Zingerone Alleviates Acetaminophen‐Induced Liver Damage by Regulating Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy

Neuroprotective effects of zingerone on the thioacetamide-induced hepatic encephalopathy in rats. Insights from oxidative stress, ER stress, BDNF signaling and apoptosis

Betaine Alleviates Favipiravir-induced Ovarian and Uterine Toxicity by Regulating Oxidative, Inflammatory, Cellular Death, Steroidogenic, Hormonal, and Histopathological Changes

Hesperidin mitigates DEHP-induced nephrotoxicity through anti-oxidant, anti-apoptotic, and anti-inflammatory pathway modulation: Evidence from Nrf2/HO-1/Keap-1, Bax/Bcl-2/caspase-3, and TLR4/NF-κB axis activation

Objective(s): This study aimed to assess the protective role of hesperidin (HSP), a citrus flavonoid, against di-(2-ethylhexyl) phthalate (DEHP)-induced kidney toxicity in rats, focusing on oxidative stress, apoptosis, inflammation, and anti-oxidant defense pathways. Materials and Methods: Thirty-five male rats were randomly assigned into five groups (7 per group): control group, DEHP-treated group (1 g/kg), DEHP + HSP (100 mg/kg) group, DEHP + HSP (200 mg/kg) group, and HSP-alone group, and treated orally for 10 consecutive days. Kidney tissues were collected for biochemical assays, including malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Gene expression of Nrf2, Keap1, HO-1, Bax, Bcl-2, Caspase-3, TLR-4, and NF-κB was analyzed using real-time PCR, and protein levels were evaluated using Western blotting. Results: DEHP significantly increased oxidative damage and the expression of inflammatory and apoptotic markers, while decreasing anti-oxidant parameters. Co-treatment with HSP, particularly at 200 mg/kg, restored anti-oxidant balance, reduced lipid peroxidation, and down-regulated the expression of TLR-4, NF-κB, and Caspase-3. Moreover, HSP increased Bcl-2 levels and enhanced Nrf2/HO-1 signaling, as confirmed by both gene and protein expression data. Conclusion: HSP demonstrates dose-dependent renoprotective effects against DEHP-induced nephrotoxicity in rats. The protective mechanism involves anti-oxidant enhancement and inhibition of oxidative stress-induced inflammation and apoptosis, supporting the therapeutic potential of HSP in managing phthalate-related renal injury.

Enhanced hepatoprotective effects of fisetin-loaded liposomal nanoparticles against DEHP-induced liver injury in rats: modulation of oxidative stress, inflammation, apoptosis, and ferroptosis pathways.

MOLECULAR EFFECTS OF QUINOA ON RAT KIDNEY: A DOSE-DEPENDENT STUDY ON PYROPTOSIS AND ANTIOXIDANT DEFENSE

Oxidative stress and inflammation contribute to renal dysfunction, and antioxidant-rich functional foods may modulate these processes. This study evaluated the effects of dietary quinoa on oxidative stress and the expression of pyroptosis, inflammation and apoptosis-related genes in healthy rat kidneys. Forty male Wistar albino rats were randomly assigned to control and diet groups containing 5%, 10% or 20% quinoa for six weeks (n=10). Rat body weight, superoxide dismutase activity, glutathione, and malondialdehyde levels in kidney tissue were measured; expression of nine genes was assessed in a representative subgroup using quantitative real-time polymerase chain reaction. Quinoa dose-dependently increased antioxidant markers, reduced lipid peroxidation, and downregulated inflammasome (Nlrp3, Casp-1,Gsdmd), inflammatory (Nf-κB, IL-1β, Tnf-α), and apoptotic (Bax,Casp-3) genes, while increasing Bcl2 expression, with the greatest effects at 10% and 20% quinoa. These findings provide evidence that dietary quinoa beneficially modulates renal molecular pathways involved in oxidative stress and inflammatory responses under physiological conditions.

Protective effects of thymoquinone against hexavalent chromium-ınduced nephrotoxicity: a multiparametric evaluation of oxidative stress, ınflammation, ferroptosis- and apoptosis-related markers