ABSTRACT
This study was aimed to probe into the mechanism of moxibustion in the treatment of Alzheimer’s disease (AD). A total of 40 male 15-month-old SD rats were randomly divided into the normal group, model group, moxibustion group and sham-operation group. Stereotactic injection of agglutinated Aβ25-35 into rat’s bilateral hippocampus was used to prepare AD models. Equal amount of normal saline was injected to rat’s bilateral hippocampus in the sham-operation group. Model rats were treated by moxibustion at the distance of 2-3 cm above points of‘BL23-Shenshu’, ‘ST36-Zusanli’ and ‘GV20-Baihui’. No intervention was given to rats in the normal group. The learning and memory ability was detected by Morris water maze test. Changes on expressions of Bcl-2, Bax and Caspase-3 of hippocampus zone were detected by immunohistochemical method. The results showed that in the model group, the average escape latency of five days and the last three days were significantly lengthened. And the times across the platform position were significantly reduced. Compared with the normal group and the sham-operation group, expressions of Bax and Caspase-3 in the hippocampus were significantly increased, and the expression of Bcl-2 was obviously decreased (P < 0.01). In the moxibustion group, the average escape latency of five days and the last three days were shortened obviously, and the times across the platform position were significantly increased. Compared with the model group, expressions of Bax and Caspase-3 were significantly reduced, and the expression of Bcl-2 was significantly increased (P < 0.01). It was concluded that the action mechanism of AD treatment with moxibustion may be through the reducing of proapoptotic protein Bax and Caspase-3 releasing, promoting the releasing of anti-apoptotic protein Bcl-2, so as to improve the learning and memory impairment caused by Aβ.
ABSTRACT
Objective To observe the effects of moxibustion on learning and memory ability and nerve cell ultrastructure in CA1 region of hippocampus of rats with Alzheimer's disease (AD);To discuss its mechanism of action to AD.Methods A total of 40 male SD mice was randomly divided into normal group, model group, moxibustion group and sham-operation group. Stereotactic injection agglutinated Aβ25-35 into bilateral hippocampus of rats in model group and moxibustion group to prepare AD models. Rats in moxibustion group were treated by moxibustion at the points which were located above 2-3 cm away from Shenshu, Zusanli and Baihui. Rats in normal group received no treatment. The learning and memory ability was detected by Morris water maze test. Morphological changes of rat nerve cell ultra structure in hippocampal CA1 region were observed by transmission electron microscope.Results In model group, the average escape latency of five days and the last three days was significantly lengthened, and the times across the platform position significantly decreased. Transmission electron microscope indicated nerve cell structures were damaged and displayed unclearly;mitochondrion swelled, even mitochondrial crista was abnormal and deformed, endoplasmic reticulum of inter organelle expanded and the deposition of lipofuscin increased. After the treatment by moxibustion, the average escape latency of five days and the last three days was shortened obviously, and the times across the platform position significantly increased. In moxibustion group, the edema of nerve cells significantly decreased;dilation of endoplasmic reticulum and mitochondria swelling significantly improved;golgi bodies, mitochondria and ribosomes obviously increased in comparison with the model group. Conclusion Moxibustion can improve the learning and memory impairment caused by Aβ by promoting repairing of nerve cells in brain.