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Sal B to improve the mechanism of aristolochic acid nephropathy study
PAGE \* MERGEFORMAT 15
Sal B to improve the mechanism of aristolochic acid nephropathy study
Of: Li-Qun, Huang Di, Wang Yun Man, Shen Liping
[Abstract] Objective Sal B on aristolochic acid nephropathy tubulointerstitial disease prevention mechanism. Methods of aristolochic acid (aristolochic acid, AA) stomach caused by aristolochic acid nephropathy model, 36 Rats were randomly divided into 3 groups: model group (n = 12), received daily intragastric AA dose of 5mg / (kg d); treatment group (n = 12), received daily intragastric AA \ [5mg / (kg d) \] immediately after receiving Sal B (salvianolic acid, SalB) ig \ [10mg / (kg d) \]; normal group (n = 12), received the same volume of saline daily gavage. drug treatment for 8 weeks. animals weighed weekly to adjust the dosage weight. The first week collection of 24h urine samples 2,4,6,8, 8 weeks after the removal of renal pathological narcotic detection, the use of RT- PCR method for the determination of renal tissue matrix metalloproteinase 9 (MMP-9), kidney tissue plasminogen activator inhibitor -1 (PAI-1), ITG-1, monocyte chemotactic factor -1 (MCP-1) , tissue inhibitor of matrix metalloproteinase -1 (TIMP-1) mRNA expression. Results of model group than in normal group was significantly widened interstitial, interstitial cells increased collagen increased significantly. Compared with model group, treatment group, PAI- 1, TIMP-1, ITG-1 mRNA expression decreased, MMP-9 mRNA increased. Conclusion isolated from Danshen SalB of chronic aristolochic acid nephropathy tubulointerstitial injury has strong anti-fibrosis.
[Keywords:] aristolochic acid nephropathy; Sal B; anti-fibrosis; rat
ABSTRACT: ObjectiveTo study the mechanism of salvianolic acid B in preventing and treating renal tubulointerstitial injury caused by aristolochic acid. MethodsRat model of aristolochic acid nephropathy was induced by intragastric administration of aristolochic acid. Thirty-six rats were randomly divided into model group, t
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