Hepatoprotective activity of andrographolide possibly through antioxidative defense mechanism in Sprague-Dawley rats. (2022)

• Record Type: Journal Article
• Authors: Mondal, Milon; Sarkar, Chandan; Saha, Sushmita; Hossain, Md Naim; Norouzi, Roghayeh; Mubarak, Mohammad S.; Siyadatpanah, Abolghasem; Wilairatana, Polrat; Hossain, Rajib; Islam, Muhammad Torequl; Coutinho, Henrique Douglas Melo
• Is Part Of: Toxicology reports. Volume 9(2022)
• Page Start: 1013
• Page End: 1022
• Publication Date: 2022
• Subjects: Andrographolide -- Acetaminophen -- Oxidative stress, Anti-oxidant, Hepatoprotective activity; Toxicology -- Periodicals; Clinical toxicology -- Periodicals; Drug-Related Side Effects and Adverse Reactions; Hazardous Substances; Poisoning; Toxicology; Electronic journals; Periodicals; Periodicals; 571.9505
• DOI: 10.1016/j.toxrep.2022.04.007
• Languages: English
• ISSNs: 2214-7500

Abstract

Abstract: The aims of this study to assess the efficiency of AGL against acetaminophen (APAP)-induced hepatic toxicity that was generated by mitochondrial oxidative stress and glutathione depletion. Free radical scavenging potentiality was analyzed by using 2, 2-diphenyl-1-picrylhydrazyl (DPPH), hydrogen peroxide, nitric oxide, and hydroxyl radical scavenging assays. APAP-induced liver toxicity was formed at a dose level of 640 mg/kg mg/kg BW each, p.o. for 14 days for all experimental rats except the vehicle control group. AGL (5 and 10 mg/kg) were treated orally with negative control and negative control silymarin (50 mg/kg) group. To assess the protective effect, we looked at the levels of serum biochemical markers, liver histoarchitecture, and hepatic antioxidant enzyme activity. AGL showed in vitro anti-oxidant potentialities by scavenging radicals in the respective assays. As evidenced by serum biochemical indicators and relative liver weight, AGL co-administration substantially reduced toxicant-induced hepatic damage. APAP-intoxication increased the malondialdehyde (MDA) level and declined in cellular endogenous antioxidant enzymes such as reduced catalase, superoxide dismutase, and glutathione, where, AGL treatment amended their level. In the same way, histopathological evaluation further verified that AGL protected the hepatocyte from APAP-induced damage. As AGL scavenges toxic free radicals, thereby protects mitochondria and other organelles from reactive oxygen and nitrogen species-mediated stress and its eventual consequence necrosis. Therefore, we propose the hepatoprotective activity of AGL through its antioxidant mechanism. Graphical Abstract: ga1 Highlights: AGL with APAP revealed substantial ameliorative effects on the liver. APAP-induced distress in oxidative stress in rat liver by elevating the levels of MDA. APAP-induced distress in oxidative stress by reducing the activities of GSH, SOD, and CAT.