ABSTRACT
Objective@#To investigate whether GIV , a coiled helix structural domain protein containing 88A , has an effect on the neuroinflammatory response in a model of cerebral ischemia⁃reperfusion injury.@*Methods@# A middle cerebral artery embolization⁃reperfusion model (MACO/R) and an oxygen glucose deprivation/reoxygenation model ( OGD 6 h + R 24 h) of BV2 microglia were constructed in C57BL/6 mice , and the area of cerebral infarction was detected by TTC staining; the Longa neurobiological score was used to evaluate the degree of neurological deficit in mice ; ELISA was used to detect the release of IL⁃6 and TNF⁃α in the supernatant of peripheral blood and cell cultures , and Western blot was used to detect the protein expression of GIV , TREM2 and TLR4 in the cortical area around the infarct foci in mice ; different concentrations of lipopolysaccharide (LPS , 1 , 5 , 10 μg/ml) were used to stimulate BV2 cells for 24 h to establish a neuroinflammation model , qRT⁃PCR was performed to detect the mRNA levels of IL⁃6 , TNF⁃α and IL⁃1β , and Western blot was used to detect the expression of GIV ; OGD/R culture treatment was performed after knocking down the expression of GIV gene using siRNA interference technique ;ELISA was performed to detect the release concentration of IL⁃6 and TNF⁃α in cell culture medium supernatant;protein immunoblotting was performed to detect the knockdown efficiency of GIV.@*Results @#Both the successfully constructed MCAO/R and OGD/R models activated the neuroinflammatory response and induced a decrease in protein expression of GIV ; MCAO/R induced increased concentrations of IL⁃6 and TNF⁃α release in peripheral blood of mice and promoted the protein expression of TREM2 and TLR4 ; LPS activated IL⁃6 , IL⁃1β and TNF⁃α expression in BV2 cells , but did not affect GIV expression ; siRNA interference with GIV gene expression further in creased the expression of inflammatory factors IL⁃6 and TNF⁃α .@*Conclusion@#The GIV gene may be characteristically involved in regulating the neuroinflammatory response induced by cerebral ischemia⁃reperfusion injury , and it may be a potential therapeutic target for cerebral ischemia⁃reperfusion injury.