| Objective: The study is to establish a rat model of subarachnoid hemorrhage(SAH),to observe the changes of neurological function in rats with melatonin,to detect the expression of Poly-ADP-ribose polymerase-1(PARP-1)and cell apoptosis in hippocampal neurons,and to detect blood brain barrier(BBB)permeability changes and brain edema,and to explore the effect of melatonin on the apoptosis of early brain injury(EBI)after SAH and its neuroprotective mechanism.Methods: Seventy-two healthy adult male rats were randomly divided into sham group(n = 18),subarachnoid hemorrhage group(n = 18),vehicle group(n = 18)and MEL group(n = 18).Then 18 rat of each group were divided into two parts,10 rat were used for immunohistochemistry and TUNEL staining,the other 8 for evaluating the brain water content.The EBI model of SAH was established by prechiasmatic cistern injection method.The melatonin was injected intraperitoneally at 2 hours and 24 hours after subarachnoid hemorrhage to MEL group and observed the Neurobehavior changes of all rats.The brain edema of temporal basal cortex,the blood brain barrier permeability changes,the expression of PARP-1 in the hippocampus,the apoptosis of neurons were recorded to explore the neuroprotective mechanism of melatonin on EBI of rat subarachnoid hemorrhage when 48 hours after operation.The data were analyzed statistically using SPSS 13.0,and when p <0.05 was considered statistically significant.Results:1.Neurobehavioral score: Compared with sham group,the neurological function of SAH group was significantly decreased,the appetite and activity ability were significantly decreased.Compared with vehicle group,the neurological function of MEL was significantly improved,and the appetite and activity were significantly increased.2.Brain edema: The water content of brain tissue in SAH group was significantly higher than that in sham group 48 hours after operation(P <0.01).There was no significant difference in water content between SAH group and vehicle group(p> 0.05),but the water content of brain tissue in MEL group was significantly less than that in vehicle group(p <0.01).3.Blood brain barrier permeability:The content of EB in the temporal basal cortex of SAH group was significantly higher than that in sham group to 48 hours after operation(p <0.01).The vehicle group and SAH group was not significantly different(p > 0.05).However,the EB content in the MEL group was lower than that in the vehicle group(p <0.01).4.Expression of PARP-1: The expression of PARP-1 in hippocampus neurons of SAH group was significantly higher than that in sham group(p <0.01).The expression in vehicle group was not significantly different from that in SAH group(p > 0.05).But the expression in MEL group was less than that of the vehicle group(p <0.01).5.Apoptosis in hippocampal: After 48 hours,SAH group hippocampus neuronal cell apoptosis was significantly extra sham group(p <0.01).There was no significant difference between the vehicle group and the SAH group(p > 0.05).However,the apoptotic cells in the hippocampus of the MEL group were significantly lower than those in the hippocampus in vehicle group(p <0.01).Conclusion:1.The neurological deficits of rats after SAH were obvious,and the neurological behavior of rats after MEL treatment was significantly improved,which indicated that MEL could alleviate the early brain injury after SAH and have neuroprotective effect.2.After SAH,cerebral edema in rats were obvious,but after MEL treatment,rat blood brain permeability improved significantly,brain edema alleviated,indicating that MEL can protect the blood-brain barrier to ease brain edema.3.The expression of PARP-1 was improved and apoptosis increased after SAH,but those was decreased after MEL treatment,which indicated that MEL could reduce the apoptosis of EBI cells after SAH by inhibiting PARP-1 pathway. |
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