Article3 Biotech2024
Morin hydrate ameliorates Di-2-ethylhexyl phthalate (DEHP) induced hepatotoxicity in a mouse model via TNF-α and NF-κβ signaling.
Article in 3 Biotech, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Liposomal Morin Attenuates DMH-Associated Colonic Oxidative Stress, Inflammation, and Apoptosis/Autophagy-Related Dysregulation in Rats.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Curcumin attenuates di(2-ethylhexyl) phthalate-induced hepatic injury in chicks via oxidative stress, glycolysis, and PANoptosis-related signaling.Poultry science · 2026Article
- Morin hydrate alleviated cisplatin-induced testicular toxicity in rats via modulating NLRP3/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Ameliorated Hepatoprotective Aptitude of Novel Lignin Nanoparticles on APAP-Induced Hepatotoxicity in a Murine Model.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Morin: a promising hepatoprotective agent against drug and chemical-induced liver injury.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Mechanism of Mongolian Medicine Batri-7 onJournal of inflammation research · 2025Article
- Analyzing the potential targets and mechanisms of liver damage induced by acetyl tributyl citrate plasticizer using network toxicology, molecular docking andFrontiers in pharmacology · 2025Article
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Authors and funding
5 authors.
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Abstract
Di-(2-ethylhexyl) phthalic acid (DEHP) pollutes the environment, and posing a significant risk to human and animal health. Consequently, a successful preventative strategy against DEHP-induced liver toxicity needs to be investigated. Morin hydrate (MH), a flavanol compound, possesses toxic preventive attributes against various environmental pollutants. However, the effects of MH have not been investigated against DEHP-induced liver toxicity. Female Swiss albino mice were divided into four groups: control, DEHP (orally administered with 500 mg/kg, DEHP plus MH 10 mg/kg, and DEHP plus MH 100 mg/kg for 14 days. The results showed that the MH treatment ameliorated the DEHP-induced liver dysfunctions by decreasing the alanine transaminase (ALT), aspartate aminotransferase (AST), total bilirubin, liver histoarchitecture, fibrosis, and markers of oxidative stress. Furthermore, DEHP increased apoptosis, increased active caspase 3 and decreased B cell lymphoma-2 (Bcl-2) expression. However, the MH treatment showed a differential effect on these proteins; a lower dose increased, and a higher dose decreased the expression. Thus, a lower dose of MH could be involved in the disposal of damaged hepatocytes. Expression of Estrogen receptors alpha (ERα) also showed a similar trend with active caspase 3. Furthermore, the expression of Tumor necrosis factor alpha (TNF-α) and Nuclear factor-κβ (NF-κβ) were up-regulated by DEHP treatment, and MH treatment down-regulated the expression of these two inflammatory markers. Since this down-regulation of TNF-α and NF-κβ coincides with improved liver functions against DEHP-induced toxicity, it can be concluded that MH-mediated liver function involves the singling of TNF-α and NF-κβ.
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