本文選題：高壓氧 + 腎臟��； 參考：《遵義醫(yī)學(xué)院》2017年碩士論文

【摘要】：目的:通過(guò)建立同系(C57BL/6J)小鼠腎缺血再灌注損傷(ischemia reperfusion injury,IRI)模型觀察血管內(nèi)皮生長(zhǎng)因子(vascular endothelial growth factor,VEGF)、B淋巴細(xì)胞瘤-2(B-cell lymphoma-2,BCL-2)、核轉(zhuǎn)錄因子(nuclear factor kappa B,NF-κB)、低氧誘導(dǎo)因子(hypoxia inducible factor-lalpha,HIF-1α)和結(jié)締組織生長(zhǎng)因子(connective tissue growth factor,CTGF)在缺血再灌注腎組織中的表達(dá)變化以及高壓氧(hyperbaric oxygenation,HBO)治療對(duì)這些因子表達(dá)的影響,進(jìn)一步研究缺血再灌注后腎組織的病理生理改變以及HBO對(duì)缺血再灌注腎損傷的治療作用和機(jī)制。方法:將C57BL/6J小鼠隨機(jī)分為正常對(duì)照組、假手術(shù)組、腎缺血組、HBO+腎缺血組、腎IR組、腎IR㧏HBO治療組,然后再分別將IR組及IR㧏HBO治療組分為1h、3h、6h、12h、24h組,每小組6只小鼠。正常對(duì)照組及切開(kāi)小鼠腹腔立即處死小鼠取雙腎,假手術(shù)組僅切開(kāi)腹腔后便將腹腔關(guān)閉;腎缺血組:切開(kāi)腹腔,雙側(cè)腎蒂阻斷45min后,立即處死小鼠,采血并切取腎臟標(biāo)本;缺血+HBO組:在進(jìn)行腎缺血組相同處理前對(duì)小鼠進(jìn)行1h高壓氧治療;腎IR組:切開(kāi)腹腔,雙側(cè)腎蒂阻斷45min后開(kāi)放血流,分別于再灌注后1、3、6、12、24h切取雙腎并采取靜脈血;IR㧏HBO治療組:切開(kāi)腹腔,雙側(cè)腎蒂阻斷45min后開(kāi)放血流,分別于再灌注后0、2、5、11、23h時(shí)行HBO治療,治療1h后切取雙腎并采取靜脈血,雙側(cè)腎蒂不阻斷,于相應(yīng)時(shí)點(diǎn)切取雙腎并采取靜脈血。采用HE染色觀察腎組織的病理改變,免疫組織化學(xué)法檢測(cè)VEGF、BCL-2、NF-κB和HIF-1α在腎組織中的表達(dá),實(shí)時(shí)熒光定量PCR(real-time PCR)檢測(cè)VEGF、CTGF的表達(dá)以及全自動(dòng)生化分析儀檢測(cè)血清肌酐(SCr)。結(jié)果:1.腎功能變化:結(jié)果顯示,假手術(shù)組與正常對(duì)照組血肌酐無(wú)明顯差異,腎缺血組和HBO+腎缺血組的血肌酐值明顯高于假手術(shù)組(P0.05),在HBO治療后,腎缺血引起的腎功能損害有改善但不明顯。再灌注后腎功能損害加重,且隨著再灌注時(shí)間的延長(zhǎng)逐漸加重,在再灌注24h時(shí)損傷最重。HBO治療則明顯改善了再灌注后的腎功能,以1h、3h、6h和12h時(shí)突出,24小時(shí)后高壓氧治療對(duì)腎功能的保護(hù)作用減弱。2.腎組織病理變化:正常對(duì)照組和假手術(shù)組可見(jiàn)腎小管細(xì)胞無(wú)明顯病理改變,缺血組及缺血+HBO組可見(jiàn)腎小管細(xì)胞明顯腫脹,HBO治療后腎小管細(xì)胞腫脹程度較前有輕微好轉(zhuǎn),IR組于1h時(shí),可見(jiàn)系膜細(xì)胞輕度增生,腎間質(zhì)血管輕度擴(kuò)張充血,腎小球體積輕度增大,腎小管上皮細(xì)胞輕度腫脹;于3h時(shí),可見(jiàn)腎小管上皮細(xì)胞腫脹進(jìn)一步加重,呈顆粒樣變性,組織血管充血;于6h時(shí),可見(jiàn)腎腎小管細(xì)胞已經(jīng)逐漸失去細(xì)胞原有形態(tài),腎小管上皮細(xì)胞腫脹進(jìn)一步加重,伴少量中性粒細(xì)胞浸潤(rùn),12h及24h可見(jiàn)大量的小管細(xì)胞破壞,腎小管細(xì)胞出現(xiàn)了相互融合,細(xì)胞結(jié)構(gòu)被完全破壞,并出現(xiàn)少量核碎裂核溶解,并出現(xiàn)大量的的中性粒細(xì)胞浸潤(rùn)。經(jīng)過(guò)高壓氧治療后各時(shí)間點(diǎn)均可見(jiàn)腎小管細(xì)胞腫脹明顯減輕,細(xì)胞破壞明顯減少,核溶解現(xiàn)象也有所減少。3.免疫組織化學(xué)法檢測(cè)VEGF、BCL-2、NF-κB和HIF-1α在腎組織中的表達(dá):(1)腎組織VEGF蛋白的表達(dá)變化:VEGF蛋白主要表達(dá)于腎小管上皮細(xì)胞胞質(zhì),細(xì)胞核少量表達(dá),高壓氧治療后胞核及胞質(zhì)表達(dá)均增加。相對(duì)定量結(jié)果顯示,腎缺血組、HBO+腎缺血組、腎IR組及腎IR+HBO組VEGF蛋白的表達(dá)均顯著高于正常對(duì)照組和假手術(shù)組(P0.05),而在腎缺血前運(yùn)用高壓氧治療可見(jiàn)VEGF表達(dá)增加(P0.05)。腎IR后,VEGF的表達(dá)較假手術(shù)組呈持續(xù)性上升并在6h達(dá)到峰值(P0.05),12h后開(kāi)始表現(xiàn)出下降趨勢(shì)但仍高于假手術(shù)組(P0.05);經(jīng)高壓氧治療后,腎IR+HBO組VEGF對(duì)應(yīng)各時(shí)間點(diǎn)的表達(dá)相較于腎IR組有明顯的增加并且在6h增加最為明顯(P0.05)。(2)腎組織HIF-1α蛋白的表達(dá)變化:HIF-1α蛋白主要表達(dá)于腎小管細(xì)胞的胞質(zhì),細(xì)胞核有少量表達(dá)。相對(duì)定量結(jié)果顯示,腎缺血組、HBO+腎缺血組、腎IR組及腎IR+HBO組HIF-1α蛋白的表達(dá)均顯著高于正常對(duì)照組和假手術(shù)組(P0.05),而在腎缺血前運(yùn)用高壓氧治療可見(jiàn)HIF-1α表達(dá)增加,但并無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)。腎缺血再灌注損傷發(fā)生后,HIF-1α的表達(dá)呈持續(xù)性上升并在6h達(dá)到峰值(P0.05),12h后開(kāi)始表現(xiàn)出下降趨勢(shì)但仍高于假手術(shù)組(P0.05);經(jīng)高壓氧治療后,HIF-1α的表達(dá)各時(shí)間點(diǎn)相比較于腎IR組有明顯的增加并且在6h增加最為明顯(P0.05)。(3)腎組織Bcl-2蛋白的表達(dá)變化:Bcl-2蛋白主要表達(dá)于腎小管上皮細(xì)胞胞質(zhì),細(xì)胞核少量表達(dá)。相對(duì)定量結(jié)果顯示,腎缺血組、HBO+腎缺血組、腎IR組及腎IR+HBO組Bcl-2蛋白的表達(dá)均顯著高于正常對(duì)照組和假手術(shù)組(P0.05),而在腎缺血前運(yùn)用高壓氧治療可見(jiàn)Bcl-2表達(dá)增加,但并無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)。腎缺血再灌注損傷發(fā)生后,Bcl-2的表達(dá)呈持續(xù)性上升并在3-6h達(dá)到峰值(P0.05),12h后開(kāi)始表現(xiàn)出下降趨勢(shì)但仍高于假手術(shù)組(P0.05);經(jīng)高壓氧治療后,Bcl-2蛋白各時(shí)間點(diǎn)的表達(dá)相比較于腎IR組均有明顯的增加并且在3-6h增加最為明顯(P0.05)。