本文選題：帕金森病 + 血管活性腸肽��； 參考：《神經(jīng)解剖學(xué)雜志》2017年03期

【摘要】：目的:研究血管活性腸肽(VIP)對(duì)1-甲基-4-苯基-1,2,3,6-四氫吡啶(MPTP)誘導(dǎo)的帕金森病(PD)模型小鼠發(fā)揮抗氧化應(yīng)激和神經(jīng)保護(hù)作用。方法:雄性C57BL/6J小鼠隨機(jī)分為生理鹽水(NS)組、MPTP組和MPTP+VIP組。Elisa法檢測(cè)紋狀體丙二醛(MDA)以及超氧化物歧化酶(SOD)、過(guò)氧化氫酶(CAT)的變化;免疫組織化學(xué)法觀察中腦黑質(zhì)紋狀體系統(tǒng)酪氨酸羥化酶(TH)、星形膠質(zhì)細(xì)胞特異性標(biāo)記物膠質(zhì)細(xì)胞纖維酸性蛋白(GFAP)和小膠質(zhì)細(xì)胞標(biāo)志物離子鈣結(jié)合蛋白(Iba-1)的表達(dá)變化;透射電子顯微鏡觀察中腦黑質(zhì)多巴胺能神經(jīng)元的超微結(jié)構(gòu)變化。結(jié)果:MPTP組與對(duì)照組相比,MDA水平顯著增高,SOD和CAT的表達(dá)顯著降低;給予VIP可顯著抑制MDA的水平(P0.01),增強(qiáng)SOD和CAT的表達(dá)(P0.05)。與對(duì)照組相比,MPTP組小鼠GFAP和Iba-1的表達(dá)明顯上升,TH表達(dá)明顯下降;給予VIP可顯著降低GFAP和Iba-1的表達(dá)(P0.05),而TH表達(dá)明顯增強(qiáng)。透射電鏡觀察顯示:NS組神經(jīng)細(xì)胞和細(xì)胞器結(jié)構(gòu)清晰完整;MPTP組神經(jīng)細(xì)胞核膜內(nèi)陷,線粒體空泡樣變;MPTP+VIP組神經(jīng)細(xì)胞和細(xì)胞器結(jié)構(gòu)基本正常。結(jié)論:VIP能夠抑制MPTP誘導(dǎo)PD小鼠中腦黑質(zhì)星形膠質(zhì)細(xì)胞和小膠質(zhì)細(xì)胞的活化,對(duì)抗氧化應(yīng)激,發(fā)揮神經(jīng)保護(hù)作用。
[Abstract]:Aim: to study the antioxidation and neuroprotective effects of vasoactive intestinal peptide (VIP) on PD model mice induced by 1-methyl-4-phenyl-1-trihydropyridine (MPTP). Methods: male C57BL/6J mice were randomly divided into two groups: MPTP group and MPTP VIP group. The changes of malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (catalase) in the striatum were detected by Elisa. The expression of tyrosine hydroxylase (THN), astrocyte-specific marker glial fibrillary acidic protein (glial fibrillary acidic protein) and microglial marker ion-calcium-binding protein (Iba-1) in the substantia nigra striatum were observed by immunohistochemical method. The ultrastructural changes of dopaminergic neurons in the substantia nigra were observed by transmission electron microscope. Results compared with the control group, the expression of sod and CAT was significantly decreased in the control group, and the expression of SOD and CAT was significantly inhibited by VIP, and the expression of SOD and CAT was enhanced by the administration of VIP. Compared with the control group, the expression of GFAP and Iba-1 in MPTP group increased significantly, and the expression of th decreased significantly in mice treated with VIP, and the expression of GFAP and Iba-1 decreased significantly, while the expression of th increased significantly. The results of transmission electron microscope showed that the structure of neurons and organelles in the VIP group was clear and intact. The nuclear membrane of the neurons in the MPTP group was trapped, and the structure of the neuronal and organelle in the MPTP VIP group was basically normal. ConclusionVIP can inhibit the activation of astrocytes and microglia in the substantia nigra of PD mice induced by MPTP, and play a neuroprotective role on antioxidant stress.
【作者單位】： 濰坊醫(yī)學(xué)院組織學(xué)與胚胎學(xué)教研室;濰坊醫(yī)學(xué)院醫(yī)學(xué)研究實(shí)驗(yàn)中心;濰坊醫(yī)學(xué)院;濰坊醫(yī)學(xué)院護(hù)理學(xué)院;
【基金】：山東省醫(yī)藥衛(wèi)生科技發(fā)展計(jì)劃項(xiàng)目(2015WS0063) 濰坊醫(yī)學(xué)院大學(xué)生科技創(chuàng)新基金項(xiàng)目(KX2016006,KX2016011)
【分類號(hào)】：R-332;R742.5

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