Neuroprotective Effect and Possible Mechanisms of Ginsenoside-Rd for Cerebral Ischemia/Reperfusion Damage in Experimental Animal: A Meta-Analysis and Systematic Review. (1st September 2022)

• Record Type: Journal Article
• Authors: Zhou, Ai-fang; Zhu, Ke; Pu, Pei-min; Li, Zhuo-yao; Zhang, Ya-yun; Shu, Bing; Cui, Xue-jun; Yao, Min; Wang, Yong-jun
• Other Names: Kumar Gaurav Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2022(2022)
• Publication Date: 2022-09-01
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2022/7650438
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : Ischemic stroke, the most common type of stroke, can lead to a long-term disability with the limitation of effective therapeutic approaches. Ginsenoside-Rd (G-Rd) has been found as a neuroprotective agent. In order to investigate and discuss the neuroprotective function and underlying mechanism of G-Rd in experimental animal models following cerebral ischemic/reperfusion (I/R) injury, PubMed, Embase, SinoMed, and China National Knowledge Infrastructure were searched from their inception dates to May 2022, with no language restriction. Studies that G-Rd was used to treat cerebral I/R damage in vivo were selected. A total of 18 articles were included in this paper, and it was showed that after cerebral I/R damage, G-Rd administration could significantly attenuate infarct volume (19 studies, SMD = − 1.75 − 2.21 to − 1.30, P < 0.00001 ). Subgroup analysis concluded that G-Rd at the moderate doses of >10- <50 mg/kg reduced the infarct volume to the greatest extent, and increasing the dose beyond 50 mg/kg did not produce better results. The neuroprotective effect of G-Rd was not affected by other factors, such as the animal species, the order of administration, and the ischemia time. In comparison with the control group, G-Rd administration could improve neurological recovery (lower score means better recovery: 14 studies, SMD = − 1.50 − 2.00 to − 1.00, P < 0.00001 ; higher score means better recovery: 8 studies, SMD = 1.57 0.93 to 2.21, P < 0.00001 ). In addition, this review suggested that G-Rd in vivo can antagonize the reduced oxidative stress, regulate Ca 2+, and inhibit inflammatory, resistance to apoptosis, and antipyroptosis on cerebral I/R damage. Collectively, G-Rd is a promising natural neuroprotective agent on cerebral I/R injury with unique advantages and a clear mechanism of action. More clinical randomized, blind-controlled trials are also needed to confirm the neuroprotective effect of G-Rd on cerebral I/R injury.