TL;DR
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.
Drug-induced liver injury is a major health concern and represents one of the most common causes of acute liver failure. Diclofenac, a widely prescribed non-steroidal anti-inflammatory drug (NSAID), is known to induce hepatotoxicity through oxidative stress, mitochondrial dysfunction, and the formation of reactive metabolites. Natural products with antioxidant properties have gained attention as potential hepatoprotective agents. Impatiens balsamina Linn. is a medicinal plant traditionally used for various therapeutic purposes and is rich in flavonoids, phenolic compounds, tannins, and other bioactive constituents with potent antioxidant activity. The present study was undertaken to evaluate the hepatoprotective activity of the hydroalcoholic extract of Impatiens balsamina leaves (HAEIB) against diclofenac-induced hepatotoxicity in experimental rats. HAEIB treatment significantly restored altered biochemical parameters, increased GSH and SOD levels, and reduced LPO levels compared with the diclofenac-treated group, indicating attenuation of oxidative stress. Histopathological examination revealed marked protection against hepatic degeneration, necrosis, and inflammatory cell infiltration. HAEIB at a dose of 400 mg/kg demonstrated hepatoprotective activity comparable to that of the standard drug silymarin. These findings suggest that the hepatoprotective effect of HAEIB may be attributed to its antioxidant phytoconstituents and support its potential use as a natural hepatoprotective agent.
Panax ginseng is a widely recognized medicinal plant known for its hepatoprotective, antioxidant, and anti-inflammatory activities. These properties are largely attributed to its active constituents, the ginsenosides. Diclofenac, a commonly used nonsteroidal anti-inflammatory drug is associated with clinically significant hepatotoxicity characterized by oxidative stress, mitochondrial dysfunction, and hepatocellular injury. This study aimed to investigate the protective and therapeutic efficacy of the alcoholic extract of Panax ginseng against diclofenac-induced hepatotoxicity in adult male rats. Forty-nine rats were allocated into seven experimental groups and administered diclofenac, P. ginseng extract, or combined treatments for 30 days according to the study design. Serum biomarkers of liver function (ALT, AST, ALP) and oxidative stress (MDA, SOD) were measured, and liver tissues were subjected to histopathological evaluation. Diclofenac administration resulted in marked elevations in liver enzyme activities and significant oxidative stress, accompanied by histological alterations including vacuolar degeneration, hepatocellular necrosis, and inflammatory infiltration. In contrast, both co-administration and post-treatment with Panax ginseng extract produced substantial improvements in biochemical and histological parameters, restoring enzyme levels, reducing lipid peroxidation, enhancing antioxidant activity, and improving liver architecture. The Panax ginseng extract alone produced no adverse hepatic effects. These findings demonstrate that the alcoholic extract of Panax ginseng possesses both preventive and therapeutic hepatoprotective properties against diclofenac-induced liver injury, likely mediated through its antioxidant and anti-inflammatory mechanisms. The results support its potential use as a natural agent for mitigating drug-induced hepatotoxicity.
Background: Liver diseases remain a major global health problem, and currently available therapies are often associated with limitations and adverse effects. Medicinal plants rich in antioxidant phytoconstituents have emerged as promising alternatives for the management of hepatic disorders. Curcuma pseudo-montana is traditionally used in folk medicine for the treatment of various ailments, including liver-related disorders. Objective: The present study was undertaken to evaluate the hepatoprotective effect of 50% methanolic extract of Curcuma pseudo-montana rhizomes against D-galactosamine-induced hepatic injury in rats. Materials and Methods: Hepatic injury was induced in Wistar albino rats using D-galactosamine (600 mg/kg, i.p.). Animals were treated with 50% methanolic extract of Curcuma pseudo-montana rhizomes at doses of 200 and 400 mg/kg body weight. Silymarin (100 mg/kg) was used as the standard hepatoprotective drug. Serum biochemical markers including SGOT, SGPT, ALP, bilirubin, and total protein were evaluated. Antioxidant parameters such as catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), and malondialdehyde (MDA) were estimated. Histopathological examination of liver tissues was also performed. Results: D-galactosamine administration produced significant hepatic injury characterized by elevated serum SGOT, SGPT, ALP, and bilirubin levels along with a reduction in total protein content. Oxidative stress was evidenced by decreased CAT, SOD, and GSH levels and increased MDA concentration. Treatment with the 50% methanolic extract significantly restored liver function markers and antioxidant enzyme levels in a dose-dependent manner. The higher dose (400 mg/kg) demonstrated greater hepatoprotective activity and significantly reduced lipid peroxidation. Histopathological examination confirmed marked protection against hepatocellular degeneration, necrosis, and inflammatory infiltration, with near-normal hepatic architecture observed in the high-dose treatment group. Conclusion: The findings demonstrate that the 50% methanolic extract of Curcuma pseudo-montana rhizomes possesses significant hepatoprotective activity against D-galactosamine-induced liver injury. The protective effect may be attributed to its antioxidant and anti-inflammatory properties, supporting the traditional use of the plant in liver disorders.
