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目的探讨血管活性肠肽(VIP)通过调控脑组织IFN-γ、IL-17A因子水平对实验性自身免疫性脑脊髓炎(EAE)大鼠防治作用。方法将60只健康雌性Wistar大鼠随机分成4组(正常对照组、EAE对照组、VIP低剂量防治组和VIP高剂量防治组),利用髓鞘碱性蛋白(MBP)+完全弗氏佐剂(CFA)诱导建立EAE模型。自造模当日起,每隔1 d分别对VIP低、高剂量防治组大鼠腹腔注射VIP 4 nmol/kg(0.2 ml)、16 nmol/kg(0.8 ml),正常对照组及EAE对照组注射0.8 ml生理盐水,连续10 d。观察大鼠发病情况;HE染色观察脑组织基本病理改变;通过免疫组化技术,利用抗胶质纤维酸性蛋白抗体(GFAP)检测脑组织内的星形胶质细胞活化情况;ELISA法检测脑组织匀浆中IFN-γ、IL-17A因子含量变化。结果 VIP各剂量防治组大鼠发病潜伏期延长、进展期缩短、发病高峰期神经功能障碍评分(NDS)降低,脑组织中炎症细胞浸润程度明显下降、活化的星形胶质细胞即GFAP+细胞数量减少,脑组织匀浆中IFN-γ、IL-17A含量降低,且高剂量组变化更明显。结论 VIP通过降低脑组织中IFN-γ、IL-17A含量,减轻脑组织炎症细胞的浸润程度,抑制星形胶质细胞活化,发挥对EAE的防治作用。
Objective To investigate the preventive and therapeutic effects of vasoactive intestinal peptide (VIP) on experimental autoimmune encephalomyelitis (EAE) rats by regulating the levels of IFN-γ and IL-17A in brain tissue. Methods Sixty healthy female Wistar rats were randomly divided into 4 groups (normal control group, EAE control group, VIP low-dose prevention group and VIP high-dose prevention group). The MBP + complete Freund’s adjuvant (CFA) induced EAE model. From the day of modeling, VIP 4 and 5 nmol / kg (0.8 ml) were intraperitoneally injected into the VIP low dose and high dose control groups, and the normal control group and EAE control group 0.8 ml normal saline for 10 days. The pathological changes of rat brain were observed by HE staining. The activation of astrocytes in brain tissue was detected by immunohistochemistry and GFAP antibody. The brain tissue was detected by ELISA The content of IFN-γ and IL-17A in the homogenate changed. Results The rats in VIP control group had longer latent period, shorter developmental duration, lower neurological deficit score (NDS), infiltration of inflammatory cells in brain tissue and decreased number of activated astrocytes, that is, GFAP + cells , The content of IFN-γ and IL-17A in brain homogenate decreased, and the change in high dose group was more obvious. Conclusion VIP can prevent and treat EAE by decreasing the levels of IFN-γ and IL-17A in brain tissue, decreasing the infiltration of inflammatory cells in brain tissue, inhibiting the activation of astrocytes.