Hsieh C L, Chen M F, Li T C, Li S C, Tang N Y, Hsieh C T, Pon C Z, Lin J G
School of Chinese Medicine, China Medical College, Taichung, Taiwan.
Am J Chin Med. 1999;27(2):257-64. doi: 10.1142/S0192415X9900029X.
This study investigated the anticonvulsant effect of Uncaria rhynchophylla (UR) and the physiological mechanisms of its action in rats. A total of 70 male Sprague-Dawley (SD) rats were selected for study. Thirty four of these rats were divided into 5 groups as follows: 1) CONTROL GROUP (n = 6): received intraperitoneal injection (i.p.) of kainic acid (KA, 12 mg/kg); 2) UR1000 group (n = 10), 3) UR500 group (n = 6) 4) UR250 group, received UR 1000, 500, 250 mg/kg i.p. 30 min prior to KA administration, respectively; 5) Contrast group: received carbamazepine 20 mg/kg i.p. 30 min prior to KA administration. Behavior and EEG were monitored from 15 min prior to drug administration to 3 hours after KA administration. The number of wet dog shakes were counted at 10 min intervals throughout the experimental course. The remaining 36 rats were used to measure the lipid peroxide level in the cerebral cortex one hour after KA administration. These rats were divided into 6 groups of 6 rats as follows: 1) Normal group: no treatment was given; 2) CONTROL GROUP: received KA (12 mg/kg) i.p.; 3) UR1000 group, 4) UR500 group, 5) UR250 group, received UR 1000, 500, 250 mg/kg i.p. 30 min prior to KA administration, respectively; 6) Contrast group: received carbamazepine 20 mg/kg i.p. 30 min prior to KA administration. Our results indicated that both UR 1000 and 500 mg/kg decreased the incidence of KA-induced wet dog shakes, no similar effect was observed in the UR 250 mg/kg and carbamazepine 20 mg/kg group. Treatment with UR 1000 mg/kg, 500 mg/kg, or 250 mg/kg and carbamazepine 20 mg/kg decreased KA-induced lipid peroxide level in the cerebral cortex and was dose-dependent. These findings suggest that the anticonvulsant effect of UR possibly results from its suppressive effect on lipid peroxidation in the brain.
本研究调查了钩藤（UR）在大鼠中的抗惊厥作用及其作用的生理机制。共选取70只雄性Sprague-Dawley（SD）大鼠进行研究。其中34只大鼠分为5组，如下：1）对照组（n = 6）：腹腔注射（i.p.）海藻酸（KA，12 mg/kg）；2）UR1000组（n = 10），3）UR500组（n = 6），4）UR250组，分别在给予KA前30分钟腹腔注射1000、500、250 mg/kg的UR；5）对照组：在给予KA前30分钟腹腔注射20 mg/kg卡马西平。从给药前15分钟至给予KA后3小时监测行为和脑电图。在整个实验过程中，每隔10分钟计数湿狗样抖动的次数。其余36只大鼠用于在给予KA后1小时测量大脑皮质中的脂质过氧化物水平。这些大鼠分为6组，每组6只，如下：1）正常组：未进行处理；2）对照组：腹腔注射KA（12 mg/kg）；3）UR1000组，4）UR500组，5）UR250组，分别在给予KA前30分钟腹腔注射1000、500、250 mg/kg的UR；6）对照组：在给予KA前30分钟腹腔注射20 mg/kg卡马西平。我们的结果表明，1000和500 mg/kg的UR均降低了KA诱导的湿狗样抖动的发生率，而在250 mg/kg的UR组和20 mg/kg的卡马西平组中未观察到类似效果。1000 mg/kg、500 mg/kg或250 mg/kg的UR以及20 mg/kg的卡马西平处理均降低了KA诱导的大脑皮质脂质过氧化物水平，且呈剂量依赖性。这些发现表明，UR的抗惊厥作用可能源于其对大脑脂质过氧化的抑制作用。
