李燕 高操 郑利 司马欣元 武阳.NaHS抑制创伤出血性休克导致的大鼠心肌组织的凋亡[J].现代生物医学进展英文版,2014,14(11):2047-2051. |
NaHS抑制创伤出血性休克导致的大鼠心肌组织的凋亡 |
Exogenous H2S Protects Cardiac Tissue Through Inhibiting Apoptosisin a Traumatic-hemorrhagic Shock Rat Model |
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DOI: |
中文关键词: 硫化氢;创伤出血性休克;心肌;凋亡;Bcl-2 Bax Caspase-8 |
英文关键词: Traumatic-hemorrhagic shock Hydrogen Sulfide Apoptosis Bcl-2 Bax Caspase-8 |
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中文摘要: |
目的:创伤导致的失血性休克是临床上常见的导致死亡的原因之一,传统的快速扩容措施会导致缺血- 再灌注损伤,诱发炎
症反应和组织细胞的凋亡坏死;新型气体信号分子硫化氢(H2S)具有抗炎、促进心血管增生等多种生理保护功能,在此实验中我们
探索了新型气体信号分子硫化氢(H2S)对出血性休克大鼠心肌的保护作用。方法:复制雄性SD大鼠出血性休克模型:复制大鼠腹
中正切口造成创伤模型,然后经右侧股动脉插管放血,造成失血性休克,右侧股静脉建立液体通道准备复苏,给药组大鼠经腹腔
给予NaHS(28 umol/kg),经左侧股动脉插管至左心室监测大鼠血流动力学的影响;取大鼠复苏后2 h静脉血,测量血清肌酸激酶
(CK)及乳酸脱氢酶(LDH)水平,比较各组心肌酶改变。以蛋白印记法观察大鼠心肌组织凋亡相关因子Bcl-2、Bax、与Caspase-8
的表达变化。结果:外源性H2S 对创伤性休克大鼠的血流动力学指标有不同程度的改善,保护了创伤休克导致的心肌细胞的损
伤,并上调了大鼠心肌组织中抗凋亡蛋白Bcl-2的表达,下调了促凋亡蛋白Bax 及Caspase-8 的表达。结论:外源性硫化氢可能通
过抑制凋亡途径来保护创伤性休克导致大鼠的心肌组织的损伤,从而起到保护作用。 |
英文摘要: |
Objective:Trauma induced hemorrhagic shock is a common death reason clinically. Traditional rapid fluid infusion
method will result in ischemia-reperfusion injury, inflammation response, and apoptosis even necrosis in cells or tissues. The new
gaseous signaling molecule H2S possesses kinds of physiological protective funciotns such as anti-infammation and pro-angiogenesis. In
the present study, we explored the protective effects of H2S on a mimetic traumatic-hemorrhagic shock rat model. Methods:Duplicate
male SD rats traumatic-hemorrhagic shock models, hemodynamic data was recorded by inserting a PE-50 catheter to left femoral artery
of the rats which were treated with NaHS (28 umol/kg) in advance. Two hours after injection NaHS, the rats' vein blood was obtained.
SerumCKand LDHlevelswere analyzed and Bcl-2, Bax and Caspase-8 in rat cardiac tissue were detected byWestern-blot assays. Results: Exogenous H2S improved rats' hemodynamic function, protected rats' cardiac tissue from traumatic-hemorrhagic shock, up-regulated expression
of Bcl-2 and down-regulated expression of the pro-apoptosis factors Bax and Caspase-8 in rats' cardiac tissue.Conclusion:Exogenous
H2S may exert cardio-protective effects through inhibiting apoptosis pathway. |
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