本文選題：小鼠 + 皮膚缺血�。� 參考：《重慶醫(yī)科大學(xué)》2012年碩士論文

【摘要】：第一部分小鼠皮膚局部缺血模型的建立 目的：研究建立穩(wěn)定的昆明小鼠皮膚局部缺血模型。 方法：取40只雌性昆明小鼠,隨機(jī)分為A/B兩組,每組20只。分別在小鼠背部建立深達(dá)皮膚筋膜層的U型皮瓣。A組為3.3×1.5cm皮瓣組,B組為2.5×1.5cm皮瓣組。皮瓣游離緣墊以醫(yī)用橡膠,縫合切口,造成皮膚缺血模型,術(shù)后觀察皮瓣發(fā)紺水腫及壞死情況,并用散斑全景實(shí)時(shí)血流成像儀(Moor FLPI)檢測(cè)皮瓣血流。 結(jié)果：肉眼觀察,3.3×1.5cm皮瓣組在術(shù)后第2天,50%小鼠皮瓣末端壞死,壞死面積達(dá)皮瓣面積的(37.20±4.83)%。術(shù)后第3天100%小鼠皮瓣末端壞死。并隨時(shí)間的延長(zhǎng),壞死面積逐漸擴(kuò)大。2.5×1.5皮瓣組在術(shù)后第1天皮瓣出現(xiàn)發(fā)紺,水腫,發(fā)紺水腫面積占(77.46±4.51)%,術(shù)后第3、第5天發(fā)紺水腫區(qū)面積逐漸減小,至術(shù)后第7天,發(fā)紺、水腫完全消退。散斑全景實(shí)時(shí)血流成像儀(Moor FLPI)檢測(cè)皮膚血流顯示,術(shù)后第1天皮瓣顯著性缺血(p0.05),術(shù)后第7天血流基本恢復(fù)到術(shù)前水平。 結(jié)論：成功建立了昆明小鼠皮膚局部缺血模型,該模型具有操作簡(jiǎn)單、成本低、穩(wěn)定、有效等優(yōu)點(diǎn)。 第二部分局部缺血對(duì)mTOR信號(hào)通路的影響 目的：通過(guò)研究缺血對(duì)組織中P-4E-BPl,P-p70S6K,P-S6蛋白表達(dá)的影響,探討缺血對(duì)蛋白質(zhì)翻譯mTOR信號(hào)通路的影響。 方法：將30只昆明小鼠隨機(jī)分為6組(每組5只)：正常對(duì)照組(即缺血0分鐘組),缺血15分鐘組,缺血30分鐘組,缺血1小時(shí)組,缺血4小時(shí)組,缺血24小時(shí)組。除對(duì)照組外,分別在其余各實(shí)驗(yàn)組小鼠背部建立2.5×1.5cm U型皮瓣缺血模型。蛋白質(zhì)免疫印跡法檢測(cè)不同缺血時(shí)相點(diǎn)組織中P-4E-BP1,P-p70S6K,P-S6蛋白的表達(dá)。 結(jié)果：在缺血30分鐘及1小時(shí)時(shí),組織中P-p70S6K,P-S6蛋白的表達(dá)量均明顯高于正常組(P0.05)；在缺血15分鐘、30分鐘及1小時(shí)時(shí),組織中P-4E-BP1蛋白的表達(dá)量表達(dá)明顯高于正常組(P0.05)；在缺血24小時(shí)時(shí),組織中P-4E-BP1、 P-p70S6K、P-S6的表達(dá)量均明顯低于正常組(P0.05或P0.01)。 結(jié)論：暫時(shí)性缺血(缺血時(shí)間小于1小時(shí))可增加4E-BP1、p70S6K、S6蛋白的磷酸化,促進(jìn)蛋白質(zhì)翻譯；而較長(zhǎng)時(shí)間缺血(缺血24小時(shí))可抑制4E-BP1、p70S6K、S6蛋白的磷酸化,抑制蛋白質(zhì)翻譯。
[Abstract]:Objective: to establish a stable skin ischemia model in Kunming mice. Methods: 40 female Kunming mice were randomly divided into two groups: group A / R B (n = 20). U type skin flaps with deep skin fascia layer were established on the back of mice respectively. Group A was 3.3 脳 1.5cm flap group and group B was 2.5 脳 1.5cm flap group. The skin ischemia model was established by using medical rubber and suture incision. The cyanotic edema and necrosis of the flap were observed after operation. The blood flow of the flap was detected by the real time speckle panoramic flow imager (moor FLPI). Results: on the second day after operation, 50% of the skin flaps in the 3. 3 脳 1.5cm skin flap group were necrotic, and the necrotic area was 37.20 鹵4. 83% of the flap area. On the third day after operation, 100% of the skin flaps were necrotic. With the extension of time, the necrotic area gradually expanded. 2.5 脳 1.5 flap group showed cyanosis, edema and cyanosis on the first day after operation. The area of cyanotic edema was 77.46 鹵4.51, and the area of cyanotic edema gradually decreased on the 3rd and 5th day after operation, and cyanosis occurred on the 7th day after operation. The edema completely subsided. Spot panoramic real time flow imager (moor FLPI) was used to detect the skin blood flow. On the first day after operation, the skin flap had significant ischemia (p0.05), and on the 7th day after operation, the blood flow was basically recovered to the preoperative level. Conclusion: the skin ischemia model of Kunming mice has been successfully established, which has the advantages of simple operation, low cost, stable and effective. Part two effects of local ischemia on mTOR signaling pathway. Objective: to investigate the effects of ischemia on the expression of P-4E-BPlP P-p70S6KTOR signal pathway. Methods: thirty Kunming mice were randomly divided into 6 groups (5 rats in each group): normal control group (0 minutes ischemia group, 15 minutes ischemia group, 30 minutes ischemia group, 1 hour ischemia group, 4 hours ischemia group, 24 hours ischemia group). In addition to the control group, 2. 5 脳 1.5cm U skin flap ischemia models were established in each experimental group. The expression of P-4E-BP1C P-p70S6KP6 protein was detected by Western blot. Results: the expression of P-p70S6KTP-S6 protein was significantly higher than that of normal group at 30 minutes and 1 hour after ischemia, and the expression of P-4E-BP1 protein in tissue was significantly higher than that in normal group at 15 minutes, 30 minutes and 1 hour after ischemia. After 24 hours of ischemia, the expression of P-4E-BP1 and P-p70S6KTP-S6 was significantly lower than that of normal group (P0.05 or P0.01). Conclusion: transient ischemia (ischemia time less than 1 hour) can increase the phosphorylation of 4E-BP1p70S6KS6 protein and promote protein translation, while prolonged ischemia (24 hours ischemia) can inhibit the phosphorylation of 4E-BP1p70S6KS6 protein and inhibit protein translation.
【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】：2012
【分類(lèi)號(hào)】：R-332;R622

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本文編號(hào)：2012151