| Objective: To investigate the joint protective effect of exogenousneuroglobin (Ngb) and hemin on ischemic brain tissue in rats and its possiblemechanisms.Methods: Sprague Dawley rats (n=175) were randomly divided intofive groups (n=35): sham, ischemia, Hemin intervention, Ngb plasmidintervention, and Hemin and plasmid joint intervention. The classic MCAOrat model of focal cerebral ischemia was used. After recovery fromanaesthesia, neurobehavioral testing was performed. The following factorswere measured24hours post-surgery: brain water content, infarct volumeratio, neuron apoptosis detected by in situ cell apoptosis technology(TUNEL), Bcl-2protein expression detected by immunofluorescence, andNgb and Bcl-2protein expression analyzed by western blot.Results: In the Ngb plasmid and hemin joint intervention group, therewere significant reductions (i.e., improvements) in neurobehavioral scores,brain water content, and infarct volume ratio. The reduction of the number ofapoptotic neurons and the increase in Ngb protein and Bcl-2protein expression in this group were both significantly different from the shamgroup (p<0.05).Conclusion: In the event of focal cerebral ischemia in rats, the jointaction of exogenous Ngb and hemin could strengthen the inhibition of cellapoptosis, which achieves its protection effect on ischemic brain tissues,possibly by up-regulating Bcl-2protein expression. |
PDF Full Text Request