细胞色素

The induction of TRAIL sensitivity by HCV core protein was due to facilitating activation of caspase-8 and its downstream pathway, and enhancing Bid processing, breakdown of mitochondrial transmembrane potential as well as cytochrome c release.

我们进而发现细胞对TRAIL敏感性的改变，是由於C型肝炎病毒的核心蛋白会促进caspase-8及其下游讯息分子的活化，这当中包括Bid活化、粒腺体膜电位的下降以及细胞色素c的释放。

In vitro experiments, the expression of cytochrome C in glial cells was detected by western blot and immunofluorescence cytochemistry.

体外实验中，免疫蛋白印迹法和免疫荧光细胞化学法测定大鼠神经胶质细胞细胞色素C的表达。

ObjectiveTo evaluate the effects of caspase-3 activation and cytochrome c release in cerebral ischemia reperfusion induced neuronal cell death.

目的探讨Caspase-3激活和细胞色素c释放在脑缺血再灌注损伤后神经元细胞凋亡中的作用。

Western blotting showed less expression of cytochrome c in Hsp90 overexpression system than in control.

Western blotting检测Hsp90细胞中细胞色素c的表达与对照组相比明显减少。

However, the conflicting findings exist between the Diptera and Lepidoptera on the cytochrome C release from the mitochondria to cytosol –important event in mitochondrial-mediated apoptosis signaling pathway.

但线粒体介导细胞凋亡信号转导途径中最终重要的事件-——细胞色素C从线粒体的释放，在双翅目昆虫和鳞翅目昆虫之间存在相互矛盾的研究结果。

Thus , nitric oxide inhibits cytochrome oxidase activity in neurones and glia , resulting in down-regulation of mitochondrial energy production .

在神经元和神经胶质细胞中，一氧化氮抑制细胞色素C氧化酶的活性，抑制线粒体能量产生。

Thus , nitric oxide inhibits cytochrome c oxidase activity in neurones and glia , resulting in down-regulation of mitochondrial energy production .

在神经元和神经胶质细胞中，一氧化氮抑制细胞色素C氧化酶的活性，抑制线粒体能量产生。

In addition, SW480 and HCT116 cells were treated with deoxycholic acid for 15, 30, 45, 60, 90 and 120 minutes. It was found that the deoxycholic acid treated cells showed an elevation of ATP activity by 12.35 %, 20.08 %, 29.69 %, 33.56 %, 45.85 %, 54.32 %, respectively. While the HCT116 treated cells, showed an elevation of ATP activity by 3.69 %, 5.59 %, 8.52 %, 12.26 %, 16.52 %, 19.71%, respectively.From the experiments conducted using the cell lines described above, it was further confirmed that genes CYP7A1 (cytochrome P450, family 7, subfamily A, polypeptide 1), AKR1D1 (aldo-keto reductase family 1, member D1), ALDH1A1 (aldehyde dehydrogenase 1 family, member A1), BAAT (bile acid Coenzyme A: amino acid N-acyltransferase), ABCA1 (ATP-binding cassette, sub-family A, member 1), APOC3 (apolipoprotein C-III), LIPA, LIPE (lipase, hormone-sensitive), PTGER2 (prostaglandin E receptor 2) and PTGS2 (prostaglandin-endoperoxide synthase 2) were up-regulated.

此外，为了证实其脂肪代谢产物胆酸对细胞癌化的影响，亦使用SW480和HCT116细胞株，经由脱氧胆酸在15分钟、30分钟、45分钟、60分钟、90分钟和120分钟处理后，其细胞增生比率分别有12.35%，20.08%，29.69%，33.56%，45.85%和54.32%(p.05)以及3.69%，5.59%，8.52%，12.26%，16.52%和19.71%(p.05)上升情形，并从这些细胞株进一步证实CYP7A1(细胞色素P450-7A1)、AKR1D1(醇醛酮还原酶-1-D1)、ALDH1A1(醛脱氢酶-1-A1)、BAAT(胆酸辅酶A：氨基酸N-醯基转移酶)、ABCA1(三磷酸腺苷结合盒转运体A1)、APOC3、LIPA、LIPE(脂肪酶/激素敏感脂肪酶)、PTGER2(前列腺素E受体2)和PTGS2(前列腺素内过氧化物合成酶2)等基因表现皆有呈现向上调控的情形。

In PN group, the light microscopic findings included inflammation cells infiltration and hepatic steatosis, and electron microscopy showed vacuole change in cytosol and rarefactive microvillus in micro-bile duct. Conclusion PN-associated liver dysfunction was related with hepatocyte oxidative injury and apoptosis.

PN肝脏损伤机制可能是PN某些配方成分应用中，脂质过氧化导致肝细胞氧化损伤，同时损伤线粒体膜，促使线粒体膜通透性增加，释放细胞色素C等凋亡相关因子，激发caspase-3等级联反应，产生肝细胞凋亡，导致肝损伤。

The OXPHOS electron transfer chain (mitochondrial respiration chain) is located on the inner membrane of mitochondrion and comprising of four large trans-membrane protein complexes (mitochondrial respiratory Complex I, II, III and IV) as well as ubiquinone between Complex I/II and III and cytochrome c between Complex III and IV.

摘 要：线粒体作为真核细胞的重要&能量工厂&，是细胞进行呼吸作用的场所，呼吸作用包括柠檬酸循环和氧化磷酸化两个过程，其中氧化磷酸化过程的电子传递链位于线粒体内膜上，由四个相对分子质量很大的跨膜蛋白复合体(I、II、III、和IV)、介于I/II 与III之间的泛醌以及介于III 与IV之间的细胞色素c共同组成。

But we don't care about Battlegrounds.

但我们并不在乎沙场中的显露。

Ah! don't mention it, the butcher's shop is a horror.

啊！不用提了。提到肉，真是糟透了。