Expression and clinical significance of miR-26b and platelet P-selectin (CD62p) in serum of patients with cerebral infarction / 中风与神经疾病杂志

@#Objective To explore the expression and clinical significance of microRNA (miR)-26b and platelet P-selectin (CD62p) in serum of patients with acute cerebral infarction.Methods A total of 128 patients with acute cerebral infarction (case group) and 128 healthy people with physical examination results (health group) were selected as the research objects.The relationship between the expression levels of serum miR-26b and CD62p and the clinicopathological parameters of the patients in the case group as well as their predictive power for poor prognosis 3 months after the onset were analyzed.Results The expression level of miR-26b in the case group was significantly lower than in the healthy group,and the expression level of CD62p was higher than that in the healthy group (P<0.05).There were significant differences in the expression levels of serum miR-26b and CD62p between patients with different degrees of neurological deficit,cerebral infarction volume and prognosis (P<0.05).Serum miR-26b in the case group was negatively correlated with mRS score,cerebral infarction volume and NIHSS score,while CD62p was positively correlated with mRS score,cerebral infarction volume and NIHSS score (P<0.05).Increased NIHSS score and cerebral infarction volume,low expression of miR-26b and high expression of CD62p were risk factors for poor prognosis in patients with acute cerebral infarction (P<0.05).The ROC curve showed that the area under the curve of serum miR-26b combined with CD62p in predicting poor prognosis of acute cerebral infarction was 0.950. Conclusion Serum miR-26b and CD62p are related to infarct volume,degree of neurological deficit and 3-month prognosis in patients with acute cerebral infarction,which are helpful for early prediction of clinical prognosis.

Pinocembrin Promotes OPC Differentiation and Remyelination via the mTOR Signaling Pathway / 神经科学通报·英文版

The exacerbation of progressive multiple sclerosis (MS) is closely associated with obstruction of the differentiation of oligodendrocyte progenitor cells (OPCs). To discover novel therapeutic compounds for enhancing remyelination by endogenous OPCs, we screened for myelin basic protein expression using cultured rat OPCs and a library of small-molecule compounds. One of the most effective drugs was pinocembrin, which remarkably promoted OPC differentiation and maturation without affecting cell proliferation and survival. Based on these in vitro effects, we further assessed the therapeutic effects of pinocembrin in animal models of demyelinating diseases. We demonstrated that pinocembrin significantly ameliorated the progression of experimental autoimmune encephalomyelitis (EAE) and enhanced the repair of demyelination in lysolectin-induced lesions. Further studies indicated that pinocembrin increased the phosphorylation level of mammalian target of rapamycin (mTOR). Taken together, our results demonstrated that pinocembrin promotes OPC differentiation and remyelination through the phosphorylated mTOR pathway, and suggest a novel therapeutic prospect for this natural flavonoid product in treating demyelinating diseases.

Pinocembrin Promotes OPC Differentiation and Remyelination via the mTOR Signaling Pathway / 神经科学通报·英文版

The exacerbation of progressive multiple sclerosis (MS) is closely associated with obstruction of the differentiation of oligodendrocyte progenitor cells (OPCs). To discover novel therapeutic compounds for enhancing remyelination by endogenous OPCs, we screened for myelin basic protein expression using cultured rat OPCs and a library of small-molecule compounds. One of the most effective drugs was pinocembrin, which remarkably promoted OPC differentiation and maturation without affecting cell proliferation and survival. Based on these in vitro effects, we further assessed the therapeutic effects of pinocembrin in animal models of demyelinating diseases. We demonstrated that pinocembrin significantly ameliorated the progression of experimental autoimmune encephalomyelitis (EAE) and enhanced the repair of demyelination in lysolectin-induced lesions. Further studies indicated that pinocembrin increased the phosphorylation level of mammalian target of rapamycin (mTOR). Taken together, our results demonstrated that pinocembrin promotes OPC differentiation and remyelination through the phosphorylated mTOR pathway, and suggest a novel therapeutic prospect for this natural flavonoid product in treating demyelinating diseases.