The Effect Of Cluster Needling Of Scalp Pointon The Expression Of The Surrounding Tubulin Of Cerebral Infarction Focus In Rats

Cong through the observation of thorns on the first point of cerebral infarction lesions around tubulin expression of the first points of regulation Cong thorn cerebral ischemia local micro-environment, to maintain the integrity of nerve cells skeleton playing an important role. To further clarify the first point Cong thorn for the resumption of cerebral infarction and cerebral infarction treated with acupuncture for the mechanism to provide an objective theory.Methods: This study elected to Wister male rats for 60 subjects objects were divided into scalp Cong thorn group and the control groups, each of the 25, the sham group 10. Longa by the improved prepared by the rat middle cerebral artery occlusion model. Scalp Cong thorn in the group to use the head-Acupoints seven areas of law, from the top, a day trip scalp Cong thorn, stay-30 minutes, the control group without any treatment. In each group after 1 d, 3d, 7d, 14d, 21d carry out acts of score and the execution of five, from brain tissue. Immunohistochemistry was used to observe each time around the focus point of cerebral infarction Tubulin expression.Results: 1.Scalp Cong thorn group of seven days, 14 days, 21 days later, the rats behavior than the score after one day, three days have greatly improved and is better than the control group (P < 0.05). 2.Scalp Cong thorn group and control group in 1,3 days infarction visible around a small number of Tubulin positive cells, the two groups was not significant (P> 0.05). 7, 14 days infarction around Tubulin positive cells have markedly increased, the first point Cong thorn Tubulin expression than the control group were significantly, the two groups had a significant (P <0.05). Tubulin 21 days of the two groups have come down, there are still significant difference between the two groups (P <0.05).Conclusion: Cong thorn scalp can promote cerebral infarction after infarction in the surrounding nerve tissue tubulin expression and inhibit brain damage after Ca2 + influx, calcium-activated and tubulin of decomposition, so as to reduce the nerve cell cytoskeleton collapse, to prevent Delayed axons fault occurred, to reduce neuron death, contribute to the recovery of neurological function.