This study investigated the protective effects of Cucumis melo var. agrestis Naudin (CM) at various doses against doxorubicin-induced liver and kidney injury in rats. Thirty male Wistar rats were randomly divided into five groups (n = 6 per group). DOX was administered intraperitoneally at a dose of 15 mg/kg on day 5. CM was administered orally at doses of 100, 250 or 500 mg/kg daily for ten consecutive days after DOX administration. Histological and immunohistochemical analyses were performed to evaluate tissue damage and the expression levels of caspase-3, HSP70, NF-κB p65 and TNF-α. Serum cytokines (IL-6, IL-1β, TNF-α and IL-10) and oxidative stress markers (TOS and TAS) were also measured. The DOX group exhibited significant liver and kidney damage, including hepatocellular degeneration, vascular congestion, and injury to the glomeruli and tubules, as well as increased immunoreactivity for Caspase-3, HSP70, NF-κB-p65, and TNF-α. The DOX+CM250 group showed a significant improvement in histological appearance and a marked reduction in immunoreactivity. Compared to the DOX group, this group also demonstrated decreased levels of pro-inflammatory cytokines and TOS, and increased IL-10 and TAS levels. CM significantly attenuates DOX-induced hepatotoxicity and nephrotoxicity, particularly at a dose of 250 mg/kg. Its protective effects are likely mediated through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. Abbreviations: ALT – Alanine aminotransferase, AST – Aspartate aminotransferase, Bax – Bcl-2–associated X protein, Bcl-2 – B-cell lymphoma 2, BUN – Blood urea nitrogen, CM – Cucumis melo var. agrestis Naudin, DOX – Doxorubicin, GGT – Gamma-glutamyl transferase, GR – Glutathione reductase, GSH – Glutathione, HSP70 – Heat shock protein 70, IHC – Immunohistochemistry, IL – Interleukin, IL-1β – Interleukin-1 beta, IL-6 – Interleukin-6, IL-10 – Interleukin-10, MDA – Malondialdehyde, NF-κB – Nuclear factor kappa B, NF-κB p65 – Nuclear factor kappa B subunit p65, PCNA – Proliferating cell nuclear antigen, ROS – Reactive oxygen species, SOD – Superoxide dismutase, TAS – Total antioxidant status, TNF-α – Tumor necrosis factor alpha, TOS – Total oxidative status
The present study is aimed at the evaluation of protective effects of Arundo donax L. (AD) against chemical-induced toxicity in rats, especially considering its antioxidant, hepatoprotective, and hematoprotective activities. The antioxidant potential of AD extract was assessed using 2,2-diphenyl-1-picrylhydrazyl (DPPH), hydrogen peroxide scavenging, and ferric reducing antioxidant power assays. Hepatoprotective activity was evaluated in Wistar rats using carbon tetrachloride- and paracetamol-induced hepatotoxicity models by estimating biochemical liver markers and histopathology. In this study, doses of 200 and 400 mg/kg body weight were selected. AD extract exhibited strong antioxidant activity, as shown by the DPPH radical scavenging activity of 77.68% at 250 µg/mL compared to ascorbic acid at 81.15%. The treatment with AD extract at 400 mg/kg significantly restored serum glutamate pyruvate transaminase of 115 IU/L, serum glutamate oxaloacetate transaminase of 252.65 IU/L, and alkaline phosphatase of 229 IU/L, whereas it increased total protein to 5.06 g/dL and albumin to 2.28 mg/dL in restoring liver function. Similarly, in the paracetamol model, AD extract at 400 mg/kg improved hepatotoxicity markers, reducing bilirubin levels to 1.23 mg/dL, while increasing total protein (10.65 g/dL) and albumin (3.65 mg/dL). Hematological suppression was significantly found after cyclophosphamide administration (hemoglobin: 7.37 g%, red blood cell: 2.48 million/mm³, white blood cell: 0.71 thousand/mm³, platelets: 335.83 × 104 per mm³). The conclusion from this study can be helpful in the usage of AD as an adjuvant therapy that minimizes toxic effects of chemotherapy and improves treatment outcomes.
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.