Aortic Valve ; Fibroma ; Heart Neoplasms ; Humans

Objective To observe the effects of icarisid Ⅱ (ICS Ⅱ)on cognitive deficits and expression of synaptophysin(SYN)in chronic cerebral hypoperfusion(CCH)rat models.Methods 40 male SD rats were randomly divided into four groups:normal group,sham operation group,model group and ICSⅡgroup.The model was established by permanent bilateral common carotid artery occlusion(BCCAO).ICS Ⅱ group was administered ICS Ⅱ at a dose of 8mg·kg -1 ·d -1 by gavage on 1st day after modeling.Sham group and CCH group were injected double -distilled water.The escape latency(s)and spatial probe times were measured by water maze test.Then,the morphology change and expression of SYN in hippocampal were assayed by HE and immunohistochemistry analysis.Results At the 1st month and 2nd month,the escape latency in the model group[(40.02 ±4.95)s,(42.29 ±5.75)s]were significantly prolonged compared with the sham operation group[(26.43 ±2.68)s,(26.84 ±2.06)s](t =4.89,5.06,all P <0.05).And those in the ICS Ⅱ group[(30.58 ±3.03)s,(29.19 ±4.23)s]were significantly decreased compared with the model group(t =3.63,4.10,all P <0.05).The space probe times in the model group[(2.6 ±0.89)times, (2.40 ±1.14)times]were significantly reduced compared with the sham operation group[(6.00 ±2.16)times, (5.75 ±2.16)times](t =3.23,4.18,P <0.05).And those in the ICS Ⅱ group[(4.40 ±1.34)times,(5.00 ± 1.58)times]were significantly increased compared with the model group (t =2.49,2.98,all P <0.05).The average optical density of SYN in hippocampal in the model group[CA1:(0.121 ±0.009),(0.122 ±0.008);CA3:(0.172 ± 0.028),(0.173 ±0.021 )]were significantly reduced compared with the sham operation group[CA1:(0.131 ± 0.006),(0.136 ±0.007);CA3:(0.218 ±0.035),(0.204 ±0.018)](t =2.43,2.53,3.12,2.34,P <0.05). Those in the ICS Ⅱ group[CA1:(0.131 ±0.006),(0.132 ±0.006);(0.212 ±0.02),(0.208 ±0.022)]were significantly increased compared with model group(t =2.41,2.41,2.31,2.77,all P <0.05).However,there was no statistically significant difference of those index between the normal group and sham operation group(P >0.05 ). Conclusion ICS Ⅱ can improve the cognitive deficits in CCH rat models and this effect may be associated with increased expressions of SYN in hippocampal.

Objective To observe the effect of IcarisideⅡ (ICSⅡ) on spatial learning and memory impairments and axonal regeneration induced by chronic cerebral hypoperfusion (CCH) in rats.Methods 90 male SD rats were randomly divided into normal group,sham operation group,CCH group and ICS Ⅱ low,middle and high-dose treatment groups.The chronic cerebral hypoperfusion model was established by permanent bilateral common carotid artery occlusion.Then these rats in ICS Ⅱ low,middle and high-dose treatment groups were given ICS Ⅱ4,8 and 16 mg/(kg · d) by gavage on the 1st day after modeling.There were 5 rats in every group at each observing time(4,8 and 12 week).Morris water maze experiment was utilized to assess the escape latency and the target quadrant residence time while HE and immunohistochemistry analysis were applied to test the morphology change and expressions of GAP-43,MAP-2 and Nogo-A in hippocampal CA 1.Results Compared with those of sham operation groups at 4,8 and 12 week respectively,the escape latency in CCH group were significantly prolonged(40.02±4.95) s,(42.29±5.75) s,(53.68±6.14) s vs (26.43±2.68) s,(26.84±2.06) s,(31.53±4.12) s,P＜0.05;the target quadrant residence time were significantly reduced(28.53±2.40) s,(28.02±4.28) s,(22.60±4.03) s vs (33.34±2.89) s,(33.31 ±4.14) s,(31.63±2.20)s,P＜0.05);the expressions of GAP-43 and Nogo-A were increased with that of MAP-2 reduced(P＜0.05).Meanwhile,the neuropathological changes with more denatured neurons and less normal neurons were found in hippocampal CA1.However,compared with those of CCH group,the escape latency of ICS Ⅱ middle and high-dose groups (30.58±3.03) s,(29.19±4.23) s,(38.77±5.80) s;(28.90±2.98) s,(26.91 ±6.63) s,(36.51 ±3.98) s) were shortened (P＜0.05);the target quadrant residence time (32.54± 3.41) s,(32.69±3.47) s,(28.27±3.57) s;(32.69±3.54) s,(33.20±4.29) s,(28.07±4.04) s) were increased (P＜ 0.05);the expression of Nogo-A was decreased while those of GAP-43 and MAP-2 were conversely increased (P＜0.05).Moreover,few denatured neurons were observed in hippocampal CA1.But there were no differences for those indexs between CCH group and ICS Ⅱ low-dose treatment groups (P＞0.05).Compared with those in 8 week and 4 week,the escape latency and the target quadrant residence time were prolonged and reduced with the expression of Nogo-A increased in all groups except normal group and sham operation group(P＜0.05),the expressions of GAP-43 and MAP-2 were decreased in CCH group and ICS Ⅱ low-dose treatment group(P＜0.05),but there were no significant differences in ICS Ⅱ middle and high-dose treatment groups at 12 week(P＞0.05).However,there were no statistical significance of all indexes between 8 week and 4 week(P＞0.05).Conclusion ICS Ⅱ can improve the spatial learning and memory in chronic cerebral hypoperfusion rats,which may be achieved by neuroprotective effects and reducing the expression of Nogo-A consequently promotes the regeneration of axons.