Study On Effects Of XFM And Its Specificity Antagonist On The LKB1 In Different Encephalic Regions Of Rats

XFM and its antagonist have an effect Indeed, safety, side effects and easy to use features. But the anesthesia and wake-up mechanism is not fully understood. With the research of cellular signaling pathway, it is the focus of the study of the mechanism of general anesthesia and the mechanism of the mechanism of awakening to search for clear drug action targets and to know the key mechanism of action. In the central nervous system which there is a very complex signal transduction network, it can be described as complex. LKB1 phosphorylate many conservative downstream kinases, is a good representative, AMPK family belongs to the serine / threonine protein kinase, LKB1 activates AMPK by phosphorylation of AMPK, negatively regulate the activity of mTOR that LKB1-AMPK-mTOR signal transduction pathway. LKB1 / AMPK / m TOR pathway plays a central role in the regulation point in cell proliferation, growth, differentiation. LKB1 plays an important role in long-term adjustment(anesthesia long-reaction) and excitability regulation of neuronal dendritic. It is closely associated with neuronal plasticity and local protein in the synthesis. This may be the point of anesthetics and their antagon ists and one of the key target pathway play a role in the central nervous system.To accurately understand the effects of XFM and its antagonists on the central nervous system of high physiological activity. The key protein LKB1 and transcription factors i n LKB1-AMPK-mTOR signal transduction pathway were selected as the research objects. From the molecular level on XFM and its antagonist interaction mechanism are discussed, and elucidate the XFM and its antagonists on the effect of rats in different brain r egions of LKB1 gene and protein. For future research mTOR signal transduction systems provide the basis for the role of the central nervous system.In this study, 72 SD rats were rando mLy divided into XFM anesthesia group(M), antagonists group(group J), XFM and antagonists interactive group(MJ group). M group were rando m Ly divided into five sub-groups respectively, M1(after injection XFM 10 min), M2(after injection XFM 20 min), M3(after injection XFM 40 min), M4(after injection XFM 60 min),C1(Injected with the same dose of M group of physiological saline); J group were rando mLy divided into five sub-groups respectively,J1(after injection antagonists 10 min),J2(after injection antagonists 20 min),J3(after injection antagonists 40 min),J4(after injection antagonists 60 min),C2(Injected with the same dose of J group of physiological saline); MJ group were rando m Ly divided into five sub-groups respectively,MJ1(injection of antagonist 10 min after injection of XFM 10 min),MJ2(injection of antagonist 20 min after injection of XFM 10 min),MJ3(injection of antagonist 40 min after injection of XFM 10 min),MJ4(injection of antagonist 60 min after injection of XFM 10 min),C3(Injected with the same dose of MJ group of physiological saline). Above 6 in each subgroup. After each subgroup rats reaches a predeter mined point in time were sacrificed by cervical brain, and isolated cerebral cortex, hippocampus, cerebellum, thalamus and brain stem. RT-PCR method was used to detect the relative transcript levels of LKB1 mRNA in each brain region. Western blot method was used to detect the relative expression of LKB1 protein and p-LKB1 protein in different brain regions.Experimental results show that:XFM can significantly affect the relative transcription o f LKB1 mRNA and the relative expression of p-LKB1 and LKB1 protein in brain cortex, hippocampus, cerebellum, thalamus and brainstem of rat. These sites may produce anesthetic effects.Antagonists for XFM can effectively complete reversal the relative trans cription of LKB1 mRNA and relative expression of p-LKB1 and LKB1 protein in rat brain cerebellum and brain stem of. Simultaneously, it can sectional reversal the relative transcription of LKB1 m RNA and relative expression of p-LKB1 and LKB1 protein in thalamus. These sites may produce wake-up effects.In summary, XFM and its antagonist have the opposite effect on LKB1 in the part of the brain region of rats. This may be one of them to produce the effects of anesthesia and wake interaction mechanism. However, antagonists is not all completely reverse the effects of XFM on LKB1 in rat brain, there may be other mechanisms have an effect. The effects of the LKB1 pathway may be just one of mechanisms.