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May 21, 2021
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May 21, 2021
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Abstract

Aim

In liver diseases VDAC has play as important role because it triggering the opening of the mitochondrial porin ion channel that leads to mitochondrial damage and induce apoptic or necrotic hepatic cell death. The present study, the relationship between expression of mitochondrial VDAC may underlie the protective effect of Rheum emodi against carbon tetrachloride (CCl4) induced liver damage in Wister rats.


Methods

The protective potential of the total Anthraquinone glycoside fraction of Rheum emodi (TAGF Rheum emodi) was determined by evaluating Aminotransferase activity, mitochondrial membrane potential, calcium-induced liver MPT (Mitochondrial permeability transition) and VDAC expression.


Results

Pretreatment with a total Anthraquinone glycoside fraction of Rheum emodi showed significant preservation of mitochondrial membrane potential as compared to CCl4 control demonstrating the mitochondrial protection. In addition, pretreatment with TAGF Rheum emodi at various concentrations exerted a dose-dependent effect against sensitivity to mitochondrial swelling induced by calcium. In addition, TAGF (400 mg/kg) significantly increased the transcription and translation of VDAC.


Conclusion

The result obtained from the study suggests that TAGF of Rheum emodi significantly prevents the damage to liver mitochondria induced by CCl4through regulating the expression of VDAC.

Keywords

Rheum emodi Total Anthraquinone glycoside content mitochondria Voltage dependent anion channels

Article Details

How to Cite
Meesala Srinivasarao, Mangamoori Lakshminarasu, Tasneem Mohammed, & Mohammed Ibrahim. (2021). Hepatoprotective potential of Rheum emodi against ccl4-induced liver damage through regulation of voltage dependent anion channel expression . International Journal of Research in Pharmacology & Pharmacotherapeutics, 5(2), 123-131. https://doi.org/10.61096/ijrpp.v5.iss2.2016.123-131
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