Therapeutic benefit of Yangxue Qingnao Granule on cognitive impairment induced by chronic cerebral hypoperfusion in rats.

OBJECTIVE: To observe the therapeutic effect of Yangxue Qingnao Granule (, YXQNG) on cognitive impairment induced by chronic cerebral hypoperfusion and to investigate its impact on oxidative stress, apoptosis, and the cholinergic system. METHODS: Adult male Wistar rats were subjected to chronic cerebral hypoperfusion by permanent occlusion of bilateral common carotid arteries (2-VO). Thirty rats were randomly assigned to one of the five treatment groups in a 1:1:1:1:1 ratio: sham operation plus normal saline treatment, 2-VO plus normal saline treatment, 2-VO plus YXQNG at a dose of 2 g·kg(-1)·d(-1) or 4 g·kg(-1)·d(-1), or 2-VO plus rivastigmine 2 mg·kg(-1)·d(-1). The Morris water maze test was used to assess the spatial memory retrieval. Apoptosis, total antioxide capacity (T-AOC), acetylcholine esterase (AchE) and choline acetyl transferase (ChAT) activities in the hippocampus and the cortex were investigated. RESULTS: In the chronic cerebral hypoperfusion model, the 2-VO plus saline treatment resulted in impaired special learning as shown by the significantly prolonged escape latency and shorter swim time in the first quadrant as compared to the sham operation. The impairment was associated with apoptosis and significant decreases in T-AOC, AchE and ChAT activities in the hippocampus and the cortex. Treatment with YXQNG at either 2 g·kg(-1)·d(-1) or 4 g·kg(-1)·d(-1) dose, or rivastigmine resulted in significantly shorter escape latencies and longer swim time in the first quadrant. YXQNG at both doses, but not rivastigmine, had significant reduction in apoptosis, and significant increases in T-AOC and ChAT activity in both the hippocampus and the cortex. Unlike rivastigmine, neither dose of YXQNG showed significant reduction in AchE activity. CONCLUSIONS: YXQNG ameliorated cognitive impairment induced by chronic cerebral hypoperfusion. The protective effect may be mediated through its regulation of apoptosis and activities of T-AOC and ChAT in the hippocampus and cortex of the rats in the chronic cerebral hypoperfusion model, a mechanism that is different from rivastigmine.

Green tea polyphenols inhibit cognitive impairment induced by chronic cerebral hypoperfusion via modulating oxidative stress.

Responses to oxidative stress contribute to damage caused by chronic cerebral hypoperfusion, which is characteristic of certain neurodegenerative diseases. We used a rat model of chronic cerebral hypoperfusion to determine whether green tea polyphenols, which are potent antioxidants and free radical scavengers, can reduce vascular cognitive impairment and to investigate their underlying mechanisms of action. Different doses of green tea polyphenols were administered orally to model rats from 4 to 8 weeks after experimentally induced cerebral hypoperfusion, and spatial learning and memory were assessed using the Morris water maze. Following behavioral testing, oxygen free radical levels and antioxidative capability in the cortex and hippocampus were measured biochemically. The levels of lipid peroxidation and oxidative DNA damage were assessed by immunohistochemical staining for 4-hydroxynonenal and 8-hydroxy-2'-deoxyguanosine, respectively. Rats that received green tea polyphenols 400 mg/kg per day had better spatial learning and memory than saline-treated rats. Green tea polyphenols 400 mg/kg per day were found to scavenge oxygen free radicals, enhance antioxidant potential, decrease lipid peroxide production and reduce oxidative DNA damage. However, green tea polyphenols 100 mg/kg per day had no significant effects, particularly in the cortex. This study suggests that green tea polyphenols 400 mg/kg per day improve spatial cognitive abilities following chronic cerebral hypoperfusion and that these effects may be related to the antioxidant effects of these compounds.

[Observation on clinical effect of Angelica injection in treating acute cerebral infarction].

OBJECTIVE: To study the therapeutic effect of Angelica Injection (AI) in treating acute cerebral infarction (ACI). METHODS: One thousand four hundred and four patients, who were treated with AI (692 patients in Group A), compound salvia (390 patients in Group B) and low molecular dextran injection (322 patients in Group C) respectively. Indexes such as CT scanning on infarcted volume, scoring of clinical neuro-function deficit taking on the 1st, 3rd, 7th, 15th and 25th day, clinical therapeutic effectiveness evaluated by the end of the 2nd week and the improvement of Barthel index scores were observed. RESULTS: The total effective rate in Group A, B and C was 78.7%, 63.6% and 59.3% respectively, that in Group A was significantly higher than in the other two groups (P < 0.05). The improvement of neuro-function deficit scores and Barthel scores in Group A were better than those in Group B and C (on the 25th day, P < 0.01), and the decrement of infarcted volume in Group A was larger than that in Group C (P < 0.01). CONCLUSION: AI has evident therapeutic effect in treating ACI.