本文選題：大鼠 + 前列腺素E1��； 參考：《昆明醫(yī)學院》2010年碩士論文

【摘要】： 目的：通過應用前列腺素E1對大鼠小腸缺血／再灌注損傷影響的研究,從腸粘膜的損傷程度,促炎因子和抗炎因子的釋放,以及細菌移位等不同方面探討前列腺素E1對大鼠小腸缺血再灌注損傷的是否具有保護作用,從而為臨床防治小腸缺血再灌注損傷提供一個新的策略。 方法：SPF級健康成年雄性SD大鼠80只,體重280g-320g,隨機分為假手術(Sham group, S)組、缺血／再灌注損傷(ischemia/reperfusion injury, IRI)組、缺血預處理組(ischemia preconditioning, IPC)和前列腺E1(Prostaglandin E1,PGE1)組(n=20),每組根據(jù)再灌注后采集標本的時間分為兩個亞組(n=10),實驗前12h使大鼠禁食,自由飲水,并于實驗前2h行含綠色熒光素蛋白大腸桿菌(Ecdi DH5α)2ml灌胃。 ①S組：麻醉后取腹正中切口,長約3cm,分離腸系膜上動脈(SMA)后關腹； ②IRI組：同S組分離SMA后,用無創(chuàng)微動脈夾夾閉SMA后關腹,45min后取出動脈夾,分別于再灌注2h、4h時采集標本； ③IPC組：同S組分離SMA后,給予SMA 3個循環(huán)的預處理(缺血2min后再灌注2min為一個循環(huán))后關腹,余同IRI組； ④PGE1組：同S組分離SMA后,用無創(chuàng)微動脈夾夾閉SMA后關腹,缺血45min后,于再灌注前5min經(jīng)尾靜脈按20ug／kg注入PGE1,余同IRI組。 ELISA法檢測血清中IL-1β,IL-6,IL-10和TNF-α的含量,同時取回腸壁組織長1cin行腸粘膜病理學檢測并行HE染色,取肝臟組織、脾臟組織及門靜脈血行細菌移位檢測。 結(jié)果： 1、小腸病理變化：S組大鼠腸絨毛完整,排列整齊,鏡下無中性粒細胞浸潤。IRI組大鼠在再灌注2h和4h后小腸絨毛上皮頂端與固有層分離并見固有層毛細血管暴露、出血和潰瘍,粘膜絨毛壞死,脫落,鏡下見大量中性粒細胞浸潤。與IRI組相比,IPC組和PGE1組在各時間點腸粘膜絨毛損傷減輕,壞死,脫落少見,鏡下中性粒細胞浸潤輕。IPC組和PGE1組損傷評分明顯低于IRI組(P0.05),IPC組和PGE1組相比,差異無統(tǒng)計學意義(P0.05)。 2、細胞因子改變：IRI組、IPC組和PGE1組再灌注2h、4h,大鼠動脈血清中炎性細胞因子IL-1β,IL-6,TNF-α含量明顯高于S組(P0.05)；IPC組和PGE1組IL-1p,IL-6,TNF-a則低于IRI組(P0.05)；IPC組和PGE1組相比,差異無統(tǒng)計學意義(P0.05)。大鼠動脈血清中抗炎因子IL-10含量在IRI組、IPC組和PGE1組各時間點明顯低于S組(氏0.05)；IPC組和PGE1組各時間點高于IRI組(P0.05)；IPC組和PGE1相比,差異無統(tǒng)計學意義(P0.05)。 3、細菌移位改變：再灌注2h、4h,S組大鼠脾臟、肝臟及門靜脈血未檢出移位細菌生長；IPC組和PGE1組明顯低于IRI組(P0.05),IPC組和PGE1組相比,差異無統(tǒng)計學意義(P0.05)。 結(jié)論： PGE1和IPC能減輕大鼠小腸缺血再灌注損傷后小腸粘膜絨毛的壞死程度：PGE1和IPC能抑制大鼠小腸缺血再灌注損傷后促炎細胞因子(IL-1p,IL-6,TNF-α)的釋放和促進抗炎細胞因子IL-10的表達：PGE1和IPC能減少大鼠小腸缺血再灌注損傷后的細菌移位。
[Abstract]:Objective: to study the effects of prostaglandin E _ 1 on intestinal ischemia / reperfusion injury in rats, and to investigate the extent of intestinal mucosal injury, the release of proinflammatory and anti-inflammatory factors, and the effects of prostaglandin E _ 1 on intestinal ischemia / reperfusion injury in rats. To explore whether prostaglandin E1 has protective effect on intestinal ischemia-reperfusion injury in rats from different aspects such as bacterial translocation, so as to provide a new strategy for clinical prevention and treatment of intestinal ischemia-reperfusion injury. Methods 80 healthy male Sprague-Dawley rats of SPF grade, weighing 280g-320g, were randomly divided into sham group (S) group and ischemia/reperfusion injury-injury (IRI) group. Ischemic preconditioning group (ischemia preconditioning, IPC) and prostaglandin E1 (PGE1) group were divided into two subgroups according to the time of reperfusion. The rats were fasting and drinking freely 12 hours before the experiment. In group 1, the median incision was taken after anesthesia, about 3 cm long, and the superior mesenteric artery (SMA) was separated and then closed. 