The Research About The Mechanism Of TWP Rescuring MG

Myasthenia Gravis (MG) is a n-Acetylcholine receptor(nAChR) specific T cells mediated , nAChR antibody regulated autoimmune disease. Tripterygium Wilfordii Polyglucosidium(TWP) has been used in the therapy of MG as a kind of immune inhibitor, and the effect is significant. The present researchs about its mechanism are mostly focused on the immune system, and based on the previous work of our Lab, TWP can enhance the transmission of excitation at the neuromuscular junction by acting on the presynapse, we used microionophoretic methods and the means of intracellular microelectrode to study whether TWP can act on the postsynapse , in addition , because there are several foreign lectures which claim the mRNA levels of all the nAChR subunits are higher than normal in MG patients, we constructed experimental autoimmune myasthenia gravis(EAMG) to study the expression of nAChR a ^subunit mRNA, preparing for future research.This work comprises two sections:The first one: In order to study the effect of TWP on the reactivity of the nAChR in the end plate membrane, we applied the exogenous AChCl to the superficial end-plates by using the microionophoretic methods, and Acetylcholine potential (AchP) was recorded as an indicator of the reactivity of the nAChR in the end plates. The results manifest:TWP can enhance the reactivity of the nAChR in the end plates, and this action have the quantity-effect relations and the time-effect relations;2) TWP can act on the postsynapse to enhance the reactivity of the nAChR in the end plates by increasing the conductance of ion channels and so on.The second one: we injected the nAChR extracted from the muscle of calf into the mice as antigen to construct EAMG, then used the semi-quantification RT-PCR to detect the expression of nAChR a rsubunit mRNA. The results indicat:1) The EAMG constructed is relatively successful with characteristic clinical, electromyographic, and immune features when compared with the controls; 2) The expression of the nAChR a rsubumt mRNA is increased in the MGsymptom group;3) The impairment of nAChR mediated by nAChRab can trigger a compensative mechanism to increase the expression of all nAChR subunits mRNA. The inheritance plays a certain role in the process of inducing MG.