ABSTRACT
Sanqi in Chinese herbal medicine is the root and rhizoma of Panax notoginseng (Burk.) F.H.Chen, which belongs to genus Panax in the Araliaceae family and is widely used as a tonic medicine in the traditional Chinese medicine. The main active constituents of sanqi are Panax notoginseng saponins, including ginsenoside Rg1, Rb1 and notoginsenoside R1. A wide variety of pharmaceutical applications of Panax notoginseng saponins have been reported in the regulation of blood circulation system, cardiovascular system and nervous system. Ischemic stroke, the most common form of stroke, leads to a high risk of morbidity and disability, which evolves serious medical, social and economic problems. Ischemia-reperfusion injury is the most important part in the progress of ischemic stroke. Abnormal energy metabolism, disturbance of the ion metabolism, free radical injury, inflammatory reactions all participate in the complex pathological mechanisms of ischemiareperfusion injury. Over the past few decades, substantial studies demonstrated that Panax notoginseng saponins possessed a significant protective effect on ischemia-reperfusion injury. However, little is known about the underlying mechanisms of the protective effects. In order to develop a new medicine from Panax notoginseng, we provide a review of the major literatures on the pharmaceutical actions and molecular mechanisms of Panax notoginseng and Panax notoginseng saponins in the protection of ischemia-reperfusion injury.
ABSTRACT
The study reports the detection of neuroprotective effect of 10 kinds of coumarin derivatives and explores their possible mechanism. MTT method was used to screen the neuroprotective effect of 10 coumarin derivatives on neurotoxic agents (Aβ25-35 and rotenone) or OGD (oxygen-glucose deprivation). A compound with better protective effect was obtained. Then the effect of this compound on neurotoxic agents on PC12 was detected by the morphological observation. Furthermore, the effect of compound 3 on microglia with lipopolysaccharide (LPS) induced inflammation was detected. And the inflammatory factor was tested. Finally, direct free radical scavenging ability was detected. Compound 3 was found to be the best compound through three neurons toxic models. Not only compound 3 ameliorated cell viability reduced by three neurons toxic models, but also significantly inhibited the production of inflammatory factor (TNF-α and IL-1β). And its free radical scavenging ability is very good, especially the effect on superoxide anion, which is comparable with vitamin C. The significant scavenging effect of compound 3 on superoxide anion might be the mechanism of the neuroprotection. Compound 3 as a potential neural cell protective agent merits further investigation.