Abstract
Zhenlong Xingnao Capsule (ZXC) is a Tibetan medicine used to treat ischemic stroke. In this study, we determined the in vitro and in vivo effects of ZXC on reactive oxygen species (ROS) in a mouse BV-2 microglial cell hypoxia-reoxygenation and rat middle cerebral artery occlusion infarction models. We aimed to clarify the role of ZXC in cerebral ischemia protection; reveal amino acid neurotransmitter changes in the frontal cortex after drug intervention; determine mRNA and protein expression changes in Bcl-2, Bax, caspase-3, P38, and nuclear factor (NF)-кB in the frontal cortex and changes in antioxidant indices in the brain; and elucidate the mechanisms underlying ZXC action. After hypoxia-reoxygenation, ROS levels were significantly increased in BV-2 cells, and their levels decreased after treatment with ZXC. ZXC had protective effects on ischemic/anoxic injury in vitro and in vivo by downregulating the expressions of caspase-3 and NF-кB mRNA during ischemia and reperfusion and that of p38 and caspase-3 during acute ischemia and reperfusion as well as the steady-state levels of excitatory amino acids/inhibitory amino acids and by improving the total antioxidant capacity and total superoxide dismutase activities during ischemia. These findings provide new molecular evidence for the mechanisms underlying ZXC action.
Highlights
Ischemic stroke, a leading cause of mortality and morbidity worldwide (Feigin et al, 2003), has become the most common cause of death in China (Zhang et al, 2003)
Zhenlong Xingnao Capsule (ZXC) chromatographic samples were prepared in three batches for ultra-performance liquid chromatography (UPLC; Figure 1)
This study aimed to explore the effects of reactive oxygen species (ROS) generation on volume in a BV-2 cell injury hypoxiareoxygenation model after intervention with ZXC to evaluate the protective role of ZXC on neurocytes (Figure 2)
Summary
A leading cause of mortality and morbidity worldwide (Feigin et al, 2003), has become the most common cause of death in China (Zhang et al, 2003). The current options for the effective treatment of ischemic stroke remain limited (Truelsen et al, 2007; Mozaffarian et al, 2015). The effect of interventional neuroendovascular therapies is still under evaluation (Chimowitz, 2013; McTaggart et al, 2015). Basic research studies in animals are conducted to investigate the pathological changes that occur after stroke and explore the efficacy of new drugs and therapies. Brain anoxia and ischemia resulting from ischemic stroke trigger the necrosis and apoptosis of nerve cells, which are important contributors
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