The Effect Of Different Concentrations Of Uric Acid On The Expression Of Intercellular Adhesion Molecule-1 In The Human Renal Tubular Epithelial Cells

OBJECTIVE:Hyperuricemia is an independent risk factor for chronic non-obstructive kidney disease. Hyperuricemia can lead to proteinuria, glomerular tissue hypertrophy, glomerular sclerosis and renal interstitial fibrosis and ultimately leads to chronic renal failure. Uric acid can cause chronic non-obstructive kidney disease by activating the renin-angiotensin system (RAS), oxidative stress response and producting inflammatory mediators and so one. Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule of the immunoglobulin superfamily,which plays a major role in the maintenance of normal tissue structure and function, inflammation and immune response and other physiological and pathological processes. So, Is ICAM-1 involved in the process that uric acid can cause chronic non-obstructive kidney disease? Now it is not clear. This is worth our considering.Our experiment:To stimulate human renal tubular epithelial cells with different concentrations of uric acid to detect the dynamic expression of sICAM-1 and NF-κB, which is used to investigate the dynamic expression of ICAM-1 and its signaling pathways.It can provide theory evidence for the pathogenesis that Uric acid causes chronic non-obstructive kidney disease. METHOD:Normal human kidney epithelial cell line (HK-2)was cultured in 1640 medium which contain 10% fetal calf serum.It was divided into four group:(1) Detecting the dynamic expression of sICAM-1:HK-2 were divided to blank group, uric acid 2mg/dl,7mg/dl,12mg/dl,17mg/dl and 22mg/dl induced group. Each group set the three-hole complex. On the time of 12h,24h and 48h, ELISA was used to assess the expression of sICAM-1 (2) Detecting the dynamic expression of NF-κB:HK-2 were divided to blank group, uric acid 2mg/dl,7mg/dl,12mg/dl,17mg/dl and 22mg/dl induced group. Each group set the three-hole complex. On the time of 12h,24h and 48h, Immunohistochemistry was used to assess the expression of NF-κB.RESULT:(1) Comparing with the blank control group, on the time of 12h,24h and 48h, the expression of sICAM-1 was unchanged in Uric acid 2mg/dl,7mg/dl and 12mg/dl induced group (P>0.05), while the expression of sICAM-1 was significantly increased in a time-and dose-dependent manner in Uric acid 17mg/dl and 22mg/dl induced group (P<0.05). (2) Comparing with the blank control group, on the time of 12h, 24h and 48h,the expression of NF-κB was unchanged in Uric acid 2mg/dl,7mg/dl and 12mg/dl induced group (P>0.05), while the expression of NF-κB was significantly increased in a time-and dose-dependent manner in Uric acid 17mg/dl and 22mg/dl induced group (P<0.05). (3) The expression of sICAM-1 and NF-κB was positively correlated(P<0.05). Conclusion:(1) Uric acid can cause the increase of the expression of Intercellular Adhesion Molecule-1 in the human renal tubular epithelial cells.(2) Uric acid may cause the increase of the expression of Intercellular Adhesion Molecule-1 in the human renal tubular epithelial cells by means of NF-κB.