Protective effects of Rosmarinus officinalis against methotrexate-induced hepatorenal toxicity in Wistar rats: Biochemical, histopathological, and immunohistochemical evaluation

Rosemary (Rosmarinus officinalis) Extract Attenuates Methotrexate-Induced Oxidative Stress, Inflammatory Disturbance, and Apoptotic Lung Injury: A Molecular and Histopathological Study.

The potential therapeutic effect of quercetin on mitochondrial dysfunction in hepatorenal toxicity induced by aluminum chloride in an experimental rat model

Aluminum is a xenobiotic element known to induce hepatorenal toxicity through mechanisms involving mitochondrial dysfunction, oxidative stress, and inflammation. Quercetin, a dietary flavonoid with potent antioxidant and anti-inflammatory properties, has shown promise as a therapeutic agent. This study aimed to evaluate the potential therapeutic effects of quercetin against aluminum chloride (AlCl₃)-induced hepatorenal toxicity and mitochondrial dysfunction in rats. Hepatorenal toxicity was induced by oral administration of hydrated aluminum chloride (75 mg/kg body weight) daily for six weeks. Quercetin was administered intraperitoneally at a dose of 30 mg/kg body weight daily for four weeks. Biochemical assays, mitochondrial gene expression analysis, and histopathological examinations were conducted to assess the therapeutic effects. Quercetin significantly ameliorated lipid, protein, and DNA oxidation parameters (MDA, AOPPs and 8-OHdG respectively), reduced inflammation marker (TNF-α), and restored mitochondrial biogenesis markers, including PGC-1α, mtTFA and mitochondrial DNA copy number (mtDNA-CN). In addition, Quercetin significantly decreased TNF-α and increased PGC-1α contents at protein levels. Histopathological findings corroborated these results, demonstrating that quercetin improved liver and kidney architecture. These findings suggest that quercetin may serve as a potential therapeutic agent for aluminum-induced hepatorenal toxicity.

Evaluation of the Hepatoprotective Activity of Serinolamide A against Paracetamol-Induced Hepatotoxicity in Rats

Paracetamol-induced hepatotoxicity is characterized by oxidative stress, inflammatory responses, and progressive liver damage. The present study aimed to evaluate the hepatoprotective effects of Serinolamide A against paracetamol-induced hepatotoxicity in rats. Experimental hepatotoxicity was induced by paracetamol administration, and rats were treated orally with Serinolamide A (1, 5, and 10 mg/kg) for 28 consecutive days. Liv52 (70 mg/kg, p.o.) was used as the standard drug. Body weight, liver weight, serum biochemical parameters, oxidative stress markers, pro-inflammatory cytokines, and histopathological changes were evaluated. Treatment with Serinolamide A significantly ameliorated paracetamolinduced alterations and restored body and liver weights. Furthermore, Serinolamide A enhanced antioxidant defense by increasing superoxide dismutase, catalase, and reduced glutathione activities and reduced lipid peroxidation. The treatment also attenuated inflammatory responses by decreasing tumor necrosis factor-α and interleukin-6 levels. Histopathological examination revealed marked protection against paracetamol-induced hepatic damage. The observed effects were dose-dependent, with the 10 mg/kg dose showing effects comparable to those of Liv52. These findings suggest that Serinolamide A possesses significant hepatoprotective activity, which may be attributed to its antioxidant and anti-inflammatory properties, and could represent a promising therapeutic candidate for the management of drug-induced liver injury

The antioxidant, anti-inflammatory and anti-apoptotic effects of Cucumis melo var. agrestis Naudin in doxorubicin-induced hepatotoxicity and nephrotoxicity in rats

CM significantly attenuates DOX-induced hepatotoxicity and nephrotoxicity, particularly at a dose of 250 mg/kg, and its protective effects are likely mediated through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms.

Nicotinamide Riboside Attenuates Cisplatin-Induced Hepatorenal Toxicity Through Restoration of NAD+ Homeostasis and Nrf2/NQO1-Dependent Antioxidant Signaling

Nicotinamide riboside exerts protective effects against cisplatin-induced hepatorenal toxicity that are mechanistically linked to activation of the Nrf2/NQO1 antioxidant pathway and restoration of hepatic NAD+ homeostasis.

Comparative Hepatoprotective Effects of Carica papaya, Azadirachta indica, and Allium sativum Extracts against Diethyl Nitrosamine-Induced Liver Injury in Wistar Rats

It is indicated that combining papaya, neem, and garlic extracts may provide greater hepatoprotection than administering the individual extracts against DEN-induced liver injury, and supports further mechanistic and preclinical evaluation of this polyherbal formulation before its potential therapeutic application in liver-disease management.