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首页> 外文期刊>World Journal of Gastroenterology >Nitric oxide synthase and heme oxygenase expressions in human liver cirrhosis.
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Nitric oxide synthase and heme oxygenase expressions in human liver cirrhosis.

机译：人肝硬化中一氧化氮合酶和血红素加氧酶的表达

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AIM: Portal hypertension is a common complication of liver cirrhosis. Intrahepatic pressure can be elevated in several ways. Abnormal architecture affecting the vasculature, an increase in vasoconstrictors and increased circulation from the splanchnic viscera into the portal system may all contribute. It follows that endogenous vasodilators may be able to alleviate the hypertension. We therefore aimed to investigate the levels of endogenous vasodilators, nitric oxide (NO) and carbon monoxide (CO) