本文選題：蛋白激酶Cβ + 炎癥趨化因子��； 參考：《遵義醫(yī)學(xué)院》2014年碩士論文

【摘要】：目的：通過建立小鼠腎移植模型，研究PKCβ受到抑制時(shí)移植腎內(nèi)細(xì)胞間質(zhì)趨化因子及外周血效應(yīng)細(xì)胞相應(yīng)指標(biāo)變化，來探討炎癥反應(yīng)可能的影響機(jī)制。 方法：建立小鼠異質(zhì)移植（allograft）和同質(zhì)移植（isograft）的腎移植模型，將其分為異質(zhì)移植對照組、異質(zhì)移植PKCβ抑制劑治療組和同質(zhì)移植對照組。PKCβ抑制劑治療組術(shù)前1天予PKCβ抑制劑灌胃，其余兩組均予等量生理鹽水灌胃，三組小鼠均于術(shù)后一天取移植腎后處死。用免疫組織化學(xué)法檢測白細(xì)胞介素4（Interleukin4，IL-4）、白細(xì)胞介素8（Interleukin8，IL-8）、單核細(xì)胞趨化蛋白1（Monocyte chemotacticprotein-1， MCP-1）、巨噬細(xì)胞移動抑制因子（Macrophage migration inhibitoryfactor,MIF）、白細(xì)胞趨化因子（Leukocyte chemotactic factor，，LCF）、白細(xì)胞移動抑制因子（Leukocyte migration inhibitory factor，LIF）這些趨化因子的表達(dá)；用逆轉(zhuǎn)錄聚合酶鏈反應(yīng)（RT－PCR）來檢測LCF、低氧誘導(dǎo)因子1（Hypoxia inducible factor1，HIF-1）、MCP-1、IL-8、LIF、MIF、氧合血紅蛋白1（Oxygenated hemoglobin1，HO-1）的表達(dá)情況。 結(jié)果： 1.免疫組化提示：異質(zhì)移植對照組IL-4、IL-8、MCP-1、MIF、LCF高表達(dá)，異質(zhì)移植PKCβ抑制劑預(yù)治療組和同質(zhì)移植腎對照組表達(dá)明顯減少；異質(zhì)移植PKCβ抑制劑預(yù)治療組表達(dá)較異質(zhì)移植對照組明顯降低（P0.01），異質(zhì)移植對照組表達(dá)較同質(zhì)移植組表達(dá)明顯增高（P0.01）。異質(zhì)移植PKCβ抑制劑預(yù)治療組與同質(zhì)對照組LIF高表達(dá)，異質(zhì)移植對照組表達(dá)明顯減少；異質(zhì)移植PKCβ抑制劑預(yù)治療組表達(dá)較異質(zhì)移植對照組明顯增高（P0.01），異質(zhì)移植對照組表達(dá)較同質(zhì)移植組表達(dá)明顯降低（P0.01）。 2.RT－PCR結(jié)果提示：異質(zhì)移植對照組IL-8、、MCP-1、LCF高表達(dá)，異質(zhì)移植PKCβ抑制劑預(yù)治療組和同質(zhì)移植腎對照組表達(dá)明顯減少；異質(zhì)移植PKCβ抑制劑預(yù)治療組表達(dá)較異質(zhì)移植對照組明顯降低（P0.05），異質(zhì)移植對照組表達(dá)較同質(zhì)移植組表達(dá)明顯增高（P0.05）。異質(zhì)移植PKCβ抑制劑預(yù)治療組與同質(zhì)對照組HIF、MIF、LIF高表達(dá)，異質(zhì)移植對照組表達(dá)明顯減少；異質(zhì)移植PKCβ抑制劑預(yù)治療組表達(dá)較異質(zhì)移植對照組明顯增高（P0.05），異質(zhì)移植對照組表達(dá)較同質(zhì)移植組表達(dá)明顯降低（P0.05）。同質(zhì)對照組HO-1高表達(dá)，異質(zhì)移植PKCβ抑制劑預(yù)治療組表達(dá)明顯減少；異質(zhì)移植PKCβ抑制劑預(yù)治療組表達(dá)較異質(zhì)移植對照組明顯增高（P0.05），異質(zhì)移植對照組表達(dá)較同質(zhì)移植組表達(dá)明顯降低（P0.05）。 結(jié)論：PKCβ受到抑制時(shí)，炎癥抑制因子表達(dá)升高，移植腎內(nèi)腎間質(zhì)炎癥趨化因子的表達(dá)降低，PKC beta抑制劑對移植術(shù)后是通過減少炎癥趨化因子的表達(dá)來抑制細(xì)胞浸潤或增加炎癥抑制因子的表達(dá)來減輕炎癥反應(yīng)，從而對移植腎起到保護(hù)與修復(fù)的作用。
[Abstract]:Aim: to study the changes of cytoplasmic chemokines and peripheral blood effector cells in renal allograft when PKC 尾 is inhibited, and to explore the possible mechanism of inflammatory response. Methods: the models of allograft and isograft in mice were established and divided into three groups: the control group, the PKC 尾 inhibitor treatment group and the homogenous transplantation control group. The PKC 尾 inhibitor was administered intragastric 1 day before the operation in the PKC 尾 inhibitor treatment group, and the PKC 尾 inhibitor therapy group was given intragastric administration one day before the operation. The other two groups were given the same amount of normal saline intragastric perfusion, and all the three groups were killed on the first day after operation. Immunohistochemical method was used to detect interleukin 4 (IL 4), interleukin 8 (IL 8), monocyte chemoattractant protein-1 (MCP 1), macrophage migration inhibitory factor (MIF), leukocyte chemoattractant factor (LCFF), leukocyte chemotactic factor (LCF), monocyte chemoattractant protein 1 (Monocyte chemoattractant protein-1), macrophage migration inhibitory factor (MIF), leukocyte chemoattractant factor (LCFF) and monocyte chemoattractant protein 1 (Monocyte chemoattractant