Hepatoprotective activity of andrographolide possibly through antioxidative defense mechanism in Sprague-Dawley rats
Issued Date
2022-01-01
Resource Type
ISSN
22147500
Scopus ID
2-s2.0-85129525015
Journal Title
Toxicology Reports
Volume
9
Start Page
1013
End Page
1022
Rights Holder(s)
SCOPUS
Bibliographic Citation
Toxicology Reports Vol.9 (2022) , 1013-1022
Suggested Citation
Mondal M., Sarkar C., Saha S., Hossain M.N., Norouzi R., Mubarak M.S., Siyadatpanah A., Wilairatana P., Hossain R., Islam M.T., Coutinho H.D.M. Hepatoprotective activity of andrographolide possibly through antioxidative defense mechanism in Sprague-Dawley rats. Toxicology Reports Vol.9 (2022) , 1013-1022. 1022. doi:10.1016/j.toxrep.2022.04.007 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/87582
Title
Hepatoprotective activity of andrographolide possibly through antioxidative defense mechanism in Sprague-Dawley rats
Other Contributor(s)
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.
