EXPLORING THE HEPATOPROTECTIVE POTENTIAL OF ETHANOL FRACTION OF ETHANOL EXTRACT FROM HIPTAGE BENGHALENSIS AGAINST THIOACETAMIDE-INDUCED HEPATOTOXICITY

Main Article Content

Gotla Anand
Dr. MD Sultan Ali Basha
Preethi. Kuruva
Shaik Mohemmed Zeeshan Ali
D. Riyazunnisa
Shaik Mahaboob Bee

Keywords

Hepatoprotective, Hiptage benghalensis, thioacetamide, liver damage, hepatotoxicity

Abstract

Liver diseases pose a significant global health burden, necessitating the search for effective hepatoprotective agents. In this study, we investigated the hepatoprotective properties of the Ethanol Fraction of Ethanol Extract (EFEE) from Hiptage benghalensis using thioacetamide (TAA)-induced hepatotoxicity models. Two distinct approaches were employed, one simulating pre-treatment and the other post-treatment scenarios, to comprehensively evaluate EFEE's potential in preventing and ameliorating liver damage. In the pre-treatment model, EFEE administration significantly mitigated TAA-induced hepatotoxicity, as evidenced by the marked reduction in elevated biochemical markers of liver damage, including ALKP, GOT, CHOL, TBL, SODIUM, and POTASSIUM, along with the restoration of depleted TPTN levels. Histological examination confirmed these findings, revealing preserved hepatic architecture and reduced fatty changes and centrilobular necrosis in rats treated with EFEE. The post-treatment model yielded parallel results, demonstrating EFEE's effectiveness in therapeutically addressing TAA-induced liver damage. EFEE significantly reduced elevated biochemical markers and enhanced depleted TPTN levels, indicating its potential as a hepatoprotective intervention even after hepatotoxic insult. Histological analysis corroborated these outcomes, highlighting reduced centrilobular necrosis and fatty changes in rats treated with EFEE. The underlying mechanisms of EFEE's hepatoprotective effects may involve interference with the metabolic pathway of TAA, including its conversion into a toxic S-oxide metabolite and subsequent generation of reactive oxygen species by cytochrome P450 enzymes. EFEE may inhibit these processes or act as a membrane stabilizer, preventing TAA-induced damage and promoting hepatocyte regeneration. Moreover, qualitative phytochemical analysis revealed the presence of phenolic compounds, flavonoids, terpenoids, and steroids in EFEE, known for their antioxidant and hepatoprotective properties. An increase in total phenolic and flavonoid content suggests their potential contribution to EFEE's hepatoprotective activity. In conclusion, this study unveils the remarkable hepatoprotective potential of EFEE from Hiptage benghalensis, both in preventing and alleviating hepatotoxicity induced by TAA. Further investigations are warranted to elucidate the precise mechanisms involved and identify bioactive compounds responsible for this activity.

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