【摘要】：目的：觀察大鼠腸缺血再灌注損傷過(guò)程中腸黏膜的組織損傷和細(xì)胞凋亡及內(nèi)質(zhì)網(wǎng)分子伴侶葡萄糖調(diào)節(jié)蛋白78（Glucose regulated protein78kD, GRP78）的表達(dá)變化，探討腸缺血再灌注損傷后腸黏膜細(xì)胞凋亡與內(nèi)質(zhì)網(wǎng)應(yīng)激的可能機(jī)制。 方法：45只雄性SD大鼠隨機(jī)分成9組:缺血再灌注0、1、3、6、12、24、48、72h組,以及假手術(shù)對(duì)照組,每組5只。實(shí)驗(yàn)組均夾閉大鼠的腸系膜上動(dòng)脈1h后灌注，建立再灌注模型，假手術(shù)對(duì)照組僅游離腸系膜上動(dòng)脈，不夾閉。然后采用HE染色觀察腸黏膜變化，TUNEL法檢測(cè)腸黏膜細(xì)胞凋亡，Western Blot和RT-PCR檢測(cè)GRP78表達(dá)。 結(jié)果：缺血再灌注后，腸黏膜損傷程度及細(xì)胞凋亡指數(shù)隨再灌注時(shí)間延長(zhǎng)而增加，于再灌注3h達(dá)峰值（與其它組各組比較均P0.001），其后逐步減輕，于再灌注72h接近正常；缺血再灌注后，，GRP78的表達(dá)明顯增加，于1h達(dá)第1個(gè)小高峰（與0h組和3h組比較P 0.05），但隨再灌注時(shí)間的延長(zhǎng)，表達(dá)量逐步減少，再灌注12h后開(kāi)始回升（與6h組比較P 0.004），于24h達(dá)峰值（與其它各組比較均P 0.05），72h降至對(duì)照組水平（與假手術(shù)對(duì)照組比較P0.069）。 結(jié)論：腸缺血再灌注損傷啟動(dòng)內(nèi)質(zhì)網(wǎng)應(yīng)激，而內(nèi)質(zhì)網(wǎng)應(yīng)激通過(guò)某些途徑誘導(dǎo)了腸黏膜細(xì)胞凋亡，且GRP78在大鼠腸缺血再灌注過(guò)程中表達(dá)變化，可能與其對(duì)腸缺血再灌注損傷保護(hù)機(jī)制有關(guān)。
[Abstract]:Aim: to observe the tissue damage and apoptosis of intestinal mucosa and the expression of endoplasmic reticulum molecular glucose regulatory protein 78 (Glucose regulated protein 78 KD, GRP78 during intestinal ischemia reperfusion injury in rats. To explore the possible mechanism of intestinal mucosal cell apoptosis and endoplasmic reticulum stress after intestinal ischemia reperfusion injury. Methods Forty-five male Sprague-Dawley rats were randomly divided into 9 groups: control group (n = 5) and sham operation group (n = 5). In the experimental group, the superior mesenteric artery was occluded for 1 hour, then the reperfusion model was established. In the sham operation control group, the superior mesenteric artery was only free and not clamped. Then HE staining was used to observe the changes of intestinal mucosa and Tunel method was used to detect the apoptosis of intestinal mucosal cells. Western Blot and RT-PCR were used to detect the expression of GRP78. Results: after ischemia-reperfusion, the degree of intestinal mucosal injury and apoptosis index increased with the prolongation of reperfusion time, and reached the peak at 3 h after reperfusion (compared with other groups, P0.001), then gradually reduced, and reached the normal level at 72 h after reperfusion. The expression of GRP78 increased significantly after ischemia reperfusion and reached the first peak at 1 h (P 0.05 compared with 0 h group and 3 h group), but decreased gradually with the prolongation of reperfusion time. After 12 hours of reperfusion, it began to rise (P 0.004 compared with 6h group), and reached its peak at 24 h (P 0.05 compared with other groups) and decreased to the control group at 72 h (P 0.069 compared with the sham operation control group). Conclusion: endoplasmic reticulum stress is initiated by intestinal ischemia-reperfusion injury, and endoplasmic reticulum stress induces intestinal mucosal cell apoptosis through some pathways, and the expression of GRP78 changes during intestinal ischemia-reperfusion injury in rats. It may be related to the protective mechanism of intestinal ischemia reperfusion injury.
【學(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R574

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相關(guān)期刊論文 前1條

1 胡國(guó)梁;何昆侖;范利;;內(nèi)質(zhì)網(wǎng)應(yīng)激誘導(dǎo)的細(xì)胞凋亡與心肌缺血再灌注損傷[J];中華保健醫(yī)學(xué)雜志;2010年01期

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