摘要
Objective: To probe into the mechanism of moxibustion preconditioning in preventive brain-protecting effect. Methods: The global brain ischemia rat model was developed by blocking 4 arteries. Seventy-eight Wistar male rats were randomly divided into 5 groups: a normal control group, a sham-operation group, a brain ischemia group, a brain ischemia preconditioning group, a moxibustion pretreating group. The brains in the 5 groups were taken at 24 h, 48 h, and 72 h after operation respectively. Superoxide dismulase (SOD) activity was determined with xanthine oxidase method and malondialdehyde (MDA) content with thiobarbituric acid method. Results: After the operation, in the moxibustion preconditioning group, SOD activity significantly increased, especially 24 h after moxibustion preconditioning; and MDA content decreased, with a very significant difference as compared with that of the cerebral ischemia group (P<0.01). Conclusion: Moxibustion preconditioning protects the ischemic and anoxic brain tissue by increasing the activity of endogenous antioxidase.
Objective： To probe into the mechanism of moxibustion preconditioning in preventive brain-protecting effect. Methods： The global brain ischemia rat model was developed by blocking 4 arteries. Seventy-eight Wistar male rats were randomly divided into 5 groups： a normal control group, a sham-operation group, a brain ischemia group, a brain ischemia preconditioning group, a moxibustion pretreating group. The brains in the 5 groups were taken at 24 h, 48 h, and 72 h after operation respectively. Superoxide dismulase （SOD） activity was determined with xanthine oxidase method and malondialdehyde （MDA） content with thiobarbituric acid method. Results： After the operation, in the moxibustion preconditioning group, SOD activity significantly increased, especially 24 h after moxibustion preconditioning; and MDA content decreased, with a very significant difference as compared with that of the cerebral ischemia group （P〈0.01）. Conclusion： Moxibustion preconditioning protects the ischemic and anoxic brain tissue by increasing the activity of endogenous antioxidase.
