INVESTIGATION OF THE HEPATOPROTECTIVE EFFECT OF ANACARDIUM IN AN ETHANOL-INDUCED HEPATITIS MODEL

Аннотация

This study explores the hepatoprotective effects of anacardic acid, a polyphenolic compound, in a rat model of acute liver injury induced by carbon tetrachloride (CCl₄). Given the increasing exposure to hepatotoxic xenobiotics from household, industrial, and agricultural chemicals, the development of effective and multi-targeted hepatoprotective agents is critical. The experiment was conducted in compliance with international animal ethics guidelines using Wistar rats. The research assessed various doses of anacardic acid administered both orally and intraperitoneally. Biochemical markers such as ALT, total protein, diene conjugates, and malondialdehyde (MDA) levels were measured to evaluate liver function and oxidative stress. The findings demonstrated that anacardic acid, particularly at a dose of 5 mg/kg administered intraperitoneally, significantly mitigated liver damage, restored biochemical parameters, and showed comparable efficacy to the standard hepatoprotective agent Karsil. These results suggest that anacardic acid possesses promising hepatoprotective properties and warrants further investigationas apotential therapeuticagent forhepatobiliary pathologies. Keywords: Anacardic acid, hepatotoxicity, carbon tetrachloride (CCl₄), hepatoprotection, oxidativestress, liver enzymes, polyphenols, ALT, MDA, rats, acute liver injury. Introduction. Toxic liver damage is one of the most common etiological factors of hepatobiliary pathology. It is associated with a significant increase in exposure to hepatotoxic xenobiotics, including household, industrial, and agricultural chemicals. These exogenous factors not only have specific mechanisms of action but also initiate a universal and potent endogenous mechanism of hepatocyte damage in the form of oxidative stress [6]. The byproducts of this process—aggressive and numerous reactive oxygen species (ROS)—lead to metabolic disorders, membranopathies, functional impairments, mutations, accelerated apoptosis, and other forms of cellular pathology. Moreover, the multifactorial nature of toxic liver injury requires hepatoprotective agents to provide multi-level protection, which is currently exhibited by only a limited number of 323 INTERNATIONAL MULTIDISCIPLINARY JOURNAL FOR RESEARCH & DEVELOPMENT SJIF2019:5.2222020:5.5522021:5.6372022:5.4792023:6.5632024:7,805 eISSN:2394-6334 https://www.ijmrd.in/index.php/imjrd Volume12,issue06(2025) hepatoprotectors (e.g., Legalon, Silybor, Hepaton) [5]. A characteristic feature of modern hepatoprotective agents is their origin from plant-based raw materials and their content of polyphenolic compounds with antioxidant activity, such as flavonoids, flavolignans, cinnamic acids, and others [2]. Materials and Methods. The study was conducted on 240 mature male and female Wistar rats weighing between 170–280 grams, in accordance with the international recommendations of the European Convention for the Protection of Vertebrate Animals Used for Experimental and Other Scientific Purposes [1]. Acute liver injury was induced by administering a 50% solution of carbon tetrachloride(CCl₄)orally using ametal atraumaticprobe [7]. In the experiments, the polyphenol anacardine under investigation was administered using oral and intraperitoneal routes. The polyphenol was given orally at doses of 100, 300, and 500 mg/kg twice daily for 12 days via gastric intubation. Additionally, it was administered intraperitoneally at doses of 5,15,and 25mg/kg twicedaily for12days. It should be noted that the tested polyphenol was administered for 5 days prior to the introduction of carbon tetrachloride, and then concurrently with it for 7 days—specifically, 1 hour before each administration ofCCl₄ [3,7]. The acute toxicity of the studied drug was assessed in accordance with methodological guidelines for evaluating the general toxic effects of pharmacological agents. The experiment was conducted based on the method of V.V. Gatsura. After 14 days of administering the investigated preparation to animals with carbon tetrachloride-induced liver damage, sodium etaminal was injected intraperitoneally at a dose of 40 mg/kg. The duration of sleep (in lateral position) was recorded in minutes. Statistical results were processed and expressed as the arithmetic mean (M) and its standard error (m). Sodium etaminal and the studied polyphenolic compound anacardin were administered orally in different doses (100, 300, and 500 mg/kg), as well as intraperitoneally in doses of 5, 15, and 125 mg/kg. The assessment was performed under acute toxic liver injury conditions induced by carbon tetrachloride, and sodium etaminal was administered intraperitoneally at a dose of 40 mg/kg on the 14th day of compound administration [6]. Control animals received the same volumeofpurified water. According to the obtained results, compared to the control group, administration of anacardin led to a significant and reliable reduction in sleep duration — particularly by 55.7% at a dose of 100 mg/kg.