Pharmacological properties and mechanisms of Notoginsenoside R1 in ischemia-reperfusion injury.
10.1016/j.cjtee.2022.06.008
- Author:
Ting ZHU
1
;
Qi WAN
2
Author Information
1. Institute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, School of Basic Medicine, Qingdao University, Qingdao, 266071, Shandong Province, China.
2. Institute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, School of Basic Medicine, Qingdao University, Qingdao, 266071, Shandong Province, China. Electronic address: qiwan1@hotmail.com.
- Publication Type:Review
- Keywords:
Chemistry;
Ischemia/reperfusion injury;
Molecular mechanism;
Notoginsenoside R1;
Pharmacological properties
- MeSH:
Humans;
Reperfusion Injury/prevention & control*;
Inflammation;
China;
Apoptosis
- From:
Chinese Journal of Traumatology
2023;26(1):20-26
- CountryChina
- Language:English
-
Abstract:
Panax notoginseng is an ancient Chinese medicinal plant that has great clinical value in regulating cardiovascular disease in China. As a single component of panax notoginosides, notoginsenoside R1 (NGR1) belongs to the panaxatriol group. Many reports have demonstrated that NGR1 exerts multiple pharmacological effects in ischemic stroke, myocardial infarction, acute renal injury, and intestinal injury. Here, we outline the available reports on the pharmacological effects of NGR1 in ischemia-reperfusion (I/R) injury. We also discuss the chemistry, composition and molecular mechanism underlying the anti-I/R injury effects of NGR1. NGR1 had significant effects on reducing cerebral infarct size and neurological deficits in cerebral I/R injury, ameliorating the impaired mitochondrial morphology in myocardial I/R injury, decreasing kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin in renal I/R injury and attenuating jejunal mucosal epithelium injury in intestinal I/R injury. The various organ anti-I/R injury effects of NGR1 are mainly through the suppression of oxidative stress, apoptosis, inflammation, endoplasmic reticulum stress and promotion of angiogenesis and neurogenesis. These findings provide a reference basis for future research of NGR1 on I/R injury.
