科研之友
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摘要
It is well-known that signal transducer and activator of transcription 3 (STAT3) plays an essential role in cell survival and proliferation. Therefore, we investigated the effects and mechanism of STAT3 is involved neuronal apoptosis in focal cerebral ischemia/reperfusion rats. Rat MCAO model was used to produce transient focal ischemia. The volume of cerebral infarction was measured by TCC stain. The localizations of STAT3, phosphorylated STAT3 Bcl-2 and Fas were immunohistochemically examined in rats after 0.5 h to 7 d of reperfusion following 3 h of middle cerebral artery occlusion (MCAO), and the neuronal apoptosis were detected by TUNEL assay. Our results showed that the amount of apoptosis cells reaches the peak at 3 h after ischemia/reperfusion. Low expressed STAT3, p-Tyr705-STAT3, Bcl-2 and Fas were detected in control group and sham operated group. In ischemia/reperfusion (I/R) group, the STAT3 firstly detected after 0.5 h reperfusion, and peaked at 24 hours in ischemic zone, including ischemic penumbra and ischemic core zone. The p-Tyr705-STAT3 positive cells peaked at 24 hours after reperfusion in the ischemic penumbra, while peaked at 3 hours after reperfusion in the ischemic core zone. The Bcl 2 positive cells peaked at 12 hours after reperfusion in the ischemic penumbra, while reached peak at 6 hours after reperfusion in the ischemic core zone. The Fas positive cells reached peak at 24 hours after reperfusion in the ischemic penumbra, while reached peak at 12 hours after reperfusion in the ischemic core zone. Correlative analysis showed that positive correlation with each other STAT3, p-Tyr705-STAT3, Bcl-2 and Fas in the ischemic zone (P<0.01). Moreover, p-Tyr705-STAT3, Bcl-2 and Fas were positive correlation with TUNEL positive cells (P<0.01), except STAT3. In conclusion, activation of STAT3 induces neuronal apoptosis in focal cerebral ischemia/reperfusion rats via Bcl 2/Fas pathway.
- 出版日期2016
- 单位中南大学