2IRI group: after SMA was separated from the same S group, the artery clamp was removed 45 minutes after the closure of the SMA, and the specimens were collected at 4 h after 2 h reperfusion, while in the same S group, the SMA was separated from the same S group. Three cycles of preconditioning (2min after ischemia and reperfusion as a circulation) were given, followed by closure of abdomen, rest in IRI group, 4PGE1 group: after isolation of SMA from group S, closure of abdomen with non-invasive microartery clamping, and after ischemia of 45min. Before reperfusion, 5min was injected into PGE1 via caudal vein according to 20ug/kg. Elisa was used to detect the contents of IL-1 尾, IL-6, IL-10 and TNF- 偽 in serum, and the long 1cin of intestinal wall was collected for intestinal mucosal pathological examination and HE staining, and liver tissue was obtained. Bacterial translocation was detected in splenic tissue and portal vein blood. Results: 1. The intestinal villi were intact and arranged neatly in the group of small intestine pathological changes. No neutrophil infiltration. IRI rats were separated from the lamina propria at 2 and 4 hours after reperfusion and showed capillary exposure hemorrhage and ulcer mucosal villi necrosis and neutrophils infiltration under microscope. Compared with IRI group, IPC group and PGE1 group had less injury, necrosis and shedding of intestinal mucosal villi at different time points. The injury scores of IPC group and PGE1 group were significantly lower than those of IRI group (P0.05) and PGE1 group (P 0.05), and the injury scores of IPC group and PGE1 group were significantly lower than those of IRI group (P0.05). There was no significant difference (P0.05). 2. The changes of cytokines in IPC group and PGE1 group were significantly higher than those in group S (P0.05), and the levels of IL-1pIL-6TNF-a in arterial serum of rats were significantly higher than those of IRI group (P0.05), and the level of IL-1pIL-6TNF-a in arterial serum of rats was significantly higher than that of IRI group (P0.05). There was no significant difference between IPC group and PGE1 group (P0.05). The levels of anti-inflammatory factor IL-10 in serum of rats in IRI group were significantly lower than those in group S (0.05) and PGE1 group (P 0.05), and were significantly higher than those in IRI group (P0.05) and IPC group and PGE1 group at each time point. There was no significant difference between the two groups (P0.05). 3. The change of bacterial translocation: the spleen, liver and portal vein blood were not detected in the spleen, liver and portal vein blood of rats in the group of 2 h reperfusion (P0.05) compared with the group of IRI (P0.05) and the group of PGE1 (PGE1), the difference of bacterial translocation between IPC group and PGE1 group was significantly lower than that in group IPC and PGE1. The difference was not statistically significant (P0.05). Conclusion: PGE1 and IPC can reduce the degree of necrosis of intestinal villi after small intestinal ischemia reperfusion injury in rats. PGE1 and IPC can inhibit the release of pro-inflammatory cytokine (IL-1pmIL-6TNF- 偽) after small intestinal ischemia-reperfusion injury in rats. And promote the expression of anti-inflammatory cytokine IL-10: PGE1 and IPC can reduce the bacterial translocation after small intestinal ischemia-reperfusion injury in rats.
【學位授予單位】：昆明醫(yī)學院
【學位級別】：碩士
【學位授予年份】：2010
【分類號】：R363

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