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| 1 | Protection mechanism of deacetylase inhibitor on spleen of rats with severe hemorrhagic shock显示文摘Objective: To explore the protection and molecular mechanism of histone deacetylase inhibitors(HDACIs) on the spleen of rats with hemorrhagic shock. Methods: A total of 60 SPF male SD rats were selected for the modeling of severe hemorrhagic shock using the method of arterial and venous cannulation with the time-divided bleeding. The measurement of mean arterial blood pressure and blood lactic acid was used to verify the modeling. The modeled rats were randomly divided into shock group, shock+suberoylanilide hydroxamic acid(SAHA) group, shock+autogenous transfusion group, and shock+SAHA+autogenous transfusion group. Three hours after the treatment, the spleen of rats was collected and TUNEL method was employed to detect the apoptosis of spleen cells in each group. Afterwards, real-time PCR and western blot were employed to detect the expression of BCL-2, BAX, and caspass3 in the spleen of rats in each group. Results: A total of 55 rats had successful modeling of severe hemorrhagic shock, with success rate of 92%. Cell apoptosis in the severe hemorrhagic model group was the most serious. After the intervention of HDACIs and the autogenous transfusion, the tissue injury was a bit recovered. Cell apoptosis was least in the shock+SAHA+autogenous transfusion group(P<0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BCL-2 was significantly increased(P<0.05), with highest relative expression of BCL-2 in shock+SAHA+autogenous transfusion group(P<0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BAX was significantly decreased(P<0.05), with lowest relative expression of BAX in the intervention group of single HDACIs. The change in the expression of caspass3 was similar to BAX, namely the relative expression of caspass3 was significantly decreased after the intervention of HDACIs and the autogenous transfusion(P<0.05). Conclusions: HDACIs and autogenous transfusion can all protect the spleen injury because of the severe hemorrhagic shock. Its molecular mechanism may be related to the regulation on the expression of BCL-2/BAX and caspass3, which may affect the apoptosis process of cells. | Gao-Rong Deng Qiang Ling Bing-Hua Wu Yu-Ying Dong Xiang Gao Tai-Qiang Li Xin Miu Zong-Fang Li | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，6： | 2 |
| 2 | 组蛋白去乙酰化酶抑制剂对重度失血性休克大鼠生存情况的影响显示文摘目的观察组蛋白去乙酰化酶抑制剂(HDACIs)对重度失血性休克大鼠生存时间的影响。方法选择SD大鼠63只,采用股动静脉导管分时放血(60%)法,成功建立重度失血性休克模型48只,按照随机原则分三组:即软木酰苯胺氧肟酸(SAHA)组、丙戊酸(VPA)组和对照组。SAHA组采用SAHA 8 mg/kg静脉泵入,VPA组VPA30 mg/kg皮下注射,对照组用等量生理盐水静脉推注治疗。三组均采用BL-420F系统收集大鼠肢体导联心电图,分析各组的生存时间及12 h内生存率。结果本实验重度失血性休克大鼠建模成功率为76.19%(48/63)。对照组生存时间(7.04±0.97)h、12 h内生存率0,SAHA组分别为(11.86±2.35)、31.25%,VPA组分别为(10.56±1.56)h、12.50%。SAHA组、VPA组生存时间、12 h内生存率均高于对照组(P均<0.05),且SAHA组生存时间、12h内生存率高于VPA组(P均<0.05)。结论 HDACIs能明显延长重度失血性休克大鼠的生存时间,而且SAHA对失血性休克大鼠的生存保护作用优于VPA。 | 邓高荣 吴炳华 高翔 董玉莹 缪锌 黄巍 凌强 李宗芳 | 2015 | 山东医药2015，55，29： | 1 |
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