Methylene Blue Mitigated Acetaminophen-Induced Hepatotoxicity in an Experimental Animal Model

Feb 3, 2026

Journal J Biochem Technol (2025) 16(4): 56-62

DOI https://doi.org/10.51847/SDmllYjuwy

Issue 4

Volume 16

Acetaminophen (AMP)-induced hepatotoxicity (AIH) is the critical side effect associated with high-dose exposure. N-acetylcysteine (NAC) is the gold standard to preserve the liver against AMP toxicity, with some drawbacks, leading to the search for alternative therapy. The antioxidant properties of methylene blue (MB), make its application plausible for AIH, as an additive therapy with NAC or alone. Therefore, the present study aimed to define the histological impact of MB on hepatoprotection. A total of 49 rats were enrolled in the present study. Rats were sub-classified into 7 groups: control group, AMP group, MB group, prophylaxis-MB low dose, prophylaxis-MB high dose, treatment-MB low dose, and treatment-MB high dose. Liver histopathological changes were examined under a microscope, and images were taken for all groups. Photomicrograph of a rat's liver section in the control group exposed to normal saline showing intact tissue. Rat liver sections from the AMP-treated group demonstrated central venous dilatation and severe portal inflammation. Rat liver section in the MB-50 prophylaxis group demonstrated mild portal inflammation with an increase in ductular proliferation. Rat liver section in the MB group with portal tracts, with no significant pathology. A rat liver section from the MB-100 prophylaxis group demonstrated a mild increase in portal ductules. The rat liver section in the MB-50 and MB-100 treatment group demonstrated a liver with a normal central vein. The MB intervention demonstrated marked protective effects against AIH in experimental rats, with interventional treatment providing better resolution than prophylaxis; nevertheless, both interventions were effective in blocking hepatotoxicity. Background: Acetaminophen induced hepatotoxicity is the critical side effect associated with high dose exposure. NAC is the gold standard to preserve liver against AMP toxicity, with some drawbacks lured searching for alternative therapy.

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THE PROTECTIVE EFFECT OF MILK OF THISTLE AGAINST DOXORUBICIN OR METHOTREXATE INDUCED CARDIOTOXICITY

Feb 3, 2026

Journal GEORGIAN MEDICAL NEWS

DOI https://www.scopus.com/pages/publications/105027043207?origin=resultslist

Issue 368

Volume 11

Background: Doxorubicin (DOX) and methotrexate (MXT) are strong anticancer agents and gold standard therapy for several malignancies, with efficacy restricted by cardiotoxicity. Milk thistle extract (MTE) has demonstrated strong antioxidant and cytoprotective properties; we sought to determine the role of MTE in protection against Dox or MXT-induced cardiac damage. Methods: A total of 35 white albino rats were divided into five groups: control, Dox alone (1.66mg/kg/48hr, IP) group, MXT alone (oral 0.5mg/kg/48hr, oral) group, Dox+MTE group (1.66mg/kg/48hr Dox IP+150mg/kg/day MTE oral), and MXT+MTE (0.5mg/kg/48hr MXT oral +150mg/kg/day MTE oral) group. The duration of experiment were seven days. A histopathological examination was done at the end of experimentation. Results: Dox and MXT use in the rat model has induced severe cardiotoxicity with inflammatory cell infiltration, structural damage of cardiac tissue, and morphological changes. Milk thistle pretreatment extensively saved cardiac architecture. Conclusions: MTE use with Dox or MXT demonstrated marked cardioprotection potential via reduced inflammatory cell infiltration and cardiac tissue protection, suggesting that MTE could potentially emerge as a valuable tool to block cardiac complications in Dox- or MXT-treated patients. Key words. Doxorubicin, methotrexate, milk thistle extract, cardiotoxicity, chemotherapy. Doxorubicin (DOX) and methotrexate (MXT) are strong anticancer agents and gold standard therapy for several malignancies, with efficacy restricted by cardiotoxicity. Milk thistle extract (MTE) has demonstrated strong antioxidant and cytoprotective properties; we sought to determine the role of MTE in protection against Dox and/or MXT-induced cardiac damage.

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