Recanalization of blood flow after ischemia can lead to ischemia/reperfusion injury, and inflammation plays an important role in the mechanisms behind cerebral ischemia/reperfusion injury. Sphingomyelin synthase 2 (SMS2) deficiency reduces inflammation; however, the effect and mechanism of action of SMS2 on the inflammatory response after cerebral ischemia/reperfusion injury are still unclear. Wild-type (WT) and SMS2 knockout C57BL/6 mice were used to establish a model of cerebral ischemia/reperfusion. The neurological deficit score was evaluated with Longa's method, and infarct volume was evaluated by magnetic resonance imaging and 2,3,5-triphenyltetrazolium chloride staining. Neurological deficit and infarct volume were used to evaluate the degree of cerebral ischemia/reperfusion injury in mice. Western blotting, reverse transcription-quantitative PCR and immunofluorescence were used to detect the expression profiles. The neurological deficit score of SMS2-/- mice was significantly lower than that of WT mice at 72 h after cerebral ischemia/reperfusion injury (P=0.027), but not significantly different at 24 h (P=0.064). Compared with WT mice at 24 and 72 h after cerebral ischemia/reperfusion, the infarct volume of SMS2-/- mice was decreased, the expression of pro-inflammatory cytokines galectin 3 and interleukin-1β were decreased, the activation of microglia was decreased, and the nuclear translocation of NF-κB p65 was decreased, but the expression of the anti-inflammatory factor arginase 1 was increased. Lack of SMS2 in mice can help to reduce the inflammatory reaction by inhibiting the activation of NF-κB signaling pathway, further attenuating cerebral ischemia/reperfusion injury in mice.
Keywords: cerebral ischemia reperfusion; inflammation; microglial; sphingomyelin synthase 2.
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