Objective: To establish the quality standard for Shenqinaoqing Granule(Radix Astragali, Radix Ginseng, Radix Angelicae Sinensis, Radix Polygoni Multiflori, etc.) Methods: Astragaloside I of Shenqinaoqing Granule was determined by TLC-scanning, Rhizome Astragali, Radix Ginseng, Radix Polygoni Multiflori, Radix Paeoniae alba were identified by TLC. Results: TLC spot developed were fairly clear, and the blank test showed no interference. Astragaloside I showed a good linear relationship in the concentration range of 0.50～5.05?g and the average recovery was up to 97.10%, RSD was 1.34%. Conclusion: The methods can be effecive for the quality control of the Shenqinaoqin Capsule.

BACKGROUND: It is indicated in the study of recent years that gingko biloba extract (EGB) is a kind of natural cleaner of free radical and it protects the body from the damage induced by free radical and improves cerebral circulatory disturbance and neuronal function. But the experimental or clinical study on the effects of EGB on high neural functional activity, like cognition, is relatively lagged.OBJECTIVE: To probe into the function of EGB on high functional activity in central neural system so as to provide the experimental evidence on clinical application of EGB in treatment of cognitive disturbance.DESIGN: Randomized controlled experiment was designed.SETTING: Department of Geriatrics of Psychiatric Hospital affiliated to Tongji Medical College of Huazhong University of Science and Technology,Department of Pathophysiology in Tongji Medical College of Huazhong University of Science and Technology and Department of Neurology in Union Hospital affiliated to Jinan Medical College of Huazhong University of Science and Technology.MATERIALS: The experiment was performed in Basic Department of Tongji Medical College of Huazhong University of Science and Technology in June 2002. Forty Wistar rats were employed and randomized into 5groups, named as normal control of aged rats (normal group), model group,EGB 75 mg/kg group, EGB 150 mg/kg group and EGB 500 mg/kg group, 8 rats in each one.METHODS: Scopolamine was used to induce disturbance of learning and memory in aged rats to simulate the model of senile dementia animals. In normal and model groups, physiological saline of same volume was used for gastric perfusion and in every EGB group, EGB of 75, 150 and 500 mg/kg was used for gastric perfusion successively, 50-400 g/time, continuously for 5 days. On the 6th day, water maze and evading-dark-room tests were performed. During the testing, the medical perfusion stopped. The assay methods of behavioral training of learning and memory, such as experiment with water maze and evading-dark-room test, and biochemical assay were used to observe the changes in learning and memory and in acetylcholine (Ach) and protein contents in cerebral hippocampus before and after medication.MAIN OUTCOME MEASURES: ① Time required in maze test of rats in each group. ② Mistakes in maze test of rats in each group. ③ Time required and mistakes in evading-dark-room test of rats in each group. ④Contents of Ach and protein in cerebral hippocampus of rats in each group.RFSULTS: Except that 1 rat was died without definite reason in EGB 150 mg/kg group and 1 rat was escaped in either EGB 75 mg/kg or 500 mg/kg group during gastric perfusion, terminally, 37 rats entered result analysis.① The time required and mistakes in maze test in every EGB group were less remarkably than model group (P＜0.05 or P＜0.01). The time required and mistakes in maze test in model group were higher remarkably than normal group (P＜0.01). ② In learning of passive escaping in evading-darkroom test, the duration of learning for the rats in EGB 500, 150, 75 mg/kg groups was shorter remarkably than that in model group [(156.78±25.97),(172.66±13.56), (198.54±17.12), (208.34±28.56) s, P ＜ 0.05 or P＜0.01].The mistakes of electric shock in EGB 500, 150, 75 mg/kg groups were less remarkably than model group [(3.41±0.26), (6.97±0.35), (7.23±0.62),(8.38±0.92) times, P＜0.01]. The times of electric shock in EGB 500 mg/kg group was less significantly than 150 mg/kg group (P＜0.01) and that in 150 mg/kg was less remarkably than 75 mg/kg group (P＜0.05). ③ Hippocampal Ach content in modeled rats in EGB 500, 150, 75 mg/kg groups was higher than that in model group [(421.89±36.32), (387.45±32.76),(380.17±41.25), (365.28±11.42) μg/g, P＜0.05 or P＜0.01]. Hippocampal Ach content in 500 mg/kg group was higher significantly than 150 and 75 mg/kg groups (P＜0.01). In addition, compared with normal group,protein content in hippocampus in rats with disturbance of learning and memory induced by scopolamine in model group was reduced significantly [(41.75±3.82), (95.13±6.34) mg/kg, P ＜ 0.01]. After administrated with EGB,even though the protein content in hippocampus was increased in experimental rats after modeling, the difference was not significant (P＞0.05).CONCLUSION: EGB improves significantly learning and memory in experimental animal in dose-dependence and increases significantly Ach content in hippocampus.

To explore the relationship between beta-amyloid (A beta) and the pathogenesis of Alzheimer disease (AD), after injection of beta-amyloid into the rat brain, the apoptosis of nerve cells and acetylcholine (Ach) content in rat hippocampus were examined by employing TUNEL technique and base hydroxylamine colorimetry respectively. The influence of age and glucocorticoid on the neurotoxic effect of A beta was also analyzed. A beta peptide could strongly induce the apoptosis of neurons in hippocampus, cortex and striate body (P < 0.05 or P < 0.01). In addition, the senility and glucocorticoid pre-treatment could enhance the toxic effect of A beta (P < 0.05 or P < 0.01). It is concluded that A beta may play an important role in the pathogenesis of Alzheimer disease via its induction of apoptosis of neurons and by decreasing the content of the Ach.
Acetylcholine/metabolism ; Aging ; Alzheimer Disease/etiology ; Amyloid beta-Protein/*toxicity ; Apoptosis/*drug effects ; Dexamethasone/*pharmacology ; Drug Synergism ; Hippocampus/metabolism ; Hippocampus/*pathology ; Injections, Intraventricular ; Neurons/pathology ; Rats, Wistar

To explore the relationship between beta-amyloid (A beta) and the pathogenesis of Alzheimer disease (AD), after injection of beta-amyloid into the rat brain, the apoptosis of nerve cells and acetylcholine (Ach) content in rat hippocampus were examined by employing TUNEL technique and base hydroxylamine colorimetry respectively. The influence of age and glucocorticoid on the neurotoxic effect of A beta was also analyzed. A beta peptide could strongly induce the apoptosis of neurons in hippocampus, cortex and striate body (P < 0.05 or P < 0.01). In addition, the senility and glucocorticoid pre-treatment could enhance the toxic effect of A beta (P < 0.05 or P < 0.01). It is concluded that A beta may play an important role in the pathogenesis of Alzheimer disease via its induction of apoptosis of neurons and by decreasing the content of the Ach.
Acetylcholine ; metabolism ; Aging ; Alzheimer Disease ; etiology ; Amyloid beta-Peptides ; toxicity ; Animals ; Apoptosis ; drug effects ; Dexamethasone ; pharmacology ; Drug Synergism ; Hippocampus ; metabolism ; pathology ; Injections, Intraventricular ; Male ; Neurons ; pathology ; Rats ; Rats, Wistar