Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=36092162&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Neuroprotective Effect and Possible Mechanisms of Ginsenoside-Rd for Cerebral Ischemia/Reperfusion Damage in Experimental Animal: A Meta-Analysis and Systematic Review #MMPMID36092162
Zhou AF; Zhu K; Pu PM; Li ZY; Zhang YY; Shu B; Cui XJ; Yao M; Wang YJ
Oxid Med Cell Longev 2022[]; 2022 (?): 7650438 PMID36092162show ga
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.
free
free
free
Oxid+Med+Cell+Longev 2022 ; 2022 (?): 7650438
