ABSTRACT
Objective To observe the influence of Qileng Decoction on the level of serum visfatin and the degree of carotid atherosclerosis in patients with acute atherosclerotic cerebral infarction(AACI). Methods One hundred and eighty AACI patients were classified into non-AACI control group (group A;N = 30), stable carotid atherosclerotic plaques group(group B;N = 75)and unstable carotid atherosclerotic plaques group(group C;N= 75)according to the results of carotid color ultrasonography. The serum visfatin level of the three groups was detected at the time of AACI attack. Group B and group C were separately randomized into conventional treatment subgroup (N = 37)and Qileng Decoction subgroup (N = 38). The conventional treatment subgroup was given basic therapy for AACI including nutrition support and symptomatic treatment , and Qileng Decoction subgroup was treated with Qileng Decoction (mainly composed of Radix Astragali,Rhizoma Sparganii, Fructus Mori,Radix Trichosanthis, Rhizoma Curcumae,Hirudo,and Fructus Aurantii)orally on the basis of treatment for the conventional treatment group. Before treatment and 15,90 and 180 days after treatment,we detected the level of serum visfatin,and measured the carotid intima-media thickness(IMT)and plaque scores(PS). Results (1)At the time of AACI attack,serum visfatin level of group B and group C was significantly higher than that of group A,and the level of serum visfatin of group C was significantly higher than that of group B,the difference being significant (P < 0.05). After treatment,serum visfatin over-expression was improved in both conventional treatment subgroup and Qileng Decoction subgroup of groups B and C at various time points (P< 0.05 compared with that before treatment), and the improvement in Qileng Decoction subgroup was superior to that in conventional treatment subgroup (P < 0.05). (2)At the end of treatment, IMT was improved in conventional treatment subgroup and Qileng Decoction subgroup of groups B and C (P < 0.05 compared with that before treatment), and the improvement in Qileng Decoction subgroup was superior to that in conventional treatment subgroup (P < 0.05). (3) The total effective rate for PS improvement of conventional treatment subgroup in groups B and C was 74.3％,68.6％ respectively,and that of Qileng Decoction subgroup in groups B and C was 94.4％, 91.7％ respectively, indicating that Qileng Decoction subgroup had better effect on improving PS than conventional treatment subgroup(P < 0.05). Conclusion Qileng Decoction exerts certain effect on regulating the over-expression of serum visfatin and improving the degree of carotid atherosclerosis in AACI patients.
ABSTRACT
Objective: To evaluate the effects and partly mechanism of Qileng decoction(QLD,芪棱汤) resisting focal cerebral ischemia/reperfusion(I/R) injury in rats by apoptosis and signal transduction pathway.Methods: The rats were randomly divided into three groups including sham operation group,normal saline(NS) control group and QLD group.The model of focal cerebral I/R injury was induced by using modified thread embolizing in rats.Rats were evaluated by neurologic function score at 2 hours after ischemia and 2,4,6,12,24 and 48 hours after cerebral reperfusion,and the pathological changes of nerve cells and mitochondria ultrastructure at pallium and hippocampus CA1 region were observed at 24 hours after reperfusion.Immunohistochemical method was performed to examine the expression of cytochrome C(cyt C) and caspase-9 at different time points after reperfusion.Apoptosis of nerve cells in ischemic penumbra(IP) was also characterized by terminal deoxynucleotidyl-transferase mediated dUTP-biotin nick end labeling(TUNEL) method.Results: Compared with NS control group,neurologic function scores at different reperfusion time points were improved and the pathological changes were ameliorated at 24 hours after cerebral I/R in QLD group.Mitochondria hydropsia was alleviated,mitochondrial cristae fragmentation and granulum basale shedding were diminished,and mitochondrial basical morphology was retained.Meanwhile,apoptosis index(AI) was decreased and the expressions of cyt C and caspase-9 were reduced in IP in QLD group.Conclusion: QLD intervenes in mitochondria mediated and caspase-9 dependent apoptopic pathway.QLD lowers AI and plays a role of protecting nerve by maintaining mitochondrial basical form,stabilizing mitochondrial membrane and inhibiting the release of cyt C and activation of caspase-9.The above actions are possibly some parts of mechanisms of QLD resisting focal cerebral I/R injury.