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作 者:苏长海[1] 傅继华[1] 单英[1] 孔树佳[1] 王渊[1]
出 处:《中国药科大学学报》2006年第1期67-71,共5页Journal of China Pharmaceutical University
摘 要:目的:通过多因素致病刺激方法,建立一种具有代谢综合征(MS)特征的动物模型,为这类疾病发病机理及治疗药物研究提供适合的动物模型。方法:选用Wistar雄性大鼠,高脂高糖喂养同时结合应激刺激(足底电击+噪声刺激)建立MS模型。动物随机分为4组:普通全价鼠饲料喂养组(A组)、单纯高脂高糖饲料喂养组(B组)、普通饲料喂养+应激组(C组)和高脂高糖喂养+应激组(D组)。C、D组每天上、下午应激刺激1次,每次2 h,连续刺激55 d。试验期间每周记录动物体重及食耗量,每周测量血压1次,45 d后检测血脂、血糖,继续刺激10 d后进行糖耐量试验。结果:在连续6周的训练过程中,D组血压明显升高,与C组血压升高相当;进食量明显增加;至第5、6周D组体重增长有所下降,而训练期间C组体重增长明显减慢。训练6周后D组血糖升高,而B、C组血糖均未见明显升高;D组血脂指标:TC、LDL、VLDL、TC/HDL、(LDL+VLDL)/HDL均显著升高,且升高幅度明显大于B组,HDL明显下降,但TG升高幅度不及B组。至连续刺激55 d后,D组糖耐量异常最严重。结论:应激伴高热量膳食喂养的大鼠可引起脂质异常、高血压、轻微高血糖及明显糖耐量异常,具备MS特征的动物模型。这种模型不是单因素致病模型的简单相加,而具有多因素的协同作用特点。Aim:To develop an animal model that could show typical characteristics of Metabolic Syndrome (MS) by multifactorial effects and be expected for application in the study of the mechanisms and therapeutic drug of MS. Methods: The model was established by stress in male Wistar rats combined with high-sugar-fat-diet. The stresses included foot-shock with addition of noise stimulation. The animals were randomly divided into four groups: group A (normal diet), group B (high-glucose-fat-diet), group C (normal diet + stress), group D (high-glucose-fat-diet + stress). In 55 days, group C and D received two times of daily stress, which lasted 2 hours each time, in the morning and afternoon, going on for 55 days. Blood pressure was examined, and body weight as well as food intake were measured every week. Plasma lipoprotein and plasma glucose were assayed after 45 days of stress, and glucose tolerance test (GRIT) was evaluated after 55 days. Results: During the 6-week stress, the food intake and blood pressure of both groups C and D were elevated significantly, but there was no statistical difference between the two groups. The extent of increase in the body weight was found to be small after the 4-week stress on group D. Compared with group A, hyperglycemia took place in group D rather than groups B and C. The levels of TC, LDL, VLDL, TC/ I-IDL, (LDL + VLDL)/HDL were found to be markedly increased in group D, and higher than those occurred to groups B and C. Furthermore, a statistically significant reduction in HDL in the group D was observed in comparison to the group A. However, the extent of increase in TG in the group D is less than the group B. GrIT abnonnity in the group D was the most obvious among these groups. Conclusion:The model of combining high-glucose-fat-diet with stress could cause significant dyslipidemia, hypertension, light hyperglyeemia and GTr abnonnity. The stress combination might exert the synergistic effects on the developed model, rather than the additiv
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