Protection Mechanism For Ethyl Pyruvate On Hemorrhage Rats Neuron Of Experimental Research

This topic research ethyl pyruvate treatment of cerebral hemorrhagerat neurons of rat protection, experimental rats by monitoring the serum NO,SOD, free radical, and Inflammatory cytokines, il-6and TNF-a apoptotic cells,apoptosis regulatory proteins Bax, the expression of Bcl-2three aspects todiscuss ethyl pyruvate on hemorrhage rats neuron protection mechanism, whichprovides new thinking for clinical treatment.Method: Use brain stereotaxicinstrument to autologous arterial blood into the caudate nucleus preparation ofcerebral hemorrhage model rats.48male SD rats, weight300g~350g, wererandomly divided into three groups, control group (F)(n=8), and cerebralhemorrhage group (ICH)(n=20), cerebral hemorrhage+ethyl pyruvateintervention group (EP)(n=20). Each group by beheading time divided into6h,24h,3d,7d, a total of four subgroups. EP group use ethyl pyruvate liquorwith40mg/kg injected into rat abdominal cavity, F group and cerebralhemorrhage groupwith equivalent physiological saline,2h after surgery, andthen give medicine every day until death, using neurobehavioral score (Longamethod) to determine whether a building is successful. Each time point in ratswith Garcia score to understand neural function defect, preparation of serum,serum NO, SOD was evaluated by colorimetric method content, usingenzyme-linked immunoassay (ELASA), serum TNF-a and il-6levels. Usingdifferent parts of the immune histochemical method to detect rats had the expression of Bax and Bcl-2, by in situ end labeling method (TUNEL method)to observe apoptosis situation around hematoma. Results:function defect scorelow in rats in the control group (P <0.05); Serum TNF-a, il-6, NO expressionquantity increased (P <0.05), hemorrhage,6h began to increase, the3dincrease was most pronounced, serum SOD from6d began to decreasebleeding, bleeding until3d the most obvious. Higher bleeding after the numberof apoptosis, apoptosis regulating proteins Bax, Bcl-2expression increased (P<0.05). EP group rats nerve function defect scale rats increase in thehemorrhage group (P <0.05), serum TNF-a, il-6, NO content in bleeding groupalso significantly reduced, SOD content increased (P <0.05), the number ofapoptotic cells around the hematoma is reduce hemorrhage group, apoptosisregulatory proteins the Bcl-2expression increased, reduced the volume of Baxprotein expression (P <0.05). Conclusion:1, nerve function damage in ratsafter cerebral hemorrhage, serum levels of inflammatory mediators and freeradical expression quantity increase, increase number of apoptosis.2, EP canrestrain the inflammatory responses of cerebral hemorrhage in rats and theoxidative damage of free radicals, improve neural function defect score.3, EPtreatment inhibit neuronal apoptosis of rats, the effect may be raised apoptosisregulatory proteins expression of Bcl-2, downgrade and Bax expression.