protein-1). The expression of some chemokines; Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the expression of LCFCs, hypoxia inducible factor-1 (HIF-1), MCP-1, IL-8, and oxygenated hemoglobulin 1 (HO-1). Results: 1. Immunohistochemistry showed that the expression of IL-4, IL-8, MCP-1, MIFF-LCF in the heterogeneous transplantation group was significantly lower than that in the PKC 尾 inhibitor pretreated group and the homogenous allograft control group. The expression of PKC 尾 inhibitor in the heterogeneous transplantation group was significantly lower than that in the heterogeneous transplantation group, and the expression of P0.01 in the heterogeneous transplantation group was significantly higher than that in the homogenous transplantation group. The expression of LIF in the PKC 尾 inhibitor pretreated group and the homogenous control group was higher than that in the heterogeneous transplantation control group. The expression of PKC 尾 inhibitor in heterogeneous transplantation group was significantly higher than that in heterogeneous transplantation control group, and the expression of P0.01in heterogeneous transplantation group was significantly lower than that in homogenous transplantation group. 2. RT-PCR results showed that IL-8 / MCP-1 / LCF expression was significantly higher in heterogeneous transplantation control group than that in heterogenous transplantation group. The expression of PKC 尾 inhibitor in heterogeneous transplantation group was significantly lower than that in heterogeneous transplantation group, and that in heterogeneous transplantation group was significantly higher than that in homogenous transplantation group. The high expression of HIF-MIFFIF was observed in the PKC 尾 inhibitor pretreated group and the homogenous control group, while the expression in the heterogeneous transplantation control group was significantly decreased. The expression of PKC 尾 inhibitor in heterogeneous transplantation group was significantly higher than that in heterogeneous transplantation group, and the expression of P0.05 in heterogeneous transplantation group was significantly lower than that in homogenous transplantation group. The high expression of HO-1 in the homogenous control group and the decrease in the expression of PKC 尾 inhibitor in the heterogeneous transplantation group; The expression of PKC 尾 inhibitor in heterogeneous transplantation group was significantly higher than that in heterogeneous transplantation group, and the expression of P0.05 in heterogeneous transplantation group was significantly lower than that in homogenous transplantation group. Conclusion the expression of inflammatory inhibitory factor increased when the PKC 尾 was inhibited. The expression of inflammatory chemokines in renal interstitial cells decreased after transplantation, the expression of inflammatory chemokines was reduced by reducing the expression of inflammatory chemokines or increasing the expression of inflammatory inhibitors. Thus, the graft plays a protective and repair role.
【學(xué)位授予單位】：遵義醫(yī)學(xué)院
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R699.2

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