Tuba Karaarslan

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 p-Coumaric Acid Against Lead-Induced Hepatic Oxidative Stress, Inflammation, and Apoptosis: Integrated Molecular and Machine Learning-Based Analysis.

Lead (Pb) exposure is a major environmental health concern that induces hepatic injury through oxidative stress, inflammation, and apoptosis. This study evaluated the hepatoprotective effects of p-coumaric acid (PCA), a phenolic compound, against Pb-induced liver toxicity using integrated molecular and machine-learning approaches. Male rats were allocated into experimental groups and exposed to Pb-acetate (30mg/kg), while PCA was orally administered at 50 and 100mg/kg for 14 days. A dataset consisting of 30 adult male rats (n = 6 per group) was analyzed using biochemical, molecular, inflammatory, and histopathological parameters. Oxidative stress markers, antioxidant and apoptotic gene expression, inflammatory protein expression, and liver tissue alterations were assessed. In addition, principal component analysis (PC analysis), correlation heatmap analysis, and Random Forest-based SHAP (Shapley Additive Explanations) analysis were applied to identify key biomarkers associated with Pb toxicity and PCA-mediated protection. Pb exposure caused a pronounced oxidative imbalance, evidenced by significant depletion of antioxidant defenses, including reduced glutathione (GSH) (p < 0.001), glutathione peroxidase (GPx) (p < 0.001), and catalase (Cat) gene expressions (p < 0.001), together with increased malondialdehyde (MDA) levels (p < 0.001). Pb also up-regulated Bax and Casp3 (p < 0.001), down-regulated Bcl-2 (p < 0.01), and activated NF-κB, IL-1β, TNF-α, IL-6, and COX-2 (p < 0.001). Histopathology confirmed severe hepatocellular degeneration and necrosis. PCA treatment attenuated these alterations in a dose-dependent manner, with 100mg/kg showing the strongest protection (p < 0.05). Overall, PCA alleviates Pb-induced hepatotoxicity by restoring antioxidant defenses, suppressing inflammatory signalling, and inhibiting mitochondrial apoptotic pathways.

Morin attenuates vancomycin-induced nephrotoxicity via Nrf-2/HO-1, SIRT1/PGC1α and AKT/FOXO1A pathways

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.

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.