Abstract
Objective To investigate the expression of Caspase-9 and heat-shock protein-90 (HSP 90) in rats after focal cerebral ischemia-reperfusion injury. Methods The male SD rats (200-250 g) were divided into three groups by the random number table: normal group, sham group and cerebral ischemia-reperfusion (CIR) group. Each group was sorted into four subgroups including group 6 h, group 24 h, group 48 h and group 72 h according to the reperfusion time. Suture-occluded method was adopted to prepare focal cerebral ischemia-reperfusion(CIR) injury in rat model. Enzyme-linked immunosorbent assay (ELISA) method was used to detect the variations of Caspase-9 and HSP-90 expression in rats. Results The changes in Caspase-9 and HSP 90 expression in the brain cells were observed by ELISA method. The expression of Caspase-9 and HSP-90 was weakly expressed in sham group, and was at peak in CIR group within 24 h-48 h, then began to decline at 72 h after the reperfusion time. The differences in the expression of caspase-9 and HSP-70 between sham group and normal group were not statistically significant. Conclusions Apoptotic cells gradually increase along with reperfusion time and reach the peak at 48 h after cerebral ischemia-reperfusion. In ischemia half dark stripe, the expression of Caspase-9 and HSP 90 is increased in neuronal cells after cerebral ischemia-reperfusion, and the positive cells number is at peak at 48 h after cerebral ischemia-reperfusion. Apoptosis of neuronal cells after cerebral ischemia and reperfusion is a dynamic evolutionary process. The expression of Caspase-9 and HSP 90 in nerve cells plays an important role in regulating cell apoptosis. Key words: Reperfusion injury; Caspase-9; Heat-shock proteins
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.