ABSTRACT
AIM To observe the oxidant stress and opoptotic effects of anisodine hydromide (AH) on chronic cerebral hypoperfusion (CCH) rats.METHODS In vivo CCH models were established in adult male SpragueDawley rats by permanent ligation of bilateral common carotid arteries [two-vessel occlusion (2-VO)] surgery.Rats were randomly divided into six groups,sham group,model group,positive group of n-butylphthalide and sodium chloride injection,and AH groups (1.2 mg/kg high-dose group,0.6 mg/kg medium-dose group,and 0.3 mg/kg low-dose group).Antioxidant indices including the activity of SOD,CAT,LDH and iNOS and the content of GSH and NO were measured.In the in vitro trial,PC12 cells were divided into control group,model group,positive group of n-butylphthalide,and AH groups (100 μmol/L high-dose group,50 μmol/L mediumdose group,and 25 μmol/L low-dose group),and the hypoxic models were established by treating PC12 cells with CoCl2.The cells had their release of NO and LDH detected,their cellular apoptosis determined by Hochest 33342 fluorescence staining,and the expression of P53 protein identified by IF (immunofluorescence) and Western blotting method.RESULTS The in vivo trial revealed AH's enhancement in serum SOD activity and inhibition in serum iNOS activityof the CCH rats,and its power in the cerebral GSH and LDH release reduction.The in vitro trial showed the resultant lower LDH and NO release,decreased number of neuro-apoptosis,and inhibited P53 pro tein expression after AH intervention.CONCLUSION The antioxidant and antiapoptotic effects of AH on CCH rats may be associated with down regulation of P53 protein.
ABSTRACT
Objective To explore the expression level and possible reasons of Tau protein in Beagle dog model of ischemic cerebral white matter(WM) demylination.Methods Sixteen adult Beagle dogs were divided into the sham operation group(A) and observation group B,C and D according to the completely random mumber table method,4 cases in each group.Different.degrees of cerebral ischemia animal models were established by 4-vessel occlusion(4-VO) method.The bilateral ventricle edge white matter (WM) was selected.The oligodendrocyte precursors(OPCs) were labeled by NG2.The mature oligodendrocytes(Ols) were labeled by CNPase.Tau,NG2 and CNPase were detected by using the immunohistochemical method.The expression level was quantified by the mean optical value.The correlation among Tau,NG2 and CNGase was analyzed by adopting the Pearson linear correlation analysis.Results The HE staining showed obvious changes of WM demylination after chronic cerebral ischemic.The scores after LFB staining in the group A,B,C and D were(0.75 ± 0.71) points,(1.38 ± 0.06) points,(1.63 ± 0.52) points and (1.88 ± 0.64)points.Compared with the group A,the scores in the group B,C and D were much higher(P＜0.05).Compared with the group A,the expression levels of Tau protein and NG2 were significantly increased(P＜0.05),while the CNPase expression level was significantly decreased(P＜0.05).The Pearson correlation analysis showed that Tau expression level was positively correlated with the NG2 expression level(r=0.277,P=0.006);Tau and NG2 were negatively correlated with the CNPase level(r=-0.303,-0.402,P=0.003,0.001).Conclusion The increase of Tau expression in Beagle dog model of ischemic cerebral WM demylination may be related to the differentiation dysmaturity of OPCs.
ABSTRACT
Objective To study the effect of endothelial progenitor cells on the behavior of chronic cerebral ischemic rats. Methods Adult rats were treated using the protocol of chronic cerebral ischemic model. Then translated the endothelial progenitor cells in vein to them, and Morris water maze was carried out to test the learning and merrory ability of the rats. The cell proliferation, vascular distribution and the plasma VEGF levels were day of 2nd to 5th of experimental group ( EPC group ) were significantly shorter than the control group ( PBS group), which were(44.45 ±9.44)s,(38.32±1.51)s,(34.95 ±6.76)s,(24.46 ±5.47)s and (52.79±6.47 ) s, ( 43.15 ± 11.21 ) s, ( 50.29 ± 11.41 ) s, ( 53.75 ± 7.35 ) s, (P ＜ 0.01 ) respectively. The time of EPC group spend in the first quadrant were significantly longer than that of the PBS group, which were (26. 76 ±of the EPC group( 26.8 ± 5.76 ) was higher than that of the conrespondering areas in the control group( 12.17 ±ments of capillaries were (P＜0.05) shorter in the PBS groups( (3.4 ±0.24) μm) than in the EPC groups( (2.8± 0.2 )μm) significantly, EPC group could significantly (P ＜ 0.05 ) increased the number of branch points in the boundary regions of ischemia compared with the number in the PBS group (respectively (210. 1 ± 13.80 ) and (164.2 ± 12.3 )). Three-dimensional cerebral vessel surface area in the ipsilateral hemisphere significantly increased in the EPC group compared with the PBS group (respectively (84365 ± 3897 )μm2/0. 002mm3 and group in the plasma VEGF levels ( ( 63.91 ± 6.71 ) pg/ml; ( 21. 81 ± 4.25 ) pg/ml, respectively (P ＜ 0.05, P ＜0.01 ). Conclusion There are positive behavioral effects of endotbelial progenitor cells in chronic cerebral ischemic rats. The possible mechanisns mavbe involve the nerve protection and regeneration of the vascular associated with the VEGF. The endothelial progenitor cells maybe have a great prospect in the therapy of chronic cerebral ischemic disease.