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目的:观察关木通所含马兜铃酸(AA)不同时间致大鼠肾损害及川芎嗪、泼尼松和贝那普利的干预作用。方法:将雄性SD大鼠随机分为六组,每组24只。正常组(C组)予蒸馏水3ml/d灌胃,模型组(M组)、泼尼松组(P组)、贝那普利组(B组)、川芎嗪Ⅰ组(LⅠ组)和川芎嗪Ⅱ组(LⅡ组)均予关木通水煎剂(含生药2g/ml、AA0.54mg/ml、AAⅠ0.46mg/ml)5g/(kg·d)灌胃。2h后C组与M组予NS,其余四组分别予泼尼松5mg、贝那普利1.7mg、川芎嗪各50mg、150mg/(kg·d)灌胃。120天和180天后检测肾功能及血常规,并观察组织病理和超微病理。120天时每组处死7只,180天时处死剩余大鼠。结果:随着时间的延长,大鼠血肌酐与血尿素氮及尿NAG与24h尿蛋白定量逐渐升高,而血红蛋白(Hb)与红细胞比容(HCT)逐渐降低。M组与C组比差异非常显著(P<0.001);其余四组与M组比较差异显著(P<0.05),其中P组和LⅡ组降低或升高尤为明显。C组为正常肾组织表现。M组光镜:120天可见肾小管上皮细胞片状空泡变性、肿胀,以近髓部小管病变较显著,刷状缘消失,大部分肾小管基膜(TBM)裸露和(或)断裂,部分肾间质有轻度灶性炎细胞浸润和部分肾小球可见轻度节段硬化;180天病变加重,小管上皮细胞呈大片状空泡变性,以皮质部小管病变较明显,部分小管萎缩,大部分肾间质有胶原纤维增生。电?
Objective: To observe the effect of aristolochic acid (AA) contained in Guanmutong on renal damage and ligustrazine, prednisone and benazepril in rats. Methods: Male SD rats were randomly divided into six groups of 24 rats. Rats in the normal group (group C) were treated with distilled water (3ml / d), and the model group (M group), prednisone group (P group), benazepril group (B group), ligustrazine group (LⅠgroup) and Chuanxiong The rats in group Ⅱ were given gavage of 5g / (kg · d) of Guanmutong decoction (containing crude drug 2g / ml, AA0.54mg / ml, AAⅠ0.46mg / ml). After 2 hours, the rats in group C and M were treated with NS, and the other four groups were treated with prednisone 5 mg, benazepril 1.7 mg, ligustrazine 50 mg and 150 mg / (kg · d) respectively. The renal function and blood routine were detected after 120 and 180 days, and histopathology and ultrastructural pathology were observed. Seven rats were sacrificed on day 120 and the remaining rats were sacrificed on day 180. Results: Serum creatinine, blood urea nitrogen, urine NAG and 24h urinary protein gradually increased with time, while hemoglobin (Hb) and hematocrit (HCT) gradually decreased. The difference between M group and C group was significant (P <0.001). The other four groups were significantly different from M group (P <0.05), especially in P group and LⅡ group. Group C was normal renal tissue. M group of light microscope: 120 days showed renal tubular epithelial cells lamellar vacuolar degeneration, swelling, proximal tuberculous lesions more significant brush edge disappeared, most of the tubular basement membrane (TBM) bare and (or) rupture, part of Renal interstitial infiltration of mild focal inflammatory cells and some glomerular mild segmental sclerosis; 180 days increased disease, tubular epithelial cells showed large lamellar degeneration, cortical tubule lesions were more obvious, part of the tubular atrophy Most of the interstitial collagen fibrosis. Electricity?