The Molecular Mechanism Of Cerebral Protection Of Putting Blood At 12 Jing Points In MCAO Rats

Objective: In these experiments, we study the influence of putting blood at 12 hand Jing Points on the expressions of NOS, Hsp70 and c-fos in Cerebral cortex in MCAO rats, in order to clarify the molecular mechenism of the protection of this therapy in ischemia.Method: We build ischemia modles by blocking one side of middle cerebral artery in rat( Middle Cerebral Artery Occlusion, MCAO ) . And adopt Histochemistry and Immunohistochemical method respectively . Then we observe the expressions of NOS, Hsp70 and c-fos postive cells and the changes in expression after giving treatment by putting blood at 2 hand Jing Points.Outcome: (1) Acute ischemic damage may induce the expression of c-fos protein in Cerebral Cortex quickly. Also, the expression increases by the ischemia time delay. It may hint that ischemia injury can rise the ability of nerve cells to tolerate ischemia and anoxia. And the expression level of c-fos can be up-regulated by putting blood of 12 hand Jing Points. So we think that treated by this therapy can rise the irritability of brain to resist the development of ischemia and enhance the ability to plerosis. (2) Acute ischemic damage may induce the expression of HspVO in Cerebral Cortex quickly. Also, the expression increases by the ischemia time delay. It may hint that ischemia injury can rise the ability of nerve cells to tolerate ischemia and anoxia. And the expression level of HspVO can be up-regulated by putting blood of 12 hand Jing Points. So we think that treated by this therapy can rise the irritability of brain to resist the development of ischemia and enhance the ability to plerosis. (S)There's an obvious increase of NOS positve cells in Cerebral Cortex in rats of moddle group and treatment grouop, and there's a marked difference among moddle group, treatment grouop and reference group(P<0.05). The expression of NOS cells in 1 hour, 3 hour treatment group much fewer than modle group (P<0.01); and 6 hour treatment group fewer than modle group also (PO.05). On the contrary, there's no marked difference among immediate treatment group, 12 hour treatment group and reference group. (4) There's an obvious increase of nNOS positve cells in Cerebral Cortex in rats of moddle group and treatment grouop, and there's a marked difference among moddlegroup, treatment grouop and reference group(P<0.05). The expession of nNOS in Cerebral Cortex in treatment group decreased marktably by giving treatment within 6 hours after ischemia. But there is no marked difference between 12h treatment group and reference group (P>0.05).Conclusions: (l)Ischemia may promote the expression of c-fos. The expression of c-fos protein has relation relatived with severity level of ischemia; and reflect the irritability of neurons also. Putting blood at 12 hand Jing points in early period of ischemia may up-regulate the expression of c-fos. Thus protect the ischemic nerve cells. (2) Putting blood at 12 hand Jing points in early period of ischemia may promote the irritability of ischemic cerebral tissues,and suppress the developement of apoptosis. Thus protect the ischemic cerebral nerve cells. (3)Ischemia may promote the expression of NOS. But the expression can be down-regulated by putting blood at 12 hand Jing points. So we think that this therapy can protect the ischemic nerve cells. It has no effect to give theatment immediately and also after 12 hours later. NOS is one and only one important synthase of NO. And the production of NO is important mechenism of nerve injury. Put blood at 12 Jing points suppress the activity of NOS, thus reduce the production of NO. (4) Ischemia may promote the expression of nNOS neuron. The expression can be down-regulated by putting blood at 12 hand Jing points within 6 hours after ischemia. Thus may protect the ischemic nerve cells. It has no protection after 12 hours.Summerize: After ischemia, putting blood at 12 hand Jing points within theraputic time windows may suppress the expression of NOS, nNOS ,reduce the over-production of NO, relive the neurotoxicity of NO. Simultaneous...