Hilla University College Journal For Medical Science
Document Type
Original Study
Keywords
Ursodeoxycholic acid, Carbon tetrachloride (CCL4), Hepatotoxicity, Oxidative stress, Inflammation
Abstract
Background: The liver is essential for the detoxification of toxic substances as well as for metabolism, storage, and secretion. The liver is the primary organ for the metabolism of proteins, lipids, and carbohydrates. Exposure to certain xenobiotics can cause oxidative stress, which can impair liver function.
Objectives: The current study aimed to evaluate the possible protective effect of ursodeoxycholic acid against the hepatotoxicity induced by carbon tetrachloride administration.
Materials and Methods: Thirty adult male albino rats weighing between 250 and 300 g and aged between 10 and 12 weeks were included in the study. Three groups were included; group A received only normal saline intraperitoneal (I.P.) for 14 days. Group B received 0.5ml/kg carbon tetrachloride (CCL4) I.P. on day 6 of the experiment, twice a week, and Group C received 50 mg/kg ursodeoxycholic acid for 14 days + CCL4 was given I.P. on day 6 of the experiment, twice a week.
Results: In contrast to the positive control group (induction by carbon tetrachloride), the results showed that ursodeoxycholic acid preserved the liver in the treated group. In comparison to the positive control group, the Ursodeoxycholic acid-treated group showed significantly higher levels of glutathione (GSH), significantly lower levels of TNF-α, and lower levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). These results proved that ursodeoxycholic acid has a hepatoprotective effect on male albino rats.
Conclusion: These findings highlight ursodeoxycholic acid's capacity to protect the liver.
How to Cite This Article
Bey, Ayala Ya seen Ali; Barabbas, Maj id Radium; and Raj, Ahmed
(2024)
"Analyzing the Possible Hepatic Protection of Ursodeoxycholic Acid in Rat Models of Carbon Tetrachloride-Induced Hepatotoxicity,"
Hilla University College Journal For Medical Science: Vol. 2:
Iss.
2, Article 8.
DOI: https://doi.org/10.62445/2958-4515.1017