Guangping ZHAO, Panpan LIU, Fei LIU, Wei LI, Yongxue CHEN, Kai ZHANG. Observations on Hemodynamics and Stress Response of the Different Anesthesia Methods in Stereotactic Intracranial Hematoma Removal for Hypertensive Intracerebral Hemorrhage[J]. Journal of Kunming Medical University, 2022, 43(5): 117-122. doi: 10.12259/j.issn.2095-610X.S20220521
Citation: Li Jun Jie . The Gene Expression Change of Inflammatory Factors TNF-α, IL-6 and IL-1βin Cerebral Ischemia-Reperfusion Rats[J]. Journal of Kunming Medical University, 2016, 37(09).

The Gene Expression Change of Inflammatory Factors TNF-α, IL-6 and IL-1βin Cerebral Ischemia-Reperfusion Rats

  • [Abstract]Objective To investigate the gene expression change of TNF-α, IL-6 and IL-1β at different time points in brain tissues of rats with cerebral ischemia reperfusion injury. Methods A total of 24 adult male SD rats were randomly divided into four groups: sham group and 3 groups with brain ischemia reperfusion of 3h, 6h and 12h. Real-Time PCR was used to analyze the gene expression of TNF-α, IL-6 and IL-1β at 3h, 6h, and 12h after reperfusion. Results In the sham group, the mRNA expression levels of TNF-α, IL-6 and IL-1βin were low, but increased immediately after brain ischemia injury and decreased gradually thereafter. The gene expression of TNF-α mRNA at 3h after reperfusion was significantly increased and reached the peak (P<0.01) then significantly decreased at 12h after reperfusion. The gene expression of IL-6 mRNA was notably increased at 3h after reperfusion and peaked at 6h (P<0.01), and significantly decreased at 12h compared with 6h (P<0.01). The gene expression of IL-1βmRNA at 3h after reperfusion was significantly increased, peaked at 6h (P<0.01) and significantly decreased at 12h (P<0.01). Conclusion The gene expression levels of TNF-α, IL-6 and IL-1β mRNA increased significantly in the early stage of reperfusion and decreased gradually after reaching the peak, which suggested that the gene expression change of TNF-α,IL-6 and IL-1β was involved in the mechanism of cerebral ischemia reperfusion injury.
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