Objective To observe the effect of kallikrein and ozagrel on hemorheology in the treatment of patients with acute cerebral infarction,provide a theoretical basis for clinical treatment.Methods 100 patients with acute cerebral infarction met the inclusion criteria were randomly divided into 50 cases of observation group and 50 cases of control group,the control group were received conventional drug therapy,the observation group were given kallikrein and ozagrel on the basis of the control group,kallikrein 0.15PNA /times,ozagrel 80mg one time,bid,14d for a course of treatment.The symptoms improvement were observed,the NIHSS score and ADL score were calculated after treatment,then the blood were extraced for detecting high shear viscosity of whole blood,red blood cell aggrega-tion index,hematocrit,fibrinogen,erythrocyte sedimentation rate,and the clinical efficacy were judged.Results The total effective rate of the observation group were 96% (48 /50),which of the control group were 66% (33 /50),the total effective of the observation group was significantly higher than the control group (χ2 =16.105,P <0.01);The high shear viscosity of whole blood,red blood cell aggregation index,hematocrit,fibrinogen,erythrocyte sedimentation rate,NHISS of the observation group and the control group after treatment were lower than before treatment (t =6.589 and 3.762,6.204 and 3.661,8.112 and 5.774,5.542 and 3.529,9.429 and 3.962,9.621 and 6.586,all P <0.05),the ADL score was significantly higher than before treatment(t =7.673 and 5.446,all P <0.05),the high shear viscosity of whole blood,red blood cell aggregation index,hematocrit,fibrinogen,erythrocyte sedimentation rate, NHISS of the observation group after treatment were lower than those of the control group (t =3.387,3.545,3.525, 3.288,3.302,4.988,all P <0.05),the ADL score was significantly higher than the control group (t =3.446,P <0.05).Conclusion The method containing kallikrein and ozagrel has exact clinical efficacy,can effectively improve blood rheology and cerebral blood perfusion ischemic area,promote neurological deficits and recover the ability of daily life,and its security is good,which is worthy of promotion.

Objective To study the inhibitory effect and mechanism of dipeptide peptidase inhibitors analogues on LPS -induced inflam-matory response on microglia .Methods Microglia cells were cultured ,isolated and purified from the neonatal Sprague-Dawley rats.Divided them into blank group ,negative control ,LPS group and medicine group ( parallel determination for 3 times each group ) after pharmacological preconditioning for 48 hours.The optimal concentration of microglia proliferation induced by LPS were measured by MTT assay .Observed the role of dipeptide peptidase inhibitors analogues on LPS-induced microglia in different concentrations .The interleukin1β( IL-1β) ,tumor necro-sis factor alpha ( TNF-α) were assayed by enzyme-linked immunorrbent assay ( ELISA ) .The expression of TLR-4 was detected by Western blotting and the expression of NF-κB was detected by RT-PCR.Results LPS induced the proliferation of microglia and significantly in-creased the release of inflammatory cytokines in LPS-stimulated primary microglia .Compared with the blank group ,dipeptide peptidase inhibi-tors analogues could inhibit this effect and the IC 50 values was 1.014 ×10 -2 mol/L to MG after pretreatment for 48 hours.Dipeptide peptidase inhibitors analogues could inhibit the release of TNF-αand IL-1 significantly(P<0.01),and it decreased the expression of TLR4 and NF-κB signif-icantly(P<0.01).Conclusion This research suggests that dipeptide peptidase inhibitors analogues restrain cell proliferation and inflammatory re-sponse of LPS-stimulated microglia,and the possible mechanism may be related to the inhibition of the expression of TLR-4 and NF-κB.