本文選題：腦梗死 + 血管內(nèi)皮生長因子　； 參考：《新鄉(xiāng)醫(yī)學(xué)院》2014年碩士論文

【摘要】：背景腦梗死對人們身體健康的危害近年來一直位居榜首,其預(yù)后直接影響到患者今后的日常生活和家庭生活。腦組織的缺血、缺氧是腦梗死最常見的損害,改善腦組織的缺血、缺氧狀態(tài)、減輕腦水腫是治療腦梗死不可缺少的手段,血管內(nèi)皮生長因子(VEGF)能夠加速缺血、缺氧區(qū)新血管的再生、重建；腦梗死發(fā)生后,腦組織中的炎癥因子也被激活,如白細(xì)胞介素-8(IL-8)、白細(xì)胞介素-17(IL-17)等,它們對白細(xì)胞有著強烈的趨化作用,這些炎癥因子聚集在一起,又反過來加重了腦血管的堵塞,進(jìn)一步加重了腦組織的缺血、缺氧狀態(tài)；如何同時能激活VEGF.抑制IL-8、IL-17等炎癥因子顯得尤為重要。近年來,大量事實證明環(huán)磷腺苷參與多種被損傷的神經(jīng)系統(tǒng)的修復(fù),環(huán)磷腺苷是核苷酸的衍生物,人們稱之為第二信使,環(huán)磷腺苷的穩(wěn)定取決于腺苷酸環(huán)化酶和磷酸二酯酶的功能狀態(tài)。研究表明,環(huán)磷腺苷能影響神經(jīng)細(xì)胞膜蛋白的結(jié)構(gòu)和功能,阻止Ca2+內(nèi)流,抑制各種有害因子的表達(dá)和產(chǎn)生,如IL等,激活有益因子如VEGF等,促進(jìn)血管再生和重建,阻止神經(jīng)元細(xì)胞的凋亡。目前關(guān)于環(huán)磷腺苷對血清中VEGF、IL影響的研究較多,對腦脊液中VEGF、IL影響的研究較少。目的 分析二丁酰環(huán)磷腺苷鈣對急性腦梗死患者腦脊液中神經(jīng)細(xì)胞因子的影響。方法采用隨機數(shù)字表法將我院神經(jīng)內(nèi)科2012年4月至2014年8月期間105例確診急性腦梗死住院患者進(jìn)行分組,對照組52例給予胞二磷膽堿治療,試驗組53例給予環(huán)磷腺苷的衍生物——二丁酰環(huán)磷腺苷鈣治療,觀察治療后3天、7天、14天患者腦脊液中VEGF、IL-8、IL-17的變化趨勢,比較兩組研究對象在不同的治療時期三個觀察指標(biāo)的差異,來判斷二丁酰環(huán)磷腺苷鈣在腦梗死患者早期治療過程中的價值。結(jié)果1.與對照組相比,腦梗死患者在使用二丁酰環(huán)磷腺苷鈣治療3天、7天后,VEGF明顯升高,兩組比較差異有統(tǒng)計學(xué)意義；治療14天后,VEGF恢復(fù)至治療前水平,兩組比較差異無統(tǒng)計學(xué)意義：2.與對照組相比,試驗組IL-8、IL-17在治療3天后顯著下降,兩組比較差異有統(tǒng)計學(xué)意義,在治療7天、14天后降至正常水平,兩組比較差異無統(tǒng)計學(xué)意義。結(jié)論1.二丁酰環(huán)磷腺苷鈣可升高VEGF水平,有可能改善腦梗死患者腦組織的缺氧缺血狀態(tài)。2.二丁酰環(huán)磷腺苷鈣能降低IL-8、IL-17水平,有可能減輕腦梗死患者腦組織的炎癥反應(yīng)。3.二丁酰環(huán)磷腺苷鈣可能促進(jìn)腦梗死患者神經(jīng)功能的康復(fù)和局部血管的再生。
[Abstract]:Background Cerebral infarction has been the most harmful to people's health in recent years, and its prognosis has a direct impact on patients' daily life and family life. Cerebral ischemia and hypoxia are the most common lesions in cerebral infarction. Improving cerebral ischemia and hypoxia, reducing cerebral edema is an indispensable means to treat cerebral infarction. Vascular endothelial growth factor (VEGF) can accelerate ischemia. The regeneration and reconstruction of new blood vessels in the anoxic region, and the activation of inflammatory factors in the brain after cerebral infarction, such as interleukin-8, interleukin-17 (IL-17), which have a strong chemotactic effect on white blood cells, and these inflammatory factors gather together. In turn, it exacerbates the blockage of cerebral vessels, further exacerbates the ischemic and anoxic state of brain tissue, and how to activate VEGFat at the same time. It is very important to inhibit the inflammatory factors such as IL-8, IL-17 and so on. In recent years, a large number of facts have proved that adenosine is involved in the repair of many damaged nervous systems. Adenosine monophosphate is a derivative of nucleotides, which is called the second messenger. The stability of cyclic adenosine depends on the functional state of adenylate cyclase and phosphodiesterase. Studies have shown that cyclophosphate adenosine can affect the structure and function of membrane