【摘要】：目的：在體內(nèi)與體外研究中,IFN-y抗肝纖維化,肺損傷纖維化已經(jīng)得到證實。本研究通過評估IFN-γ對體外培養(yǎng)的大鼠腎成纖維細胞增殖和MCP-1表達的影響,旨在探討IFN-γ治療腎間質(zhì)纖維化的可能機制。方法：體外培養(yǎng)大鼠腎成纖維細胞NRK-49F,分別設(shè)立對照組和濃度為1000U/ml、2000U/ml、3000U/ml、4000U/ml、5000U/ml的IFN-y藥物干預(yù)組,對照組使用0.9%生理鹽水。采用MTT比色法檢測NRK-49F細胞的增殖情況；RT-PCR和Western-blot方法檢測NRK-49F細胞MCP-1 mRNA和MCP-1蛋白水平。結(jié)果：1.腎成纖維細胞增殖情況：與對照組相比,采用單因素方差分析,不同濃度IFN-γ組測的OD值均高于對照組(p0.05)；IFN-γ促進NRK-49F細胞增殖呈時間依賴性(p0.05)；不同IFN-y濃度間測在490nm波長的OD值差異不具統(tǒng)計學(xué)意義(p0.05)。2. MCP-1 mRNA表達：與對照組相比,IFN-y干預(yù)組的MCP-1 mRNA表達水平均明顯升高(p0.05)：不同濃度IFN-y間的MCP-1mRNA表達水平無顯著性差異(P0.05)。3.MCP-1蛋白表達：與對照組相比,IFN-γ干預(yù)組的MCP-1蛋白表達水平均明顯升高(p0.05)；不同濃度IFN-γ間的MCP-1蛋白水平無顯著性差異(P0.05)。結(jié)論：IFN-γ呈時間依賴性的促進NRK-49F細胞的增殖。在基因水平上,IFN-γ能上調(diào)NRK-49F細胞MCP-1 mRNA表達水平；在蛋白水平上,IFN-γ能促進NRK-49F細胞分泌MCP-1蛋白。IFN-γ可能通過上調(diào)MCP-1參與腎間質(zhì)纖維化過程。
[Abstract]:Objective: in vivo and in vitro studies, IFN-y has been proved to inhibit liver fibrosis and lung injury fibrosis. The aim of this study was to evaluate the effect of IFN- 緯 on proliferation and MCP-1 expression of rat renal fibroblasts in vitro, and to explore the possible mechanism of IFN- 緯 in the treatment of renal interstitial fibrosis. Methods: in vitro cultured rat renal fibroblasts (NRK-49F,) were divided into two groups: the control group and the control group with the concentration of 1000U / ml 2000U / ml and the control group treated with 0.9% normal saline. The proliferation of NRK-49F cells was detected by MTT colorimetry, and the MCP-1 mRNA and MCP-1 protein levels of NRK-49F cells were detected by RT-PCR and Western-blot methods. The result is 1: 1. Proliferation of renal fibroblasts: compared with the control group, the OD values of IFN- 緯 groups with different concentrations were higher than those of the control group (p0.05), and IFN- 緯 promoted the proliferation of NRK-49F cells in a time-dependent manner (p0.05). There was no significant difference in OD value between different IFN-y concentrations at 490nm wavelength (p0.05). 2. MCP-1 mRNA expression: compared with the control group, the MCP-1 mRNA expression level in the IFN-y intervention group was significantly higher than that in the control group (p0.05). There was no significant difference in the MCP-1mRNA expression level between the different concentrations of IFN-y (P0.05). 3.MCP-1 protein expression: compared with the control group, IFN- 緯 intervention group MCP-1 protein expression water The average increased significantly (p0.05). There was no significant difference in MCP-1 protein level between different concentrations of IFN- 緯 (P0.05). Conclusion: IFN- 緯 promotes the proliferation of NRK-49F cells in a time dependent manner. At the gene level, IFN- 緯 can up-regulate the expression of MCP-1 mRNA in NRK-49F cells, and at the protein level, IFN- 緯 can promote the secretion of MCP-1 protein by NRK-49F cells. IFN- 緯 may participate in the process of renal interstitial fibrosis by up-regulating MCP-1.
【學(xué)位授予單位】：昆明理工大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：R692

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