| Accelerated anti-GBM antibody nephritis in rats was established, observing the protective effects of TMP and investigate its action mechanism from the aspects of serum antibody, complement and anti-oxidation damage. TMP was administered 120mg/kg/d by ip the day before the model established and the administration was consecutive for 15 days. Content of urine protein in 24 hours was detected on the 1st, 3rd, 5th, 7th, 10th, 14th day after model established and rats were killed on the 7th day or the 14th day. Contents of blood urine nitrogen (BUN) and serum creatinine (SCr) were detected. And the changes of IgG IgM IgA,C3 in serum were determined, too. Renal cortex cytoplasm and mitochondria were produced and its MDA content, anti-oxidase activities of GSH-Px, Cat, SOD were detected. Changes in membrane fluidity of renal cortex mitochondria in accelerated anti-GBM antibody nephritis of rats were measured by l,6-diphenyl-l,3,5-hexatriene(DPH). Activity of ATPase was detected by determining phosphorum. Rat kidneys were soaked in 10% formaldehyde solution and then embedded in paraffin. The tissue sections were stained with hematoxylin and eosin and lesions of glomerulus and tubules were observed under light mirror.The data displayed that TMP group was found to have significant reduction in changes of urine protein content compared with model group. And BUN, SCr decreased significantly (p<0.01)after 14 days. The concentration of IgG increased significantly on 7th, 14th day and C3 increased on 14th day significantly (p<0.01) . Both IgG and IgM increased with administration time going on, while the concentration of IgM decreased, it was more obvious in 14th day. The concentration of IgA changed little before and after administration. In TMP group GSH-Px activity raised gradually with time in both cytoplasm and mitochondria. At 7th and 14th day, the activities in cytoplasm were significantly increased by 1.72-fold (p<0.05), 1.98-fold (p<0.01), in mitochondria is 1.19-fold, 1.22-fold (p<0.05)versus model group. The activity of Cat was increased with time, at 7th and 14th day, its activity is 1.18-fold, 1.39-fold (p<0.05) , and in mitochondria is 1.44-fold, 1.68-fold respectively versus model group. On 7th and 14th day, the activity of SOD is 1.52-fold, 1.39-fold (p<0.05) versus model group. However, The content of MDA in cytoplasm is significantly decreased with time by 13% (p<0.05) ,31% (p<0.05) respectively at 7th and 14th day. It was the same to mitochondria, and its content is decreased by 12%, 31% (p<0.05) . The data displayed that TMP can increase membrane fluidity and the activity of Na+ K+-ATPase, Mg2+-ATPase, Ca2+-ATPase.Pathology determination found that there were light proliferation on model group rats glomerulus parietal layer and protein bleeding ,deposition in glomerular capsule and glomerulus was compressed , which structure was not clear on the 7th day. On the 14th day, there were significant proliferation in glomerulus parietal layer, some of which formed annular or demi-annular crescent, and a few of glomerulus were seized by crescent. There were light proliferation in glomerulus parietal layer cells and glomerulus compressed lightly without marked protein bleeding in glomerulus capsules in TMP group rats on the 7th day. On the 14th day glomerulus lesion fundamentally recovered normal and there were not significant proliferation in parietal layer cells with clear glomerulus structure free of marked damages.The results suggested that the protective effects of TMP on accelerated anti-GBM antibody nephritis in rats may produce by anti-oxidation ability reinforcement of body and lesion reduction of lipid peroxidation products on body.
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