proteins of nerve cells, block the influx of Ca2, inhibit the expression and production of various harmful factors, such as IL, activate beneficial factors such as VEGF, and promote vascular regeneration and reconstruction. Block neuronal cell apoptosis. At present, there are more studies on the effect of cyclic adenosine on VEGF IL in serum, and less on the effect of VEGF IL in CSF. Objective to analyze the effect of dibutyryl cyclic adenosine phosphate calcium on neurocytokines in cerebrospinal fluid (CSF) of patients with acute cerebral infarction. Methods from April 2012 to August 2014, 105 inpatients with acute cerebral infarction were randomly divided into two groups. 52 patients in control group were treated with citicoline. 53 patients in the experimental group were treated with calcium dibutyryl cyclic adenosine monophosphate. The changes of IL-17 in cerebrospinal fluid (CSF) of 53 patients with adenosine cyclophosphate were observed 3 days after treatment and 14 days after treatment, and the changes of IL-17 in cerebrospinal fluid of patients with adenosine cyclophosphate were observed. To evaluate the value of calcium dibutyrylcyclophosphate in the early treatment of cerebral infarction patients, we compared the difference of three observation indexes between the two groups in different treatment period. Result 1. Compared with the control group, VEGF in cerebral infarction patients increased significantly after 3 days and 7 days of treatment, the difference between the two groups was statistically significant, 14 days after treatment, VEGF returned to the level before treatment, and there was no significant difference between the two groups. Compared with the control group, IL-8 IL-17 in the experimental group decreased significantly after 3 days of treatment, the difference between the two groups was statistically significant, and the level of IL-8 IL-17 decreased to the normal level after 7 days and 14 days of treatment, but there was no significant difference between the two groups. Conclusion 1. Calcium dibutyrylcyclophosphate can increase the level of VEGF, which may improve the hypoxic-ischemic state of cerebral tissue in patients with cerebral infarction. Calcium dibutyrylcyclophosphate can decrease the level of IL-8 and IL-17, which may alleviate the inflammatory reaction of cerebral tissue in patients with cerebral infarction. Dibutyryl cyclophosphate calcium may promote the rehabilitation of nerve function and the regeneration of local blood vessels in patients with cerebral infarction.
【學(xué)位授予單位】：新鄉(xiāng)醫(yī)學(xué)院
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R743.3

【參考文獻(xiàn)】

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1 董龍禹;李江偉;吳明毅;竇林彬;郭玉潔;孫玉明;褚文彥;;二丁酰環(huán)磷腺苷鈣預(yù)防甲狀腺瘤切除術(shù)頸叢神經(jīng)阻滯麻醉時血壓升高的效果[J];武警醫(yī)學(xué);2012年04期

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