老年肝郁失眠证候大鼠模型的建立和评价

目的:建立并评价复合型老年肝郁失眠证候大鼠模型。方法:Wistar大鼠随机分为环境对照组,单因素模型组(睡眠剥夺组),复合型模型组,复合型模型+舒郁安神方35 g.kg-1.d-1治疗组。采用D-半乳糖腹腔注射60 mg.kg-1.d-1大鼠6周致亚急性衰老模型,然后采用夹尾刺激法致肝郁,每次刺激30 min,1日2次,持续1周,最后放入自制睡眠剥夺箱中进行快速眼动睡眠(REMS)剥夺48 h,制作老年肝郁失眠证候大鼠复合型模型。观测大鼠体征、脑部自由基水平及血浆6-酮-前列腺素F1a(6-keto-PGF1a)、血栓素B2(TXB2)含量。结果:与环境对照组、单因素模型组、舒郁安神方组比较,老年肝郁失眠证候复合型模型组大鼠丙二醛(MDA)、TXB2含量均显著升高(P<0.01),而超氧化物歧化酶(SOD)活性、6-keto-PGF1a含量及6-keto-PGF1a/TXB2均显著降低(P<0.01)。结论:老年肝郁失眠证候大鼠模型具有临床证候病理特征,是可行、可靠的复合型动物模型。

Establishment and Evaluation of the Old Rat Model with Ganqi Stagnation Syndromes of Insomnia

Objective: To establish and evaluate the old rat model with Ganqi stagnation syndromes of insomnia. Method: Wistar rats were randomly divided into 4 groups:control, single-factor model, the multi-factor model, the multi-factor model+Shuyu Anshen Fang treatment. The old rat model with Ganqi stagnation Syndromes of insomnia was induced by intraperitoneal injection of D-galactose 60 mg· kg^-1·d^-1 for six weeks, and then clamping tail stimulus for one week was used toestablish Ganqi stagnation model, and REM sleep deprivation for 48 hours was caried out by using modified multiple platform method (MMPM). Then features of physical sign, free radicals in brain, and the contents of 6-keto-prostaglandin F1a(6-keto-PGF1a),thromboxane B₂(TXB₂) in blood plasma were analyzed. Result: Compared with all the other groups (control group, treatment group and single-factor model group), the multi-factor model group with Ganqi stagnation showed the higher levels of malondialdehyde(MDA) and TXB₂(P<0.01), and the lower levels of superoxide dismutase (SOD), 6-keto-PGF1a and the ratio of 6-keto-PGF1a/TXB₂ (P<0.01). Conclusion: The composite animal model showed pathological features of clinical Ganqi stagnation syndromes. It is a feasible and reliable composite animal model.