Abstract
Background Reducing cerebral ischemia-reperfusion injury is crucial for improving survival and neurologic outcomes after cardiac arrest/cardiopulmonary resuscitation (CA/CPR). The purpose of this study is to investigate the neuroprotective effects of green tea polyphenols (GTPs) concern with the modulation of endogenous antioxidation and endoplasmic reticulum stress. Methods After subjecting to CA/CPR, rats were randomized into the saline group (NS, n = 40) and the GTPs group (GTPs, n = 40) and the GTPs group (GTPs, n = 40) and the GTPs group (GTPs, Results Comparing with that in NS group, GTPs increased the expression of SOD1 and SOD2 at 12 h, 24 h, 48 h, 72 h, and the expression of GRP78 at 24 h and 48 h (p < 0.05) butdecreased caspase-12, CHOP, caspase-3 level, and apoptotic number of neurons (p < 0.05) butdecreased caspase-12, CHOP, caspase-3 level, and apoptotic number of neurons (Conclusion GTPs exert neuroprotective effects via mechanisms that may be related to the enhancement of endogenous antioxidant capacity and inhibition of endoplasmic reticulum stress in CA/CPR rat models.
Highlights
Cardiac arrest is a common and intractable condition frequently encountered in hospitals and outside of hospitals [1]
Whereas in the green tea polyphenols (GTPs) group, both superoxide dismutase 1 (SOD1) and superoxide dismutase 2 (SOD2) were higher than the NS group at all time points. e above results show that GTPs exert an antioxidative role through enhancing the expression of SOD1 and SOD2 in the process of Cerebral ischemiareperfusion injury (CIRI) after cardiac arrest/cardiopulmonary resuscitation (CA/CPR)
To elucidate the additional mechanism of GTPs on antiapoptosis apart from antioxidation, we investigated the possibility of GTPs on the endoplasmic reticulum (ER) pathway concerning apoptosis in cerebral injury post-cardio arrest (CA)/PCR, since it is known that ER stress relates to pathophysiology of ischemia-reperfusion [29, 30]
Summary
Cardiac arrest is a common and intractable condition frequently encountered in hospitals and outside of hospitals [1]. Endoplasmic reticulum (ER) stress has attracted widespread attention as a new mechanism of apoptosis, which is related to the pathological process of cerebral ischemia. Reducing cerebral ischemia-reperfusion injury is crucial for improving survival and neurologic outcomes after cardiac arrest/cardiopulmonary resuscitation (CA/CPR). Comparing with that in NS group, GTPs increased the expression of SOD1 and SOD2 at 12 h, 24 h, 48 h, 72 h, and the expression of GRP78 at 24 h and 48 h (p < 0.05) butdecreased caspase-12, CHOP, caspase-3 level, and apoptotic number of neurons (p < 0.05) after restoration of spontaneous circulation (ROSC). GTPs exert neuroprotective effects via mechanisms that may be related to the enhancement of endogenous antioxidant capacity and inhibition of endoplasmic reticulum stress in CA/CPR rat models
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
