Hydrogen sulfide modulates sub-cellular susceptibility to oxidative stress induced by myocardial ischemic reperfusion injury
Hydrogen sulfide modulates sub-cellular susceptibility to oxidative stress induced by myocardial ischemic reperfusion injury
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DOI：
10.1016/j.cbi.2016.03.036
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发表时间：
2016-05-25
影响因子：
5.1
通讯作者：
Kurian, Gino A.
中科院分区：
文献类型：
--
作者：
Ansari, Shakila Banu;Kurian, Gino A.
在这项研究中，我们比较了H2S预处理（HIPC）和后处理（HPOC）对氧化应激的影响，氧化应激是心肌缺血再灌注损伤（I/R）的主要原因，在心肌的不同室，如线粒体旁边的亚群（IFM）和亚肌膜（SSM）线粒体）和微粒体组分在I/R损伤的大鼠心脏。结果表明，与I/R大鼠心脏相比，HIPC和HPOC处理的心脏显示出减轻的心肌损伤，增强的抗氧化酶活性和降低的TBARS水平在不同的细胞室。在HIPC和HPOC中，亚细胞组分的恢复程度（通过TBARS和GSH水平测量）均为以下降序：微粒体> SSM > IFM。总之，氧化应激介导的线粒体功能障碍是I/R损伤的主要原因之一，通过HIPC和HPOC治疗部分恢复，与IFM相比，SSM分数显著改善。(C)2016爱思唯尔爱尔兰有限公司版权所有。
In this study, we compared the impact of H2S pre (HIPC) and post-conditioning (HPOC) on oxidative stress, the prime reason for myocardial ischemia reperfusion injury (I/R), in different compartments of the myocardium, such as the mitochondria beside its subpopulations (interfibrillar (IFM) and sub-sarcolemmal (SSM) mitochondria) and microsomal fractions in I/R injured rat heart. The results demonstrated that compared to I/R rat heart, HIPC and HPOC treated hearts shows reduced myocardial injury, enhanced antioxidant enzyme activities and reduced the level of TBARS in different cellular compartments. The extent of recovery (measured by TBARS and GSH levels) in subcellular fractions, were in the following descending order: microsome > SSM > IFM in both HIPC and HPOC. In summary, oxidative stress mediated mitochondrial dysfunction, one of the primary causes for I/R injury, was partly recovered by HIPC and HPOC treatment, with significant improvement in SSM fraction compared to the IFM. (C) 2016 Elsevier Ireland Ltd. All rights reserved.