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目的 探讨雷公藤红素对狼疮性肾炎肾小球硬化的防治作用。方法 在不同发病时间、用不同剂量的雷公藤红素对BWF1小鼠进行连续 2 0周腹腔注射。运用考马斯亮蓝法检测 2 4h尿蛋白量 ;ELISA法检测血清抗dsDNA抗体水平 ;免疫组化法检测肾小球中纤维连接蛋白 (FN)、Ⅳ型胶原和基质金属蛋白酶 (MMP) 1、 2、 3与基质金属蛋白酶组织抑制剂 (TIMP) 1、 2的表达 ;逆转录 巢式PCR法检测小鼠肾组织中TGF β1的表达。结果 (1)雷公藤红素能抑制小鼠蛋白尿产生 ,降低其血清抗dsDNA抗体水平 ,增加肾小球中MMP 1、 2而减少FN、Ⅳ型胶原和TIMP 1、 2与TGF β1的表达 ,改善小鼠组织学病变。 (2 )雷公藤红素于蛋白尿发生前较发生后使用疗效更为显著。 (3)于蛋白尿发生前使用雷公藤红素 3mg·kg-1·w-1和 6mg·kg-1·w-1的疗效差异无显著性。 (4)用药后各组间MMP 3的表达差异亦无显著性。结论 雷公藤红素对狼疮模型鼠的肾小球硬化具有明确保护作用 ;其降低肾脏FN、Ⅳ型胶原的沉积可能是通过增加肾组织局部MMP 1、 2而抑制TGF β1及TIMP 1、 2的表达而实现的。雷公藤红素对MMP 3的作用可能不及对MMP 1、 2的疗效明显。
Objective To investigate the effect of Tripterine on glomerulosclerosis in patients with lupus nephritis. Methods BWF1 mice were injected intraperitoneally with 20 doses of tripterine for 20 consecutive weeks at different times of onset. Serum anti-dsDNA antibody levels were measured by Coomassie brilliant blue staining. Serum anti-dsDNA antibody levels were detected by ELISA. FN, MMP-1 and MMP-2 expressions in glomeruli were detected by immunohistochemistry , 3 and tissue inhibitor of metalloproteinase (TIMP) 1, 2; reverse transcription nested PCR was used to detect the expression of TGFβ1 in mouse kidney tissue. Results (1) Tripterine inhibited the proteinuria in mice, decreased the level of anti-dsDNA antibody in serum, increased the expression of FN, type IV collagen, TIMP-1 and TIMP-1 in glomeruli , Improve mouse histological lesions. (2) Tripterine in the occurrence of proteinuria than before the use of more significant effect. (3) There was no significant difference in the efficacy of triptolide between 3mg · kg-1 · w-1 and 6mg · kg-1 · w-1 before proteinuria. (4) There was no significant difference in the expression of MMP-3 between the two groups after treatment. Conclusion Tripterine has a clear protective effect on glomerulosclerosis in lupus model rats. It may reduce the deposition of FN and type IV collagen in the kidney by inhibiting the local MMP 1 and 2 of the renal tissue and inhibiting the expression of TGF-β1 and TIMP-1 and 2 Express and achieve. The effect of tripterine on MMP-3 may not be as pronounced as that of MMP-1 and 2.