Effect Of Danxingtongluo Decoction On The Expression Of FADD And Bax Protein During Cerebral Ischemic Reperfusion Injury In Rats

Objective: Cerebral ischemia reperfusion injury is an extremely complexpathological physiology process. Apoptosis and oxidative stress have been found to play animportant role in the pathogenesis of cerebral injury secondary to ischemia/reperfusion(I/R).Especially apoptosis is influenced by many genetic manipulation.FADD、Bax protein in theway of apoptosis to play a key role.Some research results discover that Danxingtongluodecoction has protective effect for cerebral ischemia and cerebral ischemia reperfusioninjury and has to improve the efficacy of ischemic stoke symptoms, but the mechanism hasnot yet completely clear. This experiment discuss protection of FADD and Bax proteinthrough the observation of FADD and Bax protein expression changes during cerebralischemia reperfusion injury tissue in rat. When give rat Danxingtongluo decoction,weobserve influence of the FADD and Bax protein and further research the mechanism ofagainst apoptosis of Danxingtongluo decoction for the clinical application and promotion toprovide the evidence.Methods:40healthy SD rats whether, male and female and their ages are3-4months.40SD rats were randoml divided into sham-operation group,model group,Nimodipine group,Danxingtongluo decoction low dosage treatment group,Danxingtongluo decoction high dosage treatment group,8rats per group. sham-operation group and model group were given to physiological saline at dose of1.0ml/100g once a day for7days;Nimodipine group were given to Nimodipine at doseof1.0ml/100g once a day for7days;Danxingtongluo decoction low dosage treatmentgroup were given to Danxingtongluo decoction at dose of0.75ml/100g once a day for7days; Danxingtongluo decoction high dosage treatment group were given to Danxingtongluo decoction at dose of1.5ml/100g once a day for7days.After7-days,therats of all the groups except sham-operation group were made into cerebral ischemiareperfusion injury models by thread embolism method.The residual rats were killed andtheir brains were taken out after2h ischemia and24h reperfusion injury.We evaluateneural function by Longa’s methods. Hippocampus tissues of eligible rats were detectedto the pathological changes by hematoxylin-eosin staining.We detect the expression ofFADD and Bax protein during hippocampus tissues in eligible rats byimmunohistochemistry and medical image analysis methods.We analyze datas by theSPSS17.0software.Results:1.Success rates of Model are68.09%,After medical treatment,neurobehavioral scores in rats was evidently lower than the model group (p<0.05).2.Take out the brain tissue and fix right to make the paraffin and thinest slices, Weobserve histomorphology of hippocampus tissues in rats by hematoxylin-eosin stainingafter cerebral ischemic reperfusion injury.Nerve cells are normal in sham-operationgroup; Nerve cells are degenerative and necrotic in model group; The levels of braintissue damage is alleviative in Nimodipine group、Danxingtongluo decoction lowdosage treatment group and Danxingtongluo decoction high dosage treatmentgroup,especially Nimodipine group and Danxingtongluo decoction high dosagetreatment group.3.We detect the optic density(OD) of FADD and Bax protein duringhippocampus tissues in rats by immunohistochemistry and medical image analysismethods. The optic density(OD) of FADD and Bax protein in sham-operation group arelower; In model group,the optic density(OD) of FADD and Bax protein are obviouslyincrease(P<0.01);After we give rats Danxingtongluo decoction, the optic density(OD)of FADD and Bax protein are reduced(P<0.01); The expression of FADD and Baxprotein during hippocampus tissues in rats by immunohistochemistry betweenDanxingtongluo decoction high dosage treatment group and Nimodipine group hassignificantly disparity(P<0.05).Conclusions:1.After2h ischemia and24h reperfusion injury, The expression ofFADD and Bax protein are increase. The FADD and Bax protein play an important rolein nerve cell apoptosis.2.Danxingtongluo decoction protects nerve cells by reduce theexpression of FADD and Bax protein. Danxingtongluo decoction resistance to cerebralischemic reperfusion injury may be ralate to inhibiting apoptosis.