The Regulation Of NF-kB-decoy To Big Mouse Seahorse Neuron In COX-2 And It's Function Research To Protect Seahorse Structure.

Background: Epilepsy is common disease of central nervous system.Its principle feature is repeating seizures, It the huge injury which brings to the patient is by epilepsy manifests suddenly repeatedly the brain damage which (seizure) causes. Had the research to indicate, causes in the brain by the epileptic paroxysm the inflammation response causes the epileptic paroxysm cerebellum organization pathology change, specially the seahorse structure damage (neuron escapes including seahorse in loses, neuron accent perishes, spongiocyte proliferation, textile fiber germinates, seahorse hardening and so on) one of primary causes, Therefore the discussion and the research by epileptic paroxysm epilepsy sensitive brain area and so on result brain in and seahorse inflammation response mechanisms, adopts measure preventing and controlling the brain damage which manifests suddenly repeatedly by epilepsy brings, still with difficulty permanently cures at epilepsy today, to improved epilepsy patient's life and the study can play the positive role. The nucleus duplication factor (NF-kB) activation may induce the widespread gene expression highly effective, the adjustment cell factor target gene duplication, is playing the regulative role in the inflammation and the immune response. Although the minority several literature had reported when epileptic paroxysm is following in the brain the NF-kB expression, and has induced the neuron death and the spongiocyte activates, promoted in epilepsy big mouse brain pathology change, but in epilepsy activity whether has regulated of as a result of the NF-kB activation a COX-2 its downstream genes high expression, only then has caused in the brain inflammation response and a series of pathological change, until now has not seen the report.Goal: Whether in the discussion epilepsy activity has regulated its downstream gene COX-2 high expression as a result of the NF-kB. activation, only then has caused in the brain inflammation response and a series of pathological change. Through provides the theory support to in vitro raise cell observation for in vivo experiment, and further for the control epilepsy brain damage and other nerve recession disease inflammation responded provides certain theory basis.Method: Takes the young mouse seahorse neuron to carry on the raise,Will synthesize widowed gathers the deaeration nucleotide with the NF-kB syn-form part consistent double strand (kBdecoy DNA oligodeoxy- nucleotides, kB-decoy) and corresponding has nothing to do with the sequence (wrong to match - decoy) to take the comparison, After the non-virus's high efficiency, the nontoxicity extension dye carrier ExGen500 to wrap, and wrong matches kB-decoy - decoy to change over to separately in the neuron, Again uses the NF-kB activating agent fat polysaccharide (lipopolysaccharide, LPS) to induce NF-kB to activate, tests the (EMSA) method with the electrophoresis transport ratio to observe NF-Kb the activation, and examines COX-2 by RT-PCR and the immune cell chemical process the expression.Finally: Through the repeatedly raise seahorse neuron, the grouping, the experiment obtains following result: Raises cell confirmation for seahorse neuron; Uses the 100ng/ml stimulation seahorse neuron as NF-kB activating agent LPS 6h, NF-κB to have the significance extension nucleus to activate, 12h achieves the peak, then starts to drop, 36h has been at the low level to maintain the condition. Also when 12h NF-κ the B activation increases along with the LPS booster dose increases; The COX-2 activeness determination demonstrated that,After LPS stimulates 12h COX-2 to express wrong matches - the decoy group and the LPS group obviously is higher than NF-kB group; the B-decoy group, but the LPS group and wrong matches - the decoy group difference non-statistics significance.Conclusion: Raises the cell for the seahorse nerve stem cell, may use in vitro experiment; LPS took NF-kB the activating agent best response time is 12 hours, the best dosage is 100ng/ml; Design synthesis NF-kB-decoy took NF-kB the inhibitor is effective; The NF-kB activation has regulated of a COX-2 its downstream genes high expression.