Dynamic Change of Hydrogen Sulfide After Traumatic Brain Injury and its Effect in Mice

Dynamic Change of Hydrogen Sulfide After Traumatic Brain Injury and its Effect in Mice
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DOI:
10.1007/s11064-013-0969-4
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发表时间:
2013-01
影响因子:
4.4
通讯作者:
Mingyang Zhang;H. Shan;Tao Wang;Weili Liu;Yaoqi Wang;Long Wang;Lu Zhang;P. Chang;W. Dong-W.
Mingyang Zhang;H. Shan;Tao Wang;Weili Liu;Yaoqi Wang;Long Wang;Lu Zhang;P. Chang;W. Dong-W.
中科院分区:
医学3区
文献类型:
--
作者:
Mingyang Zhang;H. Shan;Tao Wang;Weili Liu;Yaoqi Wang;Long Wang;Lu Zhang;P. Chang;W. Dong-W.

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硫化氢(H_2S)是一种脂溶的、内源性产生的气体信使分子,统称为气体递质。在过去的几十年里,气体递质在各种组织和细胞损伤模型中作为有效的细胞保护媒介出现。在本研究中,我们建立了成年小鼠减重创伤性脑损伤(TBI)模型,并探讨了脑损伤后H_2S的变化及其在脑损伤发病机制中的可能作用。用逆转录聚合酶链式反应(RT-β)检测小鼠脑内硫化氢产生酶--胱硫醚-DNA合成酶(CBS)的表达。RT-PCR结果显示,脑损伤后CBS在小鼠大脑皮层和海马区的表达下调。Western印迹分析表明,CBS存在于正常小鼠的大脑皮层和海马区。它逐渐下降,达到最低水平,然后上升。脑损伤后大脑皮层和海马区硫化氢含量呈动态变化,与CBS基因和蛋白的表达平行。此外,用硫化氢供体(NaHS)预处理对脑损伤后的神经元有保护作用。值得注意的是,以损伤体积评估,硫化氢供体NaHS可减轻脑损伤。这些数据表明,硫化氢可能具有治疗神经元损伤的潜力。
Hydrogen sulfide (H2S) is a lipid-soluble, endogenously produced gaseous messenger molecule collectively known as gasotransmitter. Over the last several decades, gasotransmitters have emerged as potent cytoprotective mediators in various models of tissue and cellular injury. In this study, we performed a weight-drop traumatic brain injury (TBI) model in adult mice and investigated changes of H2S and its possible role in the pathogenesis after TBI. Expression of Cystathionine-β-synthase (CBS) mRNA as H2S-producing enzymes in mouse brain was determined by reverse transcriptase-polymerase chain reaction (RT-PCR). From the results of RT-PCR, it was found that the expression of CBS was down-regulated in mouse brain cortex and hippocampus after brain injury. Western blot analysis revealed that CBS was present in normal mouse brain cortex and the hippocampus. It gradually decreased, reached its lowest level and then increased. Hydrogen sulfide in the cortex and hippocampus exhibited dynamic changes after brain injury, in parallel with CBS mRNA and protein expression. Moreover, pretreatment with the H2S donor (NaHS) could protect the neuron against the injury induced by TBI. Noticeably, the H2S donor NaHS could reduce TBI-induced injury assessed with lesion volume. These data suggested that H2S may have a therapeutic potential against neuron damage.