| Summary: | The aim of this study was to investigate whether remote ischemic preconditioning (RIPC) can promote neurological function recovery after middle cerebral artery occlusion (MCAO) in rats and its possible mechanism. A total of 32 Sprague Dawley (SD) rats were randomly divided into RIPC group (n = 16) and MCAO group (n = 16). In the RIPC group, 1 h before induction of MCAO, the rats received bilateral femoral artery ischemic preconditioning (10 min/time), followed by 10 min of relaxation, and a total of three cycles were carried out. Then, the MCAO-2h model was established. In the MCAO group, the MCAO-2h model was established at 1 h after the separation of bilateral femoral arteries. The modified neurological severity score (mNSS) was assessed. At postmodeling day 7, triphenyltetrazolium chloride (TTC) staining and immunohistochemistry were conducted, and neurological function recovery, infarct size, and the expression levels of glial fibrillary acidic protein (GFAP), synaptophysin (SYN), and neurite outgrowth inhibitor A (Nogo-A) were observed. At postmodeling day 7, the difference in mNSS was statistically significant ( P < 0.05). Infarct size was significantly smaller in the RIPC group than in the MCAO group ( P < 0.05). The number of GFAP + cells was significantly lesser in the RIPC group than in the MCAO group ( P < 0.05). The difference in thickness of the glial scar was not statistically significant ( P = 0.091). At postmodeling day 7, the expression level of SYN integrated optical density (IOD) was significantly higher in the RIPC group than in the MCAO group ( P < 0.05). The number of Nogo-A + cells was significantly lesser in the RIPC group than in the MCAO group ( P < 0.05). At day 7 after MCAO, RIPC can promote neurological function recovery in rats and reduce infarct size. The mechanism may be that after 7 days, RIPC reduces GFAP expression, inhibits the trend of glial scar formation and Nogo-A expression, and increases SYN expression.
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