ArticleApplied biochemistry and biotechnology2023
Caesalpinia bonducella Counteracts Paracetamol-Instigated Hepatic Toxicity via Modulating TNF-α and IL-6/10 Expression and Bcl-2 and Caspase-8/3 Signalling.
Article in Applied biochemistry and biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The Role of Systemic Inflammation in Paracetamol Poisoning-An Experimental Model.International journal of molecular sciences · 2026Article
- Zingerone Alleviates Acetaminophen-Induced Liver Damage by Regulating Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy.Journal of biochemical and molecular toxicology · 2026Article
- Antioxidant and Hepatotoxicity Ameliorative Potential ofFood science & nutrition · 2025Article
- Green-Synthesized Silver Nanoparticles from Garlic Peel Target NF-κB and Redox Imbalance: A Novel Therapeutic Strategy Against Pyrogallol-Induced Hepatotoxicity in Rats.Nanomaterials (Basel, Switzerland) · 2025Article
- Hepatoprotective effect of Paederia foetida on paracetamol-induced hepatobiliary disease in rats via alteration of inflammatory and Nrf2/HO-1 pathway.Acta cirurgica brasileira · 2025Article
- A multidisciplinary approach to the antioxidant and hepatoprotective activities ofJournal of enzyme inhibition and medicinal chemistry · 2024Article
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2 authors.
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Abstract
Paracetamol is the most predominantly used antipyretic and analgesic drug. As paracetamol is metabolised mostly in the liver, both deliberate and unintentional overdoses of paracetamol are reported to provoke severe hepatotoxicity, including liver failure. Caesalpinia bonducella seed is well known for its medicinal and therapeutic properties. However, there is no report on its potential protective effects against paracetamol-instigated hepatotoxicity. Therefore, we studied the protective effects of aqueous seed extract of Caesalpinia bonducella (ASECB) on paracetamol-instigated hepatotoxicity in rats. Thirty female albino rats were divided into five groups: control, paracetamol-intoxicated, ASECB + paracetamol, silymarin + paracetamol, and ASECB alone. The rats were assessed for liver enzyme markers (alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transpeptidase), antioxidant activity (superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase), lipid peroxidation (malondialdehyde), histopathological, cytokine levels (pro-inflammatory cytokines TNF-α and IL-6, and anti-inflammatory cytokine IL-10), and protein expression (pro-apoptotic markers caspase 3 and caspase 8 and anti-apoptotic marker Bcl-2) after the 8-day study period. Repercussions of paracetamol intoxication induced upregulation of liver enzyme markers, antioxidant depletion, malondialdehyde production, decreased expression of Bcl-2 and IL-10, and overexpression of apoptotic and pro-inflammatory mediators, which were attenuated by pre-treatment with ASECB. ASECB markedly mitigated paracetamol-instigated liver injury by suppressing caspase-8/3 signalling and inflammatory infiltration in liver tissue by significantly reducing TNF-α and IL-6. In conclusion, ASECB pre-treatment exerts potent liver protection against paracetamol-instigated hepatotoxicity evidenced by mitigation of oxidative stress, lipid peroxidation, inflammation, and apoptosis.
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