ArticleFrontiers in pharmacology2026
Saroglitazar protects against cadmium-induced hepatorenal injury in rats by suppressing NF-κB and upregulating Nrf2.
Article in Frontiers in pharmacology, 2026. 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
Introduction: Cadmium (Cd) toxicity is one of the major public health problems because of its long half-life (10-30 years). Exposure to Cd can cause toxicity that affects several organs, including the liver and the kidney. Saroglitazar is highlighted in this study as a potential preventative medication against hepatic-renal damage induced by Cd in rats. Methods: Cd (3 mg/kg) was injected for five successive days to induce hepatic and renal damage. Saroglitazar (2 and 4 mg/kg/day) was given orally for five successive days concurrently with Cd. Results: Saroglitazar effectively improved hepatic and renal function and structure. In the meantime, saroglitazar mitigated the oxidative stress caused by Cd; it increased the level of reduced glutathione (GSH) and the activity of superoxide dismutase (SOD) and decreased malondialdehyde (MDA) content. Saroglitazar-treated groups showed a significant reduction in hepatic and renal nuclear factor kappa B (NF-κB), tumor necrosis factor (TNF)-α, and interleukin-6 (IL-6). Furthermore, saroglitazar pretreatment significantly increased nuclear factor erythroid 2-related factor 2 (Nrf2); furthermore, there was a marked reduction in the expression of caspase-3 in both hepatic and renal tissues. Conclusion: Collectively, saroglitazar showed a protective effect against Cd-induced hepatorenal injury in rats.
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