Expression Of Caspase-3 In Hippocampus Research Articles

Right stellate ganglion block improves learning and memory dysfunction and hippocampal injury in rats with sleep deprivation

BackgroundSleep deprivation (SD) often leads to complex detrimental consequences, though the mechanisms underlying these dysfunctional effects remain largely unknown. We investigated whether the right stellate ganglion block in rats can improve the spatial learning and memory dysfunction induced by sleep deprivation by alleviating the damage of hippocampus in rats.MethodsSixty four male Sprague Dawley rats were randomly divided into four groups: Control, SD (sleep deprivation), SGB (stellate ganglion block) and SGB + SD (stellate ganglion block+ sleep deprivation) (n = 16). The SGB and SD + SGB groups were subjected to right stellate ganglion block through posterior approach method once per day. SD and SD + SGB groups were treated with modified multi-platform water environment method for 96 h sleep deprivation in rats and their body weights were analyzed. Histopathological changes of hippocampal neurons in rats and the expression of Caspase-3 in hippocampus of rats was detected by western blotting. ELISA was used to detect the content of IL-6, IL-1 in hippocampus and serum melatonin levels.ResultsCompared with the group SD, the spatial learning and memory function of the group SD + SGB was improved, the weight loss was alleviated, the pathological damage of the hippocampus was reduced and the expression of IL-6, IL-1β and Caspase-3 in the hippocampus was decreased. The content of rat serum melatonin was also increased.ConclusionsThe right stellate ganglion block can improve the spatial learning and memory dysfunction of rats with sleep deprivation, and the underlying mechanism may be related to alleviating the apoptosis and inflammation of hippocampus of rats with sleep deprivation.

The Role of Platelet-Derived Growth Factor Receptor in Early Brain Injury Following Subarachnoid Hemorrhage

This study aims to observe encephaledema and cell apoptosis in rats following subarachnoid hemorrhage (SAH) and to explore the mechanism of platelet-derived growth factor receptor (PDGFR) in the development of early brain injury (EBI). Adult and male Sprague-Dawley rats were randomly divided into 4 groups: sham operation, SAH, SAH + imatinib, and SAH + platelet-derived growth factor-BB (PDGF-BB). SAH model was established using intravascular silk puncture of the internal carotid artery crotch. The SAH + imatinib group was treated with intraperitoneal injection of imatinib 1 hour before establishing the model. The SAH + PDGF-BB group was administered with intracerebroventricular injection of PDGF-BB 1 hour before establishing the model. The mortality, encephaledema, and nerve functional scoring were observed after 24 hours in all groups. The expression of caspase-3 in hippocampus was tested by reverse transcription polymerase chain reaction and Western blotting. Mortality and encephaledema were the highest in the SAH + PDGF-BB group, which were alleviated when the rats were injected with imatinib (P < .01). PDGFR may participate in the pathogenesis of EBI following SAH. The antagonist of PDGFR, imatinib, can reduce brain damage to some degree.

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Introduction: Epinephrine (Epi) is recommended in cardiopulmonary resuscitation (CPR). Vasopressin (Vaso) has been studied for use in CPR as an alternative. Methods: The rat model of cardiac arrest (CA) after asphyxia was used in the current study. 200 rats were divided into 5 groups randomly (n=40 rats in each group) Sham-operated group: no asphyxia and no CPR, only for endotracheal intubation. Control group: after CA, CPR was performed immediately and 1 ml of saline was administered. Epi group: CPR was implemented after CA and 1 ml of Epi (0.2mg/kg) was administered. Vaso group: after CA, CPR was carried out and 1 ml of Vaso (0.8U/Kg) was injected. Combination group: CPR was performed after CA. 1 ml of Epi (0.2mg/kg) and 1 ml of Vaso (0.8U/Kg) were administered. The rats in control group exhibited the lowest survival rate and therefore were abandoned in the following experiment. The rats survived from other groups were killed in 1, 3, 6 and 12 hours after CPR, respectively, and the brains were taken out. We tested the expression of Caspase-3 in rat’s hippocampus by immunohistochemistry. The restoration of spontaneous circulation (ROSC) rate was recorded and the pathological changes of the brains were observed in each group. Results: Compared to Epi group, the expressions of Caspase-3 in Vaso group and combination group were lower (P<0.05). No significant difference was seen between Vaso group and combination group (P>0.05). HE staining demonstrated there was no difference in morphology changes among Epi, Vaso and combination group under light microscope. Compared to Sham-operated group, the edema of neurons in Hippocampus was seen in the other three groups. The damage of Mitochondria was more serious in Epi group than in Vaso and combination group under electron microscope. No difference of Mitochondria damage was seen between Vaso and combination group. Conclusions: Vaso can reduce the expression of Caspase-3 in Hippocampus of rats with CA after asphyxia and alleviate the ischemia reperfusion injury during CPR.