| A kidney is an important organs of the body, the main physiological function is to excrete metabolic waste and regulate water, electrolyte and the balance of acid-base to maintain the environmental steady-state in the body. The balance of body fluid and the maintenance of steady-state depends on the function of different channel proteins distributed in the renal tubules. The level and activity of sodium channel plays an important role in reabsorption of sodium. Based on previous animal experiments, the pattern of sodium channels distribution suggests that vesicle chloride channel (vesicular Chloride Channel, vClC) can regulate sodium channel trafficking, and this is helpful to the diagnosis and treatment of renal disease.Chronic renal failure refers to the process of gradually decreased renal function. The number of nephron decreased gradually, and formed the end-stage renal failure syndrome. According to the extent of decreased renal function, chronic renal failure can be divided into compensatory stage, decompensated stage and uremia. The mechanism of progressive deterioration of chronic renal failure has not yet been fully clarified. In chronic renal failure, the decreased reabsorption of water and sodium can cause polyuria, imbalance metabolism of water and electrolyte metabolism. The sodium channel protein distributed in different segments .The NKCC2 and ENaC express in the ascending loop of helen and the distal convoluted tube, the alteration of their expression may paticipate in the pathogenesis of chronic renal failure. In rats with chronic renal failure, the decreased expression of NKCC2 and ENaC results in polyuria and decreased serum sodium, vClC may regulate the trafficking of sodium channel in this process. Objective:with rat model of chronic renal failure, this study focus on the expression of ClC-3, 5 in renal tissues of rats with chronic renal failure, and try to prove that vClC can regulate the trafficking of NKCC2 and ENaC. Then discuss the mechnisms of both vClC and V-ATPase regulating trafficking of NKCC2 and ENaC.Methods:With successfully estabolished models of rat with chronic renal failure and the expression of epithelial sodium channel in renal tubule. HE, immunohistochemical staining was performed, and the expression and distribution of ClC-3 and ClC-5 was also detected, the mRNA and protein level of ClC-3 and ClC-5 was also analyzed with RT-PCR and Western blotting methods.Results:The results of morphological study shows that renal tissue was severely damaged in adenine treated rat, it was showed that disrupted tubular structue and interstitial fibrosis. the mRNA expression of ClC-3, ClC-5 in renal tissues of experimental rats increased. And this was similar with the expression of ENaC. The western blotting results showed decreased ClC-5 expression in renal tissues of experimental rats, and this may be affected with post-transcriptional regulation and protein loss of tubule injury. The expression of ClC-5 was paralleled with ENaC. The results of immunohistochemical staining is similar with that of western blotting, the expression of ClC-3, ClC-5 was located mainly in cytoplasm of renal tubulal epithial cells.Conclusion:The rat model with chronic renal failure is still in the compensation stage. vClC (ClC-3, ClC-5) can regulate the trafficking of sodium channel, ClC-5 facilitates the shift of ENaC,NKCC2 into cell, and ClC-3 may help the membrane location or degradation of ENaC,NKCC2. During chronic renal failure, vClC (ClC-3, ClC-5) participates in the formation of polyuria and the decreased serum sodium, and this prove further that both of them can regulate the expression and trafficking of sodium channel.
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