ArticleBiological trace element research2026
Topiramate Attenuates Cadmium-Induced Nephrotoxicity Through Modulation of Oxidative Stress, Autophagy, and Apoptosis in Rats.
Article in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Targeting oxidative stress pathways in epilepsy: mechanistic insights into the role of ascorbic acid.Molecular biology reports · 2026Review
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7 authors.
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Abstract
Besides its traditional uses for epilepsy/migraine, topiramate has demonstrated remarkable antioxidant and anti-apoptotic features. In this study, we investigated the potential role of topiramate in mitigating cadmium-induced nephrotoxicity in rats, focusing on oxidative stress, apoptosis, and autophagy. Twenty-four male Wistar rats were randomly allocated into control, topiramate, cadmium, and cadmium + topiramate groups. Nephrotoxicity was induced by oral cadmium chloride (5 mg/kg/day) for 2 months, while topiramate (50 mg/kg/day) was co-administered orally. Renal injury, oxidative stress indices, autophagy-, and apoptosis-related proteins were examined using histopathology, ELISA, and immunohistochemistry. This study showed significant renal damage, manifested as multiple histological aberrations, elevated blood urea nitrogen and serum creatinine, along with elevated renal expression of kidney injury molecule-1 (KIM-1). Topiramate co-treatment reduced blood urea nitrogen and serum creatinine by 37.7% and 39%, respectively, and lowered KIM-1 by 36.9%, while lowering the endothelial/glomerular/tubular/interstitial (EGTI) histopathological damage score by 52.9%. Mechanistically, topiramate mitigated cadmium-induced nephrotoxicity by suppressing renal pro-oxidants and augmenting several antioxidant signals, including sirtuin 1 (SIRT1), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), and heme oxygenase 1 (HO-1) by 71.3%, 120.8%, and 78.7%, respectively. It also alleviated autophagy impairment by reducing sequestosome-1/protein 62 (SQSTM-1/p62) accumulation by 52.2% while activating AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR) pathway. Additionally, topiramate curtailed apoptosis, as evidenced by increased B cell lymphoma 2 (Bcl-2) protein levels and lowered Bcl-2-associated x protein (Bax) expression and caspase-3 activity. Collectively, promoting SIRT1/Nrf2 antioxidant pathway, enhancing AMPK/mTOR-directed autophagy, and dampening renal apoptosis were involved in topiramate's protection against cadmium nephrotoxicity.
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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 OpenQuestion graph.