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Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine 2005-Jan

[Effects of Corydalis ambailis migo total alkaloids on experimental cerebral ischemia].

Само регистровани корисници могу преводити чланке
Пријави се / Пријави се
Веза се чува у привремену меморију
Xue-Yong Hu
An-Sheng Sun
Li-Mei Yu
Qin Wu

Кључне речи

Апстрактан

OBJECTIVE

To observe the protective effects of Corydalis ambailis migo total alkaloids (COAMTA) on cerebral ischemia/reperfusion injury in rats and to investigate its mechanism.

METHODS

The effects of COAMTA on decapitated gasping mouse model and rat model of middle cerebral artery ischemia (2 h)/reperfusion (22 h) were observed. The neurological scale, cerebral infarcted volume and cerebral water content subjected to cerebral middle artery ischemia/reperfusion in rats were recorded. The activities of nitric oxide synthase (NOS) and superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in the ratso brain were measured. Cell apoptosis in ischemic penumbral area was observed with light microscope in the method of terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL).

RESULTS

The average gasping time of the mice (6.0 mg/kg or 9.0 mg/kg COAMTA) was significantly prolonged, the cerebral infarcted volume and cerebral water content of the rats (5.0 mg/kg or 7.5 mg/kg COAMTA) were significantly decreased, as compared with the control groups. The average activity of SOD in cerebral tissue of the rats (5.0 mg/kg or 7.5 mg/kg COAMTA) was significantly higher than that of the control groups, meanwhile, the average activity of NOS and the content of MDA declined significantly. The cell apoptosis in ischemic penumbral area of the rats (5.0 mg/kg COAMTA) was significantly inhibited as compared with the control groups.

CONCLUSIONS

COAMTA can facilitate the protection against cerebral ischemia/reperfusion damage. The mechanism is related to inhibiting the activity of NOS and lipoperoxidation, increasing the activity of SOD and decreasing the neuronal apoptosis.

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