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目的:由于“饮食不节、过食膏粱厚味”与高尿酸血症密切相关,采用含高胆固醇的脂肪乳剂的因素诱导,观察对大鼠血清尿酸的影响,并与高嘌呤饲料造模比较,以期得到更加稳定、持续的动物模型,为中药药效评价奠定基础。方法:SD雄性大鼠分为正常对照组、高嘌呤饲料(HPD)组、脂肪乳剂(LE)组。HPD组给予高嘌呤饲料喂养,正常饮水;LE组灌胃给予脂肪乳剂10 m L·kg-1体重,正常水食,连续6周。观察大鼠行为学、摄食量和体重;每隔2周,检测血清UA,Cr,BUN,ALT,AST,HDL-c,LDL-c,TG,TC;造模4周,测血清XOD和ADA含量,收集24 h尿液测大鼠尿UA,Cr含量,计算尿酸清除率/肌酐清除率(Cua/Ccr);停止造模后第2,4周测血清UA。结果:造模2周,LE组大鼠摄食量减少、体重降低,血清UA,CR,BUN,ALT,AST,HDL-c,LDL-c,TC均升高,TG水平显著降低;造模4周,HPD组血清UA无明显变化,血清XOD含量显著升高,ADA含量无明显变化;LE组大鼠血清UA仍明显升高,血清XOD,ADA含量显著升高,Cua/Ccr显著降低;造模6周,HPD组血清UA明显升高;LE组血清UA仍显著升高;停止造模后第2周,HPD组血清UA恢复正常;LE组大鼠血清UA水平仍明显升高,第4周血清UA无统计学差异。结论:与高嘌呤饲料喂养比较,脂肪乳剂致大鼠高尿酸血症成型早、持续久、模型更稳定,与“饮食不节,过食膏粱厚味”所致代谢性疾病的发病特点更吻合,用于研究中药抗高尿酸血症的药效学有较大价值。其机制可能与其升高体内XOD,ADA酶活性,促进尿酸生成有关,同时,抑制尿酸排泄有关。
Objective: As the “diet section, overeating cream Atsumi” and hyperuricemia are closely related to the use of high cholesterol-containing fat emulsion induced factor observed in rats serum uric acid, and high-purine feed made Compared with the model, with a view to get a more stable and continuous animal model for the evaluation of Chinese medicine to lay the foundation. Methods: SD male rats were divided into normal control group, high purine feed (HPD) group and lipid emulsion (LE) group. HPD group was given high purine diet, normal drinking water; LE group was given intragastric fat emulsion 10 m L · kg-1 body weight, normal water food for 6 weeks. Serum UA, Cr, BUN, ALT, AST, HDL-c, LDL-c, TG and TC were measured every 2 weeks. The urinary UA and Cr contents in urine were collected from 24 h urine test to calculate the uric acid clearance rate and creatinine clearance rate (Cua / Ccr). Serum UA was measured at the 2nd and 4th week after the model was stopped. Results: After 2 weeks of modeling, food intake and body weight decreased, serum UA, CR, BUN, ALT, AST, HDL-c, LDL-c and TC in LE group were increased and TG level decreased significantly. Serum UA levels in HPD group were significantly higher than those in HPD group (P <0.01), serum XOD content was significantly increased, while ADA content did not change significantly. Serum UA was still significantly increased in serum of the LE group, while serum XOD and ADA levels were significantly increased and Cua / Ccr was significantly decreased Serum UA in HPD group was significantly increased at 6 weeks, while serum UA in LE group was still significantly increased. Serum UA in HPD group returned to normal at the second week after the model was established. UA serum no significant difference between weeks. CONCLUSION: Compared with high-purine feed, the hyperuricemia induced by lipid emulsion in rats is earlier and longer lasting, and the model is more stable. Compared with the high-purine feed, the incidence of metabolic disorders caused by “diet, overeating” More consistent, for the study of Chinese medicine anti-hyperuricemia pharmacodynamics have greater value. The mechanism may be related to its increase in vivo XOD, ADA enzyme activity, promote uric acid production, while inhibiting uric acid excretion.