(4)腎組織NF-κB蛋白的表達(dá)變化:NF-κB蛋白主要表達(dá)于腎小管上皮細(xì)胞胞質(zhì),細(xì)胞核少量表達(dá)。相對(duì)定量結(jié)果顯示,腎缺血組、HBO+腎缺血組、腎IR組及腎IR+HBO組NF-κB蛋白的表達(dá)均顯著高于正常對(duì)照組和假手術(shù)組(P0.05),而在腎缺血后運(yùn)用高壓氧治療預(yù)處理可見(jiàn)NF-κB表達(dá)無(wú)顯著差異(P0.05)。腎缺血再灌注損傷發(fā)生后,NF-κB的表達(dá)呈持續(xù)性上升并在6h達(dá)到峰值,12h后開(kāi)始表現(xiàn)出下降趨勢(shì)但仍高于假手術(shù)組(P0.05);經(jīng)高壓氧治療后,NF-κB各時(shí)間點(diǎn)的表達(dá)相比較于腎IR組有明顯的減少并且在6h減少最為明顯(P0.05)。4.實(shí)時(shí)熒光定量PCR(real-time PCR)檢測(cè)腎組織VEGF m RNA、CTGF m RNA的表達(dá)變化:(1)腎組織VEGF m RNA的表達(dá)變化:腎缺血組、HBO+腎缺血組,腎IR組及腎IR+HBO組VEGF m RNA的表達(dá)量較正常對(duì)照組和假手術(shù)組均增加(P0.05),經(jīng)高壓氧治療后HBO+腎缺血組VEGF m RNA的表達(dá)高于腎缺血組(P0.05)。腎IR時(shí)VEGF m RNA的表達(dá)隨著時(shí)間的延長(zhǎng)逐漸增加并在6h達(dá)到峰值(P0.05),12h后表達(dá)開(kāi)始逐漸下降。當(dāng)經(jīng)過(guò)高壓氧治療后我們可以發(fā)現(xiàn)腎IR+HBO治療組各時(shí)間點(diǎn)VEGF m RNA的表達(dá)相比較于腎IR組在1h、3h、6h、12h均有明顯增加(P0.05),24h無(wú)明顯差異(P0.05)。(2)腎組織CTGF m RNA的表達(dá)變化:腎缺血組、HBO+腎缺血組、腎IR組及腎IR+HBO組CTGF m RNA的表達(dá)均顯著高于正常對(duì)照組和假手術(shù)組(P0.05),而在腎缺血后運(yùn)用高壓氧治療預(yù)處理可見(jiàn)CTGF m RNA表達(dá)無(wú)顯著差異(P0.05)。腎缺血再灌注損傷發(fā)生后,CTGF m RNA的表達(dá)呈持續(xù)性上調(diào)(P0.05);經(jīng)高壓氧治療后,6h后各時(shí)間點(diǎn)相比較于腎IR組CTGF m RNA的表達(dá)有明顯的減少(P0.05)。結(jié)論:1.HBO治療可以通過(guò)HIF-VEGF-Notch通路顯著改善缺血再灌注腎組織的缺氧狀態(tài),促進(jìn)新生血管的生成,從而減輕腎缺血再灌注損傷。2.HBO治療可以減少CTGF表達(dá),通過(guò)減少致纖維化因子的表達(dá)在對(duì)于腎缺血再灌注損傷中減輕腎臟損傷,對(duì)腎臟起到保護(hù)作用。3.HBO治療可以通過(guò)增加Bcl-2的表達(dá)并減少NF-κB的表達(dá),對(duì)細(xì)胞凋亡上游因子的調(diào)控,從而對(duì)腎臟在缺血再灌注損傷中起到了保護(hù)作用。4.HBO治療在腎缺血再灌注早期便開(kāi)始發(fā)揮保護(hù)作用,對(duì)于新生血管的生成、纖維化因子的抑制以及對(duì)于凋亡因子的抑制都有著明顯的作用,隨著時(shí)間的推移有所減弱,因此在腎缺血再灌注損傷的預(yù)防及治療過(guò)程中應(yīng)盡早采用高壓氧治療,以減輕缺血再灌注對(duì)腎臟的損害。
[Abstract]:Objective: To observe the vascular endothelial growth factor (vascular endothelial growth factor, VEGF) and B lymphocytic tumor (ischemia reperfusion injury (IRI) model in C57BL/6J mice. The expression of ible factor-lalpha, HIF-1 alpha) and connective tissue growth factor (connective tissue growth factor, CTGF) in the renal tissue of ischemia and reperfusion and the effect of hyperbaric oxygen (hyperbaric oxygenation, HBO) on the expression of these factors, further study the pathophysiological changes of renal tissue and HBO against ischemia after blood reperfusion. Treatment and mechanism of reperfusion renal injury. Methods: C57BL/6J mice were randomly divided into normal control group, sham operation group, renal ischemia group, HBO+ kidney ischemia group, kidney IR group, kidney IR HBO treatment group, then IR group and IR HBO treatment group were divided into 1H, 3h, 6h, 12h, 6 mice in each group. The dead mice took two kidneys, and the sham operation group closed the abdominal cavity after only incision of the abdominal cavity. In the renal ischemia group, after the incision of the abdominal cavity and the bilateral renal pedicle blocking 45min, the mice were killed and the kidney specimens were harvested. The ischemic +HBO group was treated with 1H high pressure oxygen therapy before the same treatment in the kidney ischemia group; the kidney IR group: after the incision of the abdominal cavity and the bilateral renal pedicle blocking 45min The blood flow was opened and 1,3,6,12,24h was cut into two kidneys and venous blood was taken after reperfusion respectively. IR? HBO treatment