C3aR是補(bǔ)體C3a的受體.在腎臟,已發(fā)現(xiàn)C3aR表達(dá)于包括腎小管上皮細(xì)胞在內(nèi)的多種細(xì)胞.在特定的病理情況下,C3aR表達(dá)上調(diào)并參與多種腎臟疾病的病理過程,但有關(guān)C3aR在腎臟細(xì)胞中的表達(dá)調(diào)控機(jī)制仍不清楚.小管間質(zhì)缺氧是腎臟疾病中的一種常見現(xiàn)象,也是一種重要致病因素.為了探討缺氧對(duì)C3aR的表達(dá)調(diào)控作用,本文利用體外缺氧模型,對(duì)模型條件下C3aR在腎小管上皮細(xì)胞中的表達(dá)變化情況進(jìn)行了分析,同時(shí)檢測了HIF-1α和NF-κB的表達(dá)變化及活化情況,以及HIF-1α和NF-κB抑制劑對(duì)C3aR的表達(dá)影響情況.結(jié)果發(fā)現(xiàn)缺氧可誘導(dǎo)C3aR mRNA及蛋白質(zhì)水平的表達(dá)上調(diào)、HIF-1α和NF-κB的核轉(zhuǎn)移.HIF-1α和NF-κB抑制劑可阻斷缺氧對(duì)C3aR的誘導(dǎo)作用,且HIF-1α抑制劑可抑制NF-κB的核轉(zhuǎn)移.這些結(jié)果說明缺氧可通過HIF-1α/NF-κB通路誘導(dǎo)腎小管上皮細(xì)胞C3aR的表達(dá).考慮到C3aR活化可促進(jìn)腎小管的損傷,我們推測C3aR通路可能參與了缺氧和NF-κB誘導(dǎo)的腎小管損傷過程,可能是防治缺氧和NF-κB誘導(dǎo)腎組織損傷的一個(gè)新靶標(biāo).

【文章頁數(shù)】：8 頁

【文章目錄】：
1 Materials and methods
    1.1 Cell culture and experimental design
    1.2 RT-PCR
    1.3 Immunofluorescence
    1.4 Western blotting
    1.5 Statistical analysis
2 Results
    2.1 Hypoxia induced C3a R expression in HK-2cells
    2.2 Hypoxia induced translocation of HIF-1αand NF-κB into nucleus
    2.3 HIF-1αinhibitor attenuated the upregulation of C3a R and translocation of NF-κB induced by hypoxia
    2.4 The upregulation of C3a R in hypoxia condition was attenuated by NF-κB inhibitor
3 Discussion



本文編號(hào)：3902146