Background
Reducing cerebral ischemia-reperfusion injury is crucial for improving survival and neurologic outcomes after cardiac arrest/cardiopulmonary resuscitation (CA/CPR). The
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.
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 (.