group: incision of abdominal cavity, bilateral renal pedicle after blocking 45min to open blood flow, respectively after reperfusion after 0,2,5,11,23h, HBO treatment. After treatment 1H, two kidneys were cut and venous blood was taken. The two sides of kidney did not block, and the two kidneys were cut at the corresponding time points and taken static and static. Pulse blood. The pathological changes of renal tissue were observed by HE staining. Immunohistochemistry was used to detect the expression of VEGF, BCL-2, NF- kappa B and HIF-1 alpha in the renal tissue. Real-time fluorescent quantitative PCR (real-time PCR) was used to detect VEGF, CTGF expression and automatic biochemical analyzer to detect serum creatinine (SCr). Results: 1. renal function changes: the results showed sham operation group and sham operation group. There was no significant difference in serum creatinine in the normal control group. The blood creatinine value of renal ischemia group and HBO+ renal ischemia group was significantly higher than that of the sham operation group (P0.05). After HBO treatment, renal impairment caused by renal ischemia was improved but not obvious. The damage of renal function was aggravated after reperfusion, and with the prolongation of reperfusion time, the damage was the heaviest at 24h reperfusion. .HBO treatment significantly improved renal function after reperfusion, prominent in 1H, 3h, 6h and 12h. After 24 hours, the protective effect of hyperbaric oxygen therapy on renal function weakened the pathological changes of.2. renal tissue: there was no obvious pathological changes in renal tubule cells in normal control group and sham operation group, and obvious swelling of renal tubule cells in ischemic group and ischemic +HBO group, HBO After treatment, the swelling degree of renal tubular cells was slightly better than that before the treatment. When group IR was 1H, the mesangial cells were slightly proliferated, the renal interstitial vessels were slightly dilated and congested, the volume of glomeruli was slightly enlarged, and the renal tubular epithelial cells were slightly swelling. At 3h, the swelling of the tubular epithelial cells was further aggravated, with granular degeneration and hyperemia of the tissue vessels; at 6 At h, the renal tubular cells had gradually lost the original morphology of the cells. The swelling of the renal tubular epithelial cells was further aggravated, with a small amount of neutrophils infiltration. A large number of tubules were destroyed in 12h and 24h. The renal tubular cells were fused with each other, the cell structure was completely destroyed, and a small amount of nuclear disintegration was dissolved, and a large number of them appeared. Neutrophils infiltration. After hyperbaric oxygen therapy, the swelling of renal tubule cells was obviously reduced, cell destruction was significantly reduced, and nuclear dissolution also decreased the expression of VEGF, BCL-2, NF- kappa B and HIF-1 alpha in renal tissue by.3. immunohistochemistry: (1) the expression of VEGF protein in renal tissue: VEGF protein main The expression of the cytoplasm of renal tubular epithelial cells, a small amount of nuclear expression, increased nuclear and cytoplasmic expression after hyperbaric oxygen therapy. The relative quantitative