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Aslıhan Atasever

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Open access Aug 2026

Morin Protects Against Cadmium-Induced Acute Renal Toxicity by Reducing Oxidative Stress and Inflammation

Cadmium (Cd) is a highly toxic heavy metal that accumulates primarily in the kidneys, where it induces oxidative stress, inflammation, and cellular damage. Cd exposure is a major environmental and occupational concern due to its persistence and bioaccumulative nature. Morin, a natural flavonoid abundant in various fruits and medicinal plants, possesses potent antioxidant and anti-inflammatory properties. However, its potential protective efficacy against Cd-induced nephrotoxicity has not been fully elucidated. This study aimed to evaluate the protective effects of Morin against Cd-induced oxidative and inflammatory damage in rat kidney tissue and to assess its association with oxidative stress and inflammatory responses. Fifty adult male Sprague-Dawley rats were randomly divided into five groups: Control, Cd (6.5 mg/kg, i.p.), Morin100+Cd (100 mg/kg Morin + Cd), Morin200+Cd (200 mg/kg Morin + Cd), and Morin200 (200 mg/kg Morin alone). Cadmium was administered intraperitoneally for 5 consecutive days, while Morin was given intragastrically one hour before Cd injection. Cadmium exposure significantly elevated malondialdehyde (MDA) levels and proinflammatory cytokines (TNF-α, IL-1β, IL-6, IFN-γ) while reducing the activities of antioxidant enzymes (SOD, CAT, GPx, GSH) and anti-inflammatory cytokines (IL-10, IL-4). Morin treatment, particularly at 200 mg/kg, markedly ameliorated these alterations by suppressing oxidative stress, restoring antioxidant enzyme activities, and modulating cytokine balance. These findings indicate that Morin exerts a strong nephroprotective effect against Cd-induced renal toxicity through attenuation of oxidative stress and inflammation, possibly associated with its antioxidant and anti-inflammatory properties. Therefore, Morin may represent a promising natural therapeutic candidate for the prevention of heavy metal-induced renal injury.

Burak Batuhan Laçin, Furkan Aykurt, S. Tekin et al. · 0 citations
Aug 2026

p-Coumaric Acid Attenuates Lead Acetate-induced Neurotoxicity in Rats by Improving Behavioral Dysfunction and Suppressing Oxidative Stress, Neuroinflammation, Apoptosis, and Plasticity-related Molecular Alterations.

It is suggested that p-coumaric acid exerts neuroprotective effects against PbAc-induced brain injury by attenuating oxidative stress, neuroinflammation, and apoptosis while supporting neuronal plasticity.

Tuba Karaarslan, Merve Bolat, İsmail Bolat et al. · 0 citations

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