| Purpose：sugar cortical hormone to send the nerve pathological ache model toSNI model big mouse；Neuropathic pain (neuropathic pain, NPP) is defined as the nervous system(peripheral or central) injury or dysfunction induced by and chronic pain(IASP,1994), can be a variety of forms. According to the survey, neuropathicpain in a population with high incidence of up to1.5%. In many patients, suchas diabetic polyneuropathy patients, HIV patients, poststroke syndrome patients,patients with multiple sclerosis, often thus affect their quality of life.Because NPP have a complex mechanism, pain degree, poor treatment effect, longcourse of treatment, has become a troubled patients, affecting their qualityof life and even cause the main reason of individual patients world-weary mood.How to control this disease, have become scientists and clinical medicalpersonnel’s primary responsibility. With randomized controlled trials publishednumber of steady growth, evidence-based treatments are becoming feasible.Neuropathic pain is defined as pains resulting from disease or damage ofthe peripheral or central nervous system, and from dysfunction of nervous system.It is often associated with the significant appearance of abnormal sensory signsof allodynia, hyperalgesia and spontaneous pain. Neuropathic pain is calledchronic pain in clinic, for its long time lasting and complication. Neuropathicpain is not only a tough disease in clinic,but also a hot research topic inthe field of neuroscience. Now, mechanism of Pains is not clear, the traditionalview about pain and its modulation connected only with purely neural, and spinalglial cells have no relationship with intercellular signaling transportation,for it have no axon. But the explanation can’t answer the question aboutextra-territorial pain and mirror-image pain. More and more researches haverevealed that glial cells and intercellular signaling transportation play thekey role on Neuropathic pain.Nerve pathological pain influence goal this research through the establishment partial sciatic nerve branch damage (sparednerveinjury neuronthic pain model), and by the different dosage betamethasonetook the intervention factor, then through the behavior study, the immunityfluorescence method observation nerve pathological ache big mouse’s achebehavior study change and the spinal cord small sol delicate work (OX-42reaches)Materials and methods:Experimental1.SNI rats model making methodThe unilateral sciatic nerve of the tibial nerve and common peroneal nerve branchcut, retention of the sural nerve branch2paw withdrawal reflex threshold determination method:The use of Von Frey cilia vertical stimulation of rat left plantar soles, duration<4S, lift foot or licking foot acts as a positive, or negative reaction. Startingfrom2.0g, for1.2seconds, to observe whether rats paw withdrawal reflexresponses appear.3thermal foot reflex threshold (TWD) measuring method:The heat pain stimulation (BME-410) switch in the debug files (light intensityweak), start alignment rat plantar stimulation, calculate the thermal footreflex time.4immunofluorescence determination method:Were calculated for each experimental group animal postoperative uninterrupteddays taken out the same number of rats, remove spinal segment in30%sucrose,a temperature of4degrees Celsius, until the tissue sink. Were embedded inparaffin, section observation, measurementIn5experimental animal grouping:The use of SD rat (male)64, n=16, randomly assigned, divided into4groups:Group first: only the sciatic and tibial nerve, common peroneal nerve exposure,but no damage to the exposed nerve (group Sh)Group second: sciatic nerve injury model group (SNI group) In third groups: group SNI+local injection of betamethasone (D1group).(doses:a single injection of compound betamethasone1mg/1ml)In fourth groups: group SNI+intraperitoneal injection of betamethasone group(D2group).(doses: a single injection of compound betamethasone1mg/1ml)Experiments D1and D2group from animal models produced before1days to seventhdays a day is divided into two local and abdominal single injection of1mg/1mlbetamethasone. Packet details experimental animal behavior indices: themechanical paw withdrawal reflex threshold (MWT) and the thermal foot reflexduration (TWD) at all time points (1days before the operation and onpostoperative days1,3days,7days,14days) changes.Observation of play behavior indicators, each experimental animal at all timepoints in each group of4randomly chosen, its execution. Out the correspondingsegment of spinal cord, staining of tissue sections, using microscope to observethe changes in the number of OX-42.6statistical processing:Data using the mean+standard deviation to said, the experimental data throughSPSS11.5software for processing, group and group compared with single factoranalysis of variance or t test, carries on statistics processing, P <0.05thinkthere is statistical difference.Knot fruit:In1experiments on rats with postoperative day, part of the rat sciatic nervebranches injury group have significantly decreased and TWD MWT value is extended,and the preoperative and postoperative Sh compared, each time using statisticsstatistical comparisons are different, but the difference is small.2.D1and D2group in comparison, MWT value decreased, the TWD was prolonged. Butthe degree of change has no obvious statistical difference. While in D1groupand D2group and SNI group when compared to corresponding to time, MWT valuedecreased in amplitude and TWD value of extended degree have significant change. 3.D1and D2group and SNI group when compared, spinal microglia appear dose datareduction, and no significant correlation with the injection site.Knot theory:In1experiments on rats after sciatic nerve branch which is selectively afterinjury, the emergence of a more obvious thermal allodynia and mechanicalsensitivity and pain reaction.2betamethasone injection and intraperitoneal injection in inhibiting theactivation of spinal microglia, thus reducing the rat hyperalgesia and allodyniaphenomenon, indicating that the activation of microglia not only play a role,it is also involved in a portion of the branches of the sciatic nerve injurycaused by the development of neuropathic pain.In3experiments that the spared nerve injury model and glial cell changes inthe number of shows, on neuropathic pain. It plays an important role. |
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