Shang Ya-Zhen, Miao Hong, Cheng Jian-Jun, Qi Jie-Min
Institute of Traditional Chinese Medicine, Chengde Medical College, China.
Biol Pharm Bull. 2006 Apr;29(4):805-10. doi: 10.1248/bpb.29.805.
Previous studies reported that the total flavonoids from the stems and leaves of Scutellaria baicalensis Georgi (TFSS) could enhance and improve learning and memory abilities in experimental animals, and reduce the neuronal pathologic alterations induced by some reagents in mice. The present study examined whether TFSS can improve memory dysfunction, neuronal damage, and abnormal free radicals induced by permanent cerebral ischemia in rats. The permanent cerebral ischemic model in rats was produced by bilateral ligation of the common carotid arteries. The influence of permanent cerebral ischemia on learning and memory was determined in the Morris water maze. The neuronal damage in the hippocampus and cerebral cortex was assessed by the neuronal morphologic observations. The contents of malondialdehyde (MDA) and nitric oxide (NO), and the activities of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus and cerebral cortex were measured using thiobarbituric acid, nitrate reductase, xanthine-xanthine oxidase, and ammonium molybdate spectrophotometric methods, respectively. In learning and memory performance tests, cerebral ischemic rats always required a longer latency time to find the hidden platform and spent a shorter time in the target quadrant in the Morris water maze. TFSS 17.5-70 mg.kg(-1) daily orally administered to ischemic rats for 20 d, from day 16-35 after operation differently reduced the prolonged latency and increased swimming time spent in the target quadrant. In neuronal morphologic observations, daily oral TFSS 17.5-70 mg.kg(-1) for 21 d, from day 16-36 after operation markedly inhibited the ischemia-induced neuronal damage. In addition, the increased contents of MDA and NO, and SOD activity, and the decreased activity of CAT in the hippocampus and cerebral cortex induced by cerebral ischemia were differently reversed. The reference drug piracetam (140 mg.kg(-1) per day for 20-21 d) similarly improved impaired memory and neuronal damage but had no significant effects on free radicals in ligated rats. TFSS can improve memory deficits and neuronal damage in rats after permanent cerebral ischemia, which may be beneficial in the treatment of cerebrovascular dementia.
先前的研究报道,黄芩茎叶总黄酮(TFSS)可增强和改善实验动物的学习记忆能力,并减少小鼠中某些试剂诱导的神经元病理改变。本研究检测了TFSS是否能改善大鼠永久性脑缺血诱导的记忆功能障碍、神经元损伤和异常自由基。通过双侧结扎颈总动脉制备大鼠永久性脑缺血模型。在Morris水迷宫中测定永久性脑缺血对学习记忆的影响。通过神经元形态学观察评估海马和大脑皮层中的神经元损伤。分别使用硫代巴比妥酸、硝酸还原酶、黄嘌呤 - 黄嘌呤氧化酶和钼酸铵分光光度法测量海马和大脑皮层中丙二醛(MDA)和一氧化氮(NO)的含量,以及超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性。在学习和记忆性能测试中,脑缺血大鼠在Morris水迷宫中找到隐藏平台总是需要更长的潜伏期,并且在目标象限花费的时间更短。从术后第16天至35天,每天给缺血大鼠口服17.5 - 70 mg·kg⁻¹的TFSS,持续20天,不同程度地缩短了延长的潜伏期,并增加了在目标象限的游泳时间。在神经元形态学观察中,从术后第16天至36天,每天口服17.5 - 70 mg·kg⁻¹的TFSS,持续21天,显著抑制了缺血诱导的神经元损伤。此外,脑缺血诱导的海马和大脑皮层中MDA和NO含量增加、SOD活性增加以及CAT活性降低均不同程度地得到逆转。参比药物吡拉西坦(每天140 mg·kg⁻¹,持续20 - 21天)同样改善了受损的记忆和神经元损伤,但对结扎大鼠的自由基没有显著影响。TFSS可以改善大鼠永久性脑缺血后的记忆缺陷和神经元损伤,这可能对治疗脑血管性痴呆有益。