Glycyrrhizic acid ameliorates myocardial ischemic injury by the regulation of inflammation and oxidative state
Authors Xu CL, Liang CH, Sun WX, Chen JD, Chen XH
Received 10 February 2018
Accepted for publication 28 March 2018
Published 18 May 2018 Volume 2018:12 Pages 1311—1319
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Anastasios Lymperopoulos
Chongli Xu,1,2 Caihong Liang,2 Weixin Sun,3 Jiandong Chen,3 Xiaohu Chen3
1Nanjing University of Chinese Medicine, Nanjing 210029, People’s Republic of China; 2Jiangnin Hospital of Nanjing, Nanjing 211100, People’s Republic of China; 3Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, People’s Republic of China
Background: Glycyrrhizic acid (GA), a bioactive triterpenoid saponin isolated from the roots of licorice plants (Glycyrrhiza glabra), has been shown to exert a variety of pharmacological activities and is considered to have potential therapeutic applications. The purpose of the present study was to investigate the cardioprotective effect of GA on myocardial ischemia (MI) injury rats induced by isoproterenol (ISO), and explore the potential mechanisms underlying these effects.
Materials and methods: The rats were randomized into five groups: control, ISO, ISO+diltiazem (10 mg/kg), ISO+GA (10 mg/kg), and ISO+GA (20 mg/kg). Electrocardiogram and histopathological examination were performed. Markers of cardiac marker enzymes (creatine kinase-MB, lactate dehydrogenase), oxidative stress (superoxide dismutase, malondialdehyde [MDA]), and inflammation (TNF-α, IL-1β, and IL-6) were also measured in each group. Proteins involved in NF-κB and Nrf-2/HO-1 pathway were detected by Western blot.
Results: GA decreased the ST elevation induced by MI, decreased serum levels of creatine kinase, lactate dehydrogenase, malondialdehyde, IL-6, IL-1β, and TNF-α, and increased serum superoxide dismutase and malondialdehyde activities. Furthermore, GA increased the protein levels of Nrf-2 and HO-1 and downregulated the phosphorylation of IκB, and NF-κB p65 in ISO-induced MI.
Conclusion: These observations indicated that GA has cardioprotective effects against MI, and these effects might be related to the activation of Nrf-2/HO-1 and inhibition of NF-κB signaling pathway in the myocardium.
Keywords: glycyrrhizic acid, myocardial ischemia, Nrf-2/HO-1, oxidative stress, inflammation
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