Protective Effects of Virgin Olive Oil Against Titanium Dioxide Nanoparticle-Induced Hepato-Renal Toxicity: Evidence from Oxidative Stress Biomarkers and Restoration of Antioxidant Enzyme Activities.

Synergistic protective effects of curcumin nano-emulsion and virgin coconut oil against thermal oxidation of sunflower oil and its hepatorenal toxicity in rats

Introduction Repeated heating of vegetable oils leads to the generation of toxic oxidation products, which activate systemic oxidative stress and cause multi-organ injuries. This study examined the hepatorenal synergistic protection of Curcumin Nano-Emulsion (CNE) and virgin coconut oil (VCO) against the toxicity of thermally stressed sunflower oil (HSO) and explored the underlying antioxidant and anti-inflammatory mechanisms. Methods CNE was characterized by nanoscale particle size, high encapsulation efficiency, and excellent stability. HSO was supplemented with VCO (20% w/w) and CNE (200 ppm) to evaluate improvements in oxidative stability in vitro by measuring peroxide value, p-anisidine value, total polar compounds, and toxic aldehydes. For the in vivo study, sixty-four male Wistar rats were fed different oil-based diets for two months. Biochemical parameters, oxidative stress markers, inflammatory indices, and histopathological changes in liver and kidney tissues were assessed. Immunohistochemical analysis was performed to evaluate NF-κB and Nrf2 signaling pathways. Results Supplementation of HSO with VCO and CNE significantly improved oxidative stability compared with individual treatments and TBHQ, with marked reductions in peroxide value, p-anisidine value, total polar compounds, and toxic aldehydes. HSO induced significant hepatorenal injury, dyslipidemia, oxidative stress, and inflammation in rats. The combined treatment (HSO + VCO + CNE) markedly ameliorated these alterations, nearly restoring biochemical parameters to normal levels and minimizing histopathological damage. A strong downregulation of the NF-κB pathway and activation of the Nrf2 antioxidant pathway were observed. Discussion Co-administration of curcumin nano-emulsion and virgin coconut oil effectively enhances the oxidative stability and safety of thermally stressed edible oils. These findings suggest a promising natural strategy to reduce oil-induced toxicity and support safer industrial oil processing approaches aligned with public health protection.

Biochemical Antioxidant Effects of Ellagic Acid Against Di-(n)-butyl Phthalate–Induced Oxidative Stress in Rat Brain Tissue

Di-n-butyl phthalate (DBP), a widely used plasticizer, induces oxidative stress and neurotoxicity through the generation of reactive oxygen species. Ellagic acid (EA), a natural polyphenolic antioxidant, may counteract these effects. This study aimed to evaluate the protective role of EA against DBP-induced oxidative brain injury. Thirty-two male rats were randomly divided into four groups: Control, DBP, EA, and DBP+EA. DBP was administered orally at a dose of 500 mg/kg/day, while EA was given by gavage at 2 mg/kg/day for four weeks. Oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities were analyzed in brain tissue. DBP exposure significantly increased TBARS levels while decreasing GSH and SOD activities, indicating lipid peroxidation and antioxidant depletion. In contrast, CAT activity was elevated, suggesting a compensatory enzymatic response to excess hydrogen peroxide. EA treatment markedly attenuated oxidative damage by restoring GSH and SOD levels and normalizing CAT activity. These findings indicate that DBP disrupts redox homeostasis by inducing lipid peroxidation, while EA mitigates this effect through restoration of antioxidant defenses.

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.

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

Green-synthesized Salvia officinalis-conjugated Selenium Nanoparticles Mitigate Diabetic Complications via Multi-target Molecular and Histopathological Restoration in STZ-induced Mice

Diabetes mellitus is a chronic metabolic disease characterized by hyperglycemia and oxidative stress, which can lead to serious complications. In recent years, with the development of nanomedicine, selenium nanoparticles (SeNPs) have emerged as promising therapeutic agents due to their antioxidant and insulin-mimetic properties. This experiment aimed to evaluate the therapeutic efficacy of selenium nanoparticles prepared from Salvia officinalis leaves extract (SOLE–SeNPs) on metabolic, oxidative, inflammatory, and histopathological complications in STZ-induced diabetic mice SOLE-SeNPs were synthesized by an aqueous leaf extract as both a natural reducing and capping agent. TEM, DLS, zeta potential, UV–Vis spectroscopy, and FTIR techniques were used for the characterization of nanomaterials with regard to morphology, particle size, surface charge, optical properties, and biomolecular interaction. Male mice were classified into five groups, and two doses of SOLE-SeNPs (21.4 and 53.5 mg/kg) or glibenclamide (600 µg/kg) were administered for 21 days after STZ treatment to induce diabetes. Glucose, insulin, lipid profile, oxidative stress markers (GSH, SOD, and MDA), cytokine levels (IL-6 and TGF-β1), gene expression analysis (Bcl-2, GK, and GLUT2), as well as hepatic histopathology were evaluated for therapeutic assessment. Nanoparticle characterisation verified the successful synthesis with spherical shape (diameter 75 nm), good dispersity (DLS peak 60 nm), and high colloidal stability (zeta potential: - 44.84 mV). SOLE-SeNPs, especially at high doses, significantly decreased plasma glucose and triglyceride levels, accompanied by increased insulin and HDL-C levels, along with total cholesterol recovery. Elevated GSH and SOD, along with decreased MDA, confirm the powerful antioxidant effect of SOLE-SeNPs. Pro-inflammatory cytokines were markedly reduced. At the molecular level, we observed upregulation of Bcl-2 and GK in the pancreas and modest modulation of GLUT2 in the liver. Histopathological evaluation indicated almost restored hepatic architecture with high-dose SOLE-SeNPs treatment, outperforming glibenclamide in most parameters The results of this study showed that the SeNPs synthesized by SOLE extract have notable antidiabetic and antioxidant activities, which implies a combination of selenium bioactivity and some other phytochemical compounds in S. officinalis. These findings confirm the mode of action previously reported for nanoparticle-mediated therapy through an exciting new, environmentally friendly synthesis method. Limitations: Brief treatment duration and no assessment of long-term toxicities SOLE-SeNPs possessed strong and dose-dependent efficacy in preventing diabetic complications through a comprehensive set of metabolic, antioxidant, anti-inflammatory, and gene-modulatory actions. The phytoconjugated character assures their synergistic bioactivity, making them a novel green nanoplatform for diabetes treatment. The long-term safety, biodistribution, and cellular pathways must be investigated in future studies to further confirm the clinical application.

Antioxidant and anti-inflammatory effects of polyphenol-rich Illicium verum extract on lipopolysaccharide-induced liver injury in rats

Pretreatment with PEIV significantly mitigated effects of LPS-induced liver injury by regulating biochemical parameters, reducing oxidative stress and inflammation, and preserving liver architecture, suggesting its potential as a natural therapeutic agent for liver diseases.