| [Background] Nephrotic syndrome is one of the primary renal disease of children, and glucocorticoid (GC) is the first therapeutic choice of nephrotic syndrome. However, there are still some children with nephrotic syndrome have bad response to GC, or infrequent relapse, resulting in renal progressive damage. Parts of the children come into end stage renal disease at last. Nowadays, lots of studies suggest that reactive oxygen free radical (OFR) might play an important role in renal progressive damage, it's exist might result in renal injury. And the renal intrinsic cells especially messangial cells injury would result in messangial cells excreating lots of inflammatory factor. Because there existing lots of inflammatory factor continually, it would result in releasing of reactive OFR. existing lots of reactive OFR in vivo,which would result in glomerular damage, renal intrinsic cells proliferation and extracellular matrix formation. Catechin had been proved that it could eliminate reactive OFR in vivo effectively. However the effect of catechin on treating nephrotic syndrome and the detail mechanisms still remain unclearly elucidated.[Obiective] In order to elicit the mechanism of catechin on treating nephritic syndrome(NS), and provide theoretical basis and scientific measure for clinic threapeutic NS, the effect of catechin on treatment NS and how catechin to impress the renal intrinsic cells proliferation through regulting and controlling the expression of the regulted protein of cell cycle have been studied.[Method] 36 female SD rats were randomly divided into six groups: control group,nephrotic group, dexamethasone-treated group, catechin-prevented group, catechin-treated group, dexamethasone+catechin-treated. group. In the first day of experiment, adriamycin (5mg/Kg) was intravenously administered to all rats except control group, and catechin-prevented group rats received catechin(500mg/Kg.d) bygastric pcrfusion on the moment. In the end of two weeks, catechin-treated group and dexamethasone+catechin-treated group rats received catechin (500mg/Kg.d) by gastric perfusion; dexamethasone-treated group, catechin-prevented group, catechin-treated group and dexamethasone+catechin-treated group received dexamethasone (1.8mg/Kg.d) by injection. Alb (Albumin, Alb), TP(Total protein, TP), TG (Trilyceride, TG), BUN (Blood Urea Nitrogen, BUN), ?OH (Hydroxyl group free radical), MDA (Malonydialdehyde, MDA), endogenous anti-oxidease including tSOD (Total Superoxide Dismutase, tSOD) and GSH-PX (Glutathione peroxidase, GSH-PX) in serum and 24hrs urinary protein were detected by biochemical techniques, a semiquantitative score was used to evaluate the degree of glomerular and tubulointerstitium lesions. The expression ofCyclinDK PCNA, P16^ P2K P27, TGF-TGF- 3 K TGF-3 1-mRNA in renal tissue were measured by general immunohistochemical method, the expression of CyclinD 1 ^ P21, TGF- 3 1-mRNA in renal tissue were measured by in situ hybridization method.[Results] 1. The excretion of 24hr urinary protein of catechin-prevented group and catechin-treated group rats were lower than that of nephrotic group and dexamethasone-treated group rats in the end of second week (p<0.01,0.05 respectively). The excretion of 24hr urinary protein of dexamethasone-treated group and dexamethasone+catechin-treated group rats were lower than that of nephrotic group rats in the end of experiment (p<0.01).2. In the end of experiment, -OH in serum of catechin-prevented group and catechin-treated group rats were lower than that of nephrotic group rats (p<0.01,0.05 respectively), ?OH and MDA in serum of dexamethasone+catechin-treated group rats were lower than that of dexamethasone-treated group rats (p<0.01), MDA in serum of catechin-prevented group and catechin-treated group rats were lower than that of nephrotic group rats (p<0.01), and ?OH in serum was positively correlated well with MDA in serum (p<0.01).3. In the end of experiment, tSOD and GSH-PX in serum of catechin-prevented group and catechin-treate...
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