results showed that the expression of VEGF protein in renal ischemia group, HBO+ renal ischemia group, kidney IR group and renal IR+HBO group was significantly higher than that of normal control group and artificial hand group (P0.05), and hyperbaric oxygen therapy was used before renal ischemia. The expression of VEGF increased (P0.05). After IR, the expression of VEGF was higher than that in the sham operation group and reached the peak value at 6h (P0.05). After 12h, the expression of VEGF began to decline but was still higher than that of the sham operation group (P0.05). After hyperbaric oxygen therapy, the expression of VEGF in the renal IR+HBO group was significantly higher than that in the IR group and increased in the 6h. The expression of HIF-1 alpha protein in renal tissue was significantly (P0.05) (2): the expression of HIF-1 alpha protein was mainly expressed in the cytoplasm of renal tubular cells and a small amount of expression in the nucleus. The relative quantitative results showed that the expression of HIF-1 alpha protein in renal ischemia group, HBO+ renal ischemia group, kidney IR group and kidney IR+HBO group were significantly higher than that of normal control group and sham operation group (P0.05), but in kidney, the renal tissue was significantly higher than that of the normal control group and the sham operation group (P0.05). The expression of HIF-1 alpha was increased in hyperbaric oxygen therapy before ischemia, but there was no statistical significance (P0.05). After renal ischemia-reperfusion injury, the expression of HIF-1 alpha increased continuously and reached a peak in 6h (P0.05). After 12h, it began to show a downward trend but still higher than that of the sham operation group (P0.05). After hyperbaric oxygen therapy, the expression of HIF-1 a was at all time points. Compared with the renal IR group, there was a significant increase in the 6h (P0.05). (3) the expression of Bcl-2 protein in the renal tissue: the expression of Bcl-2 protein was mainly expressed in the cytoplasm of renal tubular epithelial cells and a small number of nuclei. The relative quantitative results showed that the expression of Bcl-2 protein in the renal ischemia group, the HBO+ kidney deficiency group, the renal IR group and the renal IR+HBO group were all significant. It was higher than the normal control group and the sham operation group (P0.05), but the expression of Bcl-2 increased with hyperbaric oxygen therapy before renal ischemia, but there was no statistical significance (P0.05). After renal ischemia-reperfusion injury, the expression of Bcl-2 increased continuously and reached the peak value at 3-6h (P0.05). After 12h, the decline trend began to decline but still higher than that of the sham operation group (P0.05). After hyperbaric oxygen therapy, the expression of Bcl-2 protein at all time points was significantly increased compared with that in group IR and increased in 3-6h (P0.05). (4) the expression of NF- kappa B protein in renal tissue: the expression of NF- kappa B protein was mainly expressed in the cytoplasm of renal tubular epithelial cells and a small amount of nuclear expression. The relative quantitative results showed that the renal ischemia group, HBO+ kidney was a relative quantitative result. In the ischemic group, the expression of NF- kappa B protein in the renal IR group and the kidney IR+HBO group was significantly higher than that in the normal control group and the sham operation group (P0.05), but there was no significant difference in the expression of NF- kappa B (P0.05) in the preconditioning with hyperbaric oxygen therapy after renal ischemia. The expression of NF- kappa B increased continuously and reached the peak in 6h after renal ischemia-reperfusion injury. The downward trend was still higher than the sham operation group (P0.05). After the hyperbaric oxygen therapy, the expression of NF- kappa B at each time point was significantly decreased compared to the renal IR group and the most obvious (P0.05).4. real-time quantitative PCR (real-time PCR) was most obvious in 6h (real-time PCR), and the expression changes of renal tissue were observed. (1) the expression of renal tissue was changed. The expression of VEGF m RNA in renal ischemia group, HBO+ renal ischemia group, kidney IR group and renal IR+HBO group increased (P0.05). The expression of VEGF m RNA in HBO+ renal ischemia group was higher than that in renal ischemia group after hyperbaric oxygen therapy. After 12h, the expression of VEGF m RNA in the renal IR+HBO treatment group was significantly increased in 1H, 3h, 6h and 12h in the renal IR+HBO treatment group (P0.05). (2) the renal ischemia group, renal ischemia group, renal ischemia group and renal failure group were in the renal ischemia group. The expression of CTGF m RNA in group O was significantly higher than that in the normal control group and the sham operation group (P0.05), but there was no significant difference in the expression of CTGF m RNA (P0.05). After renal ischemia and reperfusion, the expression of CTGF m RNA was continuously up-regulated after renal ischemia-reperfusion injury, and the time points were compared after hyperbaric oxygen therapy. The expression of CTGF m RNA in group IR was significantly decreased (P0.05). Conclusion: 1.HBO therapy can improve the hypoxia state of renal tissue of ischemia and reperfusion through HIF-VEGF-Notch pathway and promote the formation of new blood vessels, thus reducing the expression of CTGF in renal ischemia reperfusion injury by.2.HBO therapy, and reducing the expression of fibrotic factors by reducing the expression of fibrotic factors in the renal ischemia reperfusion injury. Renal ischemia reperfusion injury alleviates renal injury, and the protective effect of.3.HBO on kidney can be protected by increasing the expression of Bcl-2 and reducing the expression of NF- kappa B, regulating the upstream factors of apoptosis, and thus protecting the kidney from ischemia-reperfusion injury,.4.HBO treatment begins to play in the early stage of renal ischemia and reperfusion. The protective effect has obvious effect on the formation of new blood vessels, the inhibition of fibrotic factors and the inhibition of apoptosis factors, which weaken with time. Therefore, hyperbaric oxygen therapy should be adopted as early as possible in the prevention and treatment of renal ischemia-reperfusion injury, in order to reduce the damage to renal ischemia and reperfusion.
【學(xué)位授予單位】：遵義醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R692.5

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