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Volume 17, Issue 4 (In Press 2023)                   IJT 2023, 17(4): 0-0 | Back to browse issues page

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John P, Bhatia N, Kale P, Doshi G. Benefit of Betaine in Isoniazid-Rifampicin (INH-RMP)-induced hepatotoxicity in rats. IJT 2023; 17 (4)
URL: http://ijt.arakmu.ac.ir/article-1-1241-en.html
1- Research Scholar
2- Medical Affairs Executive
3- Assistant Professor
4- Assistant Professor , gaurav.pharmacology@gmail.com
Abstract:   (86 Views)
Background: Recently, advances in the field of medicine and pharmacotherapeutics, novel treatment modalities have emerged for the treatment of tuberculosis (TB). It is noteworthy that long-term drug consumption in the line of TB treatment often leads to hepatotoxicity, which is a serious and fatal side effect. In this context, many studies have been focused on the assessment of the hepatoprotective effects of betaine, a glycine derivative. The present study was aimed at evaluating the effects of betaine and understand underlying biochemical mechanisms in Isoniazid-Rifampicin (INH-RMP) induced hepatotoxicity in rats.
Methods: Animal models with isoniazid-rifampicin (INH-RMP)-induced hepatotoxicity toxicity was used to determine the protective effects of betaine at three different doses (125mg/kg, 250mg/kg and 500 mg/kg).
Results: Treatment with INH and RMP led to a significant upregulation of hepatic damage markers, along with marked alteration in the liver histopathology. The results were found to be satisfactory at 500 mg/kg comparable to silymarin (200mg/kg). The hepatotoxicity was also found to be associated with generation of reactive oxygen species (ROS) and oxidative stress, indication deterioration of the antioxidant defense system. However, pretreatment with betaine seemed to ameliorate the INH-RMP-induced hepatotoxicity, along with marked downregulation of oxidative stress and hepatotoxicity markers.
Conclusion: The present study findings indicated that betaine treatment may help in the alleviating INH-RMP-induced liver damage in terms of reduced inflammation and oxidative stress via mitochondrial GSH regeneration, ROS alleviation, and protection of mitochondria complex II. Further studies are needed to warrant and validate these outcomes.
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Type of Study: Research | Subject: General

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