Near infrared light protects cardiomyocytes from hypoxia and reoxygenation injury by a nitric oxide dependent mechanism.
Near infrared light protects cardiomyocytes from hypoxia and reoxygenation injury by a nitric oxide dependent mechanism.
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DOI：
10.1016/j.yjmcc.2008.09.707
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发表时间：
2009-01
影响因子：
5
通讯作者：
Bienengraeber, Martin
中科院分区：
文献类型：
--
作者：
Zhang, Rong;Mio, Yasushi;Pratt, Philip F.;Lohr, Nicole;Warltier, David C.;Whelan, Harry I.;Zhu, Daling;Jacobs, Elizabeth R.;Medhora, Meetha;Bienengraeber, Martin
关键词：
利用近红外光（NIR）的光生物调节在各种疾病模型中提供细胞保护。以前，低能量激光器发出的红外光已被证明可以显着改善犬心脏缺血性损伤的恢复。本研究的目的是检验来自发光二极管的NIR（670 nm）对缺氧和再氧合诱导的心肌细胞损伤产生细胞保护的假设。此外，一氧化氮（NO）作为一个潜在的细胞介质的近红外光谱进行了研究。我们的研究结果表明，暴露于近红外线在复氧时保护新生大鼠心肌细胞和HL-1细胞的损伤，通过乳酸脱氢酶释放和MTT法评估。同样，凋亡指数，包括caspase 3活性，膜联蛋白结合和细胞色素c从线粒体释放到胞质溶胶中，在NIR处理后下降。NIR增加心肌细胞中的NO，并且NIR的保护作用被NO清除剂羧基PTIO和氧合血红蛋白完全逆转，但仅被NO合酶（NOS）抑制剂L-NMMA部分阻断。线粒体代谢，测量ATP合酶活性，增加了近红外，和NO诱导的抑制耗氧量与底物复合物I或复合物IV被逆转暴露于近红外。总之，这些数据提供了证据，保护心肌细胞缺氧和复氧损伤的NIR的方式是依赖于NO来源于NOS和非NOS来源。
Photobiomodulation with near infrared light (NIR) provides cellular protection in various disease models. Previously, infrared light emitted by a low-energy laser has been shown to significantly improve recovery from ischemic injury of the canine heart. The goal of this investigation was to test the hypothesis that NIR (670 nm) from light emitting diodes produces cellular protection against hypoxia and reoxygenation-induced cardiomyocyte injury. Additionally, nitric oxide (NO) was investigated as a potential cellular mediator of NIR. Our results demonstrate that exposure to NIR at the time of reoxygenation protects neonatal rat cardiomyocytes and HL-1 cells from injury, as assessed by lactate dehydrogenase release and MTT assay. Similarly, indices of apoptosis, including caspase 3 activity, annexin binding and the release of cytochrome c from mitochondria into the cytosol, were decreased after NIR treatment. NIR increased NO in cardiomyocytes, and the protective effect of NIR was completely reversed by the NO scavengers carboxy-PTIO and oxyhemoglobin, but only partially blocked by the NO synthase (NOS) inhibitor L-NMMA. Mitochondrial metabolism, measured by ATP synthase activity, was increased by NIR, and NO-induced inhibition of oxygen consumption with substrates for complex I or complex IV was reversed by exposure to NIR. Taken together these data provide evidence for protection against hypoxia and reoxygenation injury in cardiomyocytes by NIR in a manner that is dependent upon NO derived from NOS and non-NOS sources.
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影响因子：
15.9
作者：
GOTTLIEB, RA;BURLESON, KO;ENGLER, RL
通讯作者：
ENGLER, RL
DOI：
10.1073/pnas.85.14.4971
发表时间：
1988-07-01
影响因子：
11.1
作者：
CHANCE, B;LEIGH, JS;BORETSKY, R
通讯作者：
BORETSKY, R
DOI：
10.1196/annals.1341.022
发表时间：
2005-01-01
期刊：
COMMUNICATIVE CARDIAC CELL
影响因子：
--
作者：
Honda, HM;Korge, P;Weiss, JN
通讯作者：
Weiss, JN
影响因子：
5
作者：
Jones, SP;Bolli, R
通讯作者：
Bolli, R
影响因子：
6.7
作者：
Conlan, MJ;Rapley, JW;Cobb, CM
通讯作者：
Cobb, CM