CAJ | 학술논문

背景:慢性肾衰竭进展过程中的一个重要病理改变是炎症和纤维化,主要包括肾小球和肾小管的炎症和纤维化.目前大多数研究主要集中于肾小球,对于肾小管病变的研究相对较少.但实际上部分疾病的肾小管病变出现在肾小球病变之前,其对于疾病预后更具有指导意义.目的:观察转化生长因子β1对人类肾小管上皮细胞 HK-2增殖的影响,探索转化生长因子β1在肾小管炎症和纤维化方面的作用.方法:将传代培养的 HK-2细胞分成空白对照组和转化生长因子β1作用组,分别使用 DMEM/F12培养液,以及含转化生长因子β1(2,5,10μg/L)的 DMEM/F12培养液培养,在倒置显微镜下观察各组细胞形态的改变,并使用 MTT 法检测细胞增殖情况.结果与结论:转化生长因子β1能显著抑制人肾小管上皮细胞的增殖,并促使细胞向纤维样改变,与空白对照组相比差异有显著性意义(P <0.05),其抑制增殖作用并不随转化生长因子β1质量浓度的增大而显著增强,作用时间可持续至72 h.结果可见转化生长因子β1能够抑制人肾小管上皮细胞的增殖,并具有促进肾间质纤维化的作用.
배경:만성신쇠갈진전과정중적일개중요병리개변시염증화섬유화,주요포괄신소구화신소관적염증화섬유화.목전대다수연구주요집중우신소구,대우신소관병변적연구상대교소.단실제상부분질병적신소관병변출현재신소구병변지전,기대우질병예후경구유지도의의.목적:관찰전화생장인자β1대인류신소관상피세포 HK-2증식적영향,탐색전화생장인자β1재신소관염증화섬유화방면적작용.방법:장전대배양적 HK-2세포분성공백대조조화전화생장인자β1작용조,분별사용 DMEM/F12배양액,이급함전화생장인자β1(2,5,10μg/L)적 DMEM/F12배양액배양,재도치현미경하관찰각조세포형태적개변,병사용 MTT 법검측세포증식정황.결과여결론:전화생장인자β1능현저억제인신소관상피세포적증식,병촉사세포향섬유양개변,여공백대조조상비차이유현저성의의(P <0.05),기억제증식작용병불수전화생장인자β1질량농도적증대이현저증강,작용시간가지속지72 h.결과가견전화생장인자β1능구억제인신소관상피세포적증식,병구유촉진신간질섬유화적작용.
BACKGROUND: An important pathological change in the progression of chronic renal failure means inflammation and fibrosis, including glomerular and tubular inflammation and fibrosis. At present, most of the research has focused on the glomerulus rather than renal tubular lesions. But actual y, for a part of diseases, renal tubular lesions appear before glomerular lesions, which is of more guiding significance for the prognosis of diseases.OBJECTIVE: To observe the effect of transforming growth factor beta 1 on the cel proliferation of HK-cells and to explore the role of transforming growth factor beta 1 in renal tubular inflammation and fibrosis. METHODS: HK-2 cells were cultured in Dulbecco’s modified Eagle’s medium/F12 or Dulbecco’s modified Eagle’s medium/F12 containing different concentrations of transforming growth factor beta 1. HK-2 cells were divided into four groups, control group, 2 μg/L transforming growth factor beta 1 group, 5 μg/L transforming growth factor beta 1 group and 10 μg/L transforming growth factor beta 1 group. Morphological changes were assessed by inverted phase contrastmicroscopy and cel ular proliferation was detected by MTT assay. RESULTS AND CONCLUSION: The morphology of HK-2 cells changed from epithelial cobblestone to myofibroblast-like elongated and spindly and gap among cells also widened. The proliferation of HK-2 cells was inhibited significantly by transforming growth factor beta 1, but not in a dose-dependent manner. The inhibitory effect on the cel ular proliferation lasted for 72 hours. These findings indicate that transforming growth factor beta 1 inhibits the cel ular proliferation of HK-2 cells and promotes the occurrence of renal interstitial fibrosis.