Lack of sphingomyelin synthase 2 reduces cerebral ischemia/reperfusion injury by inhibiting microglial inflammation in mice
- Yu Yang
- Fengxian Hu
- Guifeng Yang
- Qingmei Meng
Affiliations: Department of Radiology, The Third People's Hospital of Qingdao, Qingdao, Shandong 266041, P.R. China
- Published online on: October 22, 2020 https://doi.org/10.3892/etm.2020.9371
Copyright: © Yang
et al. This is an open access article distributed under the
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Commons Attribution License.
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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.