Objective: To investigate whether CXCL3 is involved in cerebral ischemia-reperfusion injury (CIRI) by mediating inflammatory response. Methods: The SD male rats were randomly divided into three groups: the sham operation group, the model group, and the CXCL3 injection group (200 ng per rat). The sham surgery group only underwent surgical exposure of the blood vessels. The model group established a middle cerebral artery occlusion/reperfusion (MCAO/R) model using the Longa suture method, with 1 hour of ischemia followed by 24 hours of reperfusion. The CXCL3 injection group used stereotactic brain surgery to inject recombinant CXC chemokine ligand 3 (CXCL3) protein into the lateral ventricle on the side of the MCAO/R model. The local cerebral blood flow changes in the MCAO model were detected using the moorFLPI-2 laser speckle perfusion imager. The degree of neurological dysfunction in rats was assessed using a neurological function scoring system. The volume of cerebral infarction was measured by TTC staining. The protein expression levels of CXCL3, interleukin-1 (IL-1) and interleukin-6 (IL-6), were measured by western blotting (WB). Results: Compared with the baseline blood flow, the blood flow in the MCAO model rats decreased by approximately 70% (P<0.001). Compared with the blood flow after 1 hour of ischemia, the blood flow values significantly increased after suture was removed (P<0.001). Additionally, there was no significant difference compared with the baseline blood flow (P>0.05). Twenty-four hours after reperfusion, compared with the sham operation group, the neurological function score and cerebral infarction volume in the model group both significantly increased (P<0.001). Compared with the sham operation group, the expression of CXCL3 protein in the ischemic area of the model group was upregulated (P<0.001), and the expressions of the inflammatory factors IL-1 and IL-6 were both increased (P<0.05). Compared with the model group, injection of recombinant CXCL3 protein further upregulate the expression of CXCL3 protein (P<0.05), and significantly increased the expression levels of the inflammatory factors IL-1 and IL-6 (P<0.05). Conclusion: High level of CXCL3 may contribute to CIRI by upregulating the expression of pro-inflammatory factors.
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