本文選題：脂多糖 + 熱休克蛋白70��； 參考：《山西醫(yī)科大學(xué)》2008年碩士論文

【摘要】： 目的本實(shí)驗(yàn)旨在觀察內(nèi)毒素血癥大鼠不同時間點(diǎn)肺組織熱休克蛋白70(HSP70)、丙二醛(MDA)、超氧化物歧化酶(SOD)的變化,以及谷氨酰胺(Gln)對大鼠內(nèi)毒素血癥肺組織損傷的影響,探討HSP70在內(nèi)毒素血癥大鼠肺組織損傷中的作用以及Gln的干預(yù)效應(yīng)。 方法第一部分實(shí)驗(yàn)選取健康雌性Wistar大鼠,隨機(jī)分為兩組,對照組(C組),內(nèi)毒素血癥組(E組)。E組于尾靜脈注射5mg/kg的內(nèi)毒素脂多糖(LPS),LPS注射后開始計(jì)時,于1h、2h、4h、6h頸動脈放血處死,對照組給予等量的生理鹽水,其余同E組。取左肺組織①光鏡觀察肺組織形態(tài)學(xué)變化②免疫組織化學(xué)方法測定HSP70。取右肺組織用分光光度計(jì)法測肺組織MDA含量及SOD活性。在第一部分實(shí)驗(yàn)的基礎(chǔ)上,第二部分實(shí)驗(yàn)選取健康雌性Wistar大鼠隨機(jī)分為三組:E組,Gln預(yù)處理組(G_1組),Gln后處理組(G_2組)。G_1組,G_2組分別在LPS注射前1h和后1h,給予0.75g/kg的Gln,在LPS注射后6h處死大鼠,取左肺組織①光鏡觀察肺組織形態(tài)學(xué)變化②免疫組織化學(xué)方法測定HSP70,取右肺組織用分光光度計(jì)法測肺組織MDA含量及SOD活性,觀察Gln的干預(yù)效應(yīng)。 結(jié)果同對照組相比,E組1h、2h、4h、6h肺組織HSP70表達(dá)均增多(P0.05或P0.01),E組2h、4h、6h與1h組相比,肺組織HSP70表達(dá)均增多(P0.05或P0.01)且在2h達(dá)到峰值; E組1h、2h、4h、6h肺組織MDA含量在均高于對照組(P0.05);E組各時間點(diǎn)肺組織SOD活性均低于對照組(P0.05),4h、6h與1h組相比肺組織SOD活性明顯降低(P0.01)。與E組相比,G_1,G_2組肺組織HSP70表達(dá)增多(P㩳0.05),SOD活性增高(P㩳0.05),MDA含量明顯降低(P㩳0.05);G_1組與G_2組在肺組織HSP70表達(dá),SOD活性,MDA含量等方面比較差異無統(tǒng)計(jì)學(xué)意義(P㧐0.05)。 結(jié)論氧自由基參與內(nèi)毒素性肺損傷的過程,內(nèi)毒素性肺損傷后的肺組織HSP70表達(dá)增多,可能與其參與LPS所致肺損傷后的組織應(yīng)激保護(hù)有關(guān)。Gln預(yù)處理或后處理都能減輕內(nèi)毒素血癥大鼠肺損傷,作用機(jī)制可能與Gln提高機(jī)體抗氧化能力以及增加HSP70的表達(dá)有關(guān),尚不能認(rèn)為二者在減輕大鼠LPS所致肺損傷有差別。
[Abstract]:Objective to observe the changes of heat shock protein 70 (HSP70), malondialdehyde (MDA) and superoxide dismutase (SOD) in lung tissue of rats with endotoxemia at different time points and the effect of glutamine (GLN) on lung injury in rats with endotoxemia. To investigate the role of HSP70 in lung tissue injury in rats with endotoxemia and the intervention effect of GLN. Methods in the first part of the experiment, the healthy female Wistar rats were randomly divided into two groups: control group (C group), endotoxemia group (E group). The control group was given the same amount of normal saline, and the others were the same as the E group. The morphological changes of left lung tissue were observed by light microscope. 2. Immunohistochemical method was used to detect HSP70. The content of MDA and the activity of SOD in right lung tissue were measured by spectrophotometer. On the basis of the first part of the experiment, In the second part of the experiment, healthy female Wistar rats were randomly divided into three groups: one hour before injection of 0.75g/kg and one hour after injection, then the rats were killed 6 hours after 0.75g/kg injection, and then the rats were divided into three groups: group G _ (1), group G _ (2), group G _ (1) and group G _ (1), respectively, one hour before and one hour after injection of 0.75g/kg, respectively. The morphologic changes of left lung tissue were observed by light microscope. The content of MDA and the activity of SOD in right lung tissue were measured by immunohistochemical method, and the intervention effect of GLN was observed. Results compared with the control group, the expression of HSP70 in the lung tissue of the E group was significantly higher than that of the control group (P0.05 or P0.01), and the expression of HSP70 in the lung tissue of the E group was significantly higher than that of the control group (P0.05 or P0.01). The expression of HSP70 in lung tissue increased (P0.05 or P0.01) and reached the peak at 2h, and the MDA content of lung tissue in group E was significantly higher than that in control group (P0.05) at 1h, 2h, 4h and 6h (P0.05). The SOD activity in group E was significantly lower than that in control group (P0.05) at 4h and 6h (P0.01). Compared with group E, the expression of HSP70 in lung tissue increased (P0. 05) and SOD activity increased (P0. 05). MDA content decreased significantly in group G1 and group 2. There was no significant difference between group 1 and group 2 in the expression of SOD activity and MDA in lung tissue (P0. 05). Conclusion oxygen free radicals are involved in the process of endotoxin induced lung injury, and the expression of HSP70 in lung tissue after endotoxin induced lung injury is increased. It may be related to the involvement of GLN in the tissue stress protection after LPS induced lung injury. GLN pretreatment or post-treatment can reduce the lung injury in rats with endotoxemia, and the mechanism may be related to the increase of GLN's antioxidant ability and the expression of HSP70. It can not be concluded that there is a difference between the two groups in reducing the lung injury induced by LPS in rats.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2008
【分類號】：R363

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