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目的:观察雷公藤甲素对局灶节段硬化性肾小球肾炎(FSGS)大鼠血清及肾组织尿激酶型纤溶酶原激活物受体(u PAR)和β3整合素的影响。方法:取健康清洁级雄性SD大鼠随机分为对照组,FSGS模型组,雷公藤甲素低、中、高剂量组。通过行5/6肾切除术建立FSGS大鼠模型。雷公藤甲素低、中、高剂量组从术后第8天开始定时灌胃治疗,给药10周。检测大鼠第4、8、12周24h尿蛋白水平,肾组织病理,血清及肾组织中的u PAR和β3整合素表达。结果:模型组及各给药组24h尿蛋白定量高于正常组同期(P<0.01),与模型组同期比较,雷公藤甲素中剂量组大鼠24h尿蛋白定量在第12周时明显减少(P<0.01),雷公藤甲素高剂量组大鼠24h尿蛋白定量从第8周开始明显减少(P<0.01)。与雷公藤甲素低剂量组比较,雷公藤甲素高剂量组大鼠24h尿蛋白定量第8周时明显减少(P<0.05)。肾脏病理提示模型组可见不同程度肾小球硬化,系膜细胞及基质中度至重度增生,小管上皮细胞损伤,间质萎缩并可见不同程度纤维化,经雷公藤甲素干预后,肾小球硬化程度明显减轻。u PAR和β3整合素在正常大鼠肾组织及血清中只有少量表达,与正常组比较,在模型组肾组织及血清中表达较强(P<0.01),各治疗组治疗后,表达较模型组明显下降,其中雷公藤素高剂量组差异有统计学意义(P<0.01)。结论:雷公藤甲素能减少尿蛋白,改善肾小球硬化、球囊粘连及系膜基质增生的情况,下调血清及肾组织中的u PAR和β3整合素的表达,延缓肾脏病变程度。
Objective: To observe the effects of Triptolide on uPAR and β3 integrins in serum and kidney of focal segmental glomerulonephritis (FSGS) rats. Methods: Healthy male SD rats were randomly divided into control group, FSGS model group and triptolide low, medium and high dose groups. FSGS rat model was established by line 5/6 nephrectomy. Triptolide low, medium and high dose groups from the eighth day after the start of regular gavage treatment, administration of 10 weeks. The levels of urinary protein, renal histopathology, uPAR and β3 integrin expression in serum and kidney were detected at the 4th, 8th and 12th week. Results: The urinary protein excretion of model group and each administration group was higher than that of the normal group at the same period (P <0.01). Compared with the model group at the same period, the urinary protein excretion of the middle-dose triptolide group was significantly decreased at the 12th week (P <0.01). The urinary protein excretion of high dose triptolide group decreased significantly from the 8th week (P <0.01). Compared with the low-dose triptolide group, the high-dose triptolide group had a significant decrease of 24h urinary protein at the 8th week (P <0.05). Kidney pathology prompted the model group showed varying degrees of glomerulosclerosis, mesangial cells and matrix moderate to severe proliferation, tubular epithelial cell damage, interstitial atrophy and fibrosis can be seen to varying degrees, after triptolide intervention, glomerular Hardening significantly reduced. The expression of PAR and β3 integrin in renal tissue and serum of normal rats was only a small amount, compared with normal group, the expression of PAR and β3 in renal tissue and serum of model group was stronger (P <0.01) Group was significantly decreased, of which the high-dose tripterygium group differences were statistically significant (P <0.01). Conclusion: Triptolide can reduce urinary protein, improve glomerular sclerosis, balloon adhesion and mesangial matrix hyperplasia, down regulate serum and renal tissue u PAR and β3 integrin expression, delay the degree of renal disease.