The polar tube protein is the major component of polar tube, and can specifically locate on the polar tube of microsporidia and plays an important role in invasion host cell. In this study, we analyzed the potential O- and Nglycosylation sites in polar tube protein 1 from Nosema bombycis. NbPTP1 was successfully cloned to eukaryotic expression vector pMT/Bip/V5-His A, involved V5 and His tags. After transfection, NbPTP1 gene could be efficiently expressed in Drosophila S2 cells. In addition, Lectin blotting and beta elimination analysis showed that NbPTP1 expressed in Drosophila S2 cells was O-glycosylation. These studies provided a basis for understanding the relationship between glycosylation and function of NbPTP1, helped us to reveal the infection mechanism of microsporidia and established effective diagnosis and prevention methods for microsporidia.

ObjectiveTo establish an ischemia-reperfusion model in cynomolgus macaques and to analyse the effects of edaravone intervention. MethodsA total of fifteen adult male cynomolgus macaques were randomly divided into three groups: sham operation (Sham group, n=3), ischemia-reperfusion model (Model group, n=6) and edaravone treatment (Edaravone group, n=6). Ischemic-reperfusion model of cynomolgus macaques was established by clamping the M1 branch of the left cerebral artery for 1 h. After 2 h of reperfusion, the animals in Edaravone group were injected with 0.5 mg/kg edaravone intravenously for intervention treatment, while the animals in Sham and Model groups were injected with an equal volume of normal saline intravenously, twice a day, from the 2nd to 7th day. The behavioral video recordings, clinical observations and neurological deficit scores of cynomolgus macaques were obtained, and brain edema volume and cerebral ischemia volume were statistically analyzed. ResultsCompared with the Sham group, the animals in Model group showed typical symptoms of ischemic stroke, with a significant increase in the neurological deficit score， the volumes of edema and infarct of brain tissue (all P＜0.01). Compared with Model group, the neurological deficit score, the volumes of edema and infarct of brain tissue were significantly reduced in Edaravone group (all P＜0.05). ConclusionAn animal model of ischemia-reperfusion in cynomolgus macaques was successfully established, and edaravone was confirmed to alleviate the damage caused by ischemia-reperfusion.