical and Biotechnology, SASTRA Deemed University, Tirumalaisamudram, Thanjavur, Tamil Nadu, India.
Gino A KurianSchool of Chemical and Biotechnology, SASTRA Deemed University, Tirumalaisamudram, Thanjavur, Tamil Nadu, India. kurian@scbt.sastra.edu.

Funding

Council of Scientific and Industrial Research (IN) 09/1095/(0040)/2018-EMR-1
6 · The paper itself

Abstract

objectiveSodium Thiosulfate (STS), a clinically approved agent for cyanide poisoning and vascular calcification, possesses antioxidant, anti-inflammatory, mitochondrial preservation, and metal chelation capabilities, rendering it a promising candidate for managing ischemia-reperfusion (IR) injury. The detrimental impact of high-fat diets (HD) on the outcomes of IR during renal surgeries is well-documented. However, the potential of STS to ameliorate renal IR injury in rat fed with high fat diet is not known.

methodsMale Wistar rats were fed a standard diet (SD) or a high-fat diet (HD) for 16 weeks before undergoing an IR protocol (45 min of ischemia followed by 24 h of reperfusion). STS (10 mg/kg) was administered 30 min before IR.

resultsSTS effectively mitigated IR-induced physiological decline and tissue damage in SD rats but was less effective in HD rats. To explore this difference, we measured renal mitochondrial quality. STS improved mitochondrial bioenergetics, balanced mitochondrial dynamics, and increased mitochondrial copy number in SD-IR rats more than in HD-IR rats. Additionally, STS significantly reduced oxidative stress and upregulated Pgc-1α, Polg, and Tfam genes in SD-IR rats but had a lesser effect in HD-IR rats. The 16-week HD significantly reduced renal mitochondrial quality at the basal level, hindering STS-mediated protection.

conclusionThese findings highlight the efficacy of STS in managing renal IR and emphasize the need for nutritional support to restore mitochondrial function in high-fat diet subjects.

Indexed as

Diet, High-FatKidneyMitochondriaReperfusion InjuryThiosulfatesAnimalsAntioxidantsMaleOxidative StressRatsRats, WistarAntioxidantssodium thiosulfateThiosulfatesHigh fat dietMitochondriaOxidative stressRenal ischemia reperfusionSodium thiosulfate

Identifiers

PMID40826372
PMCPMC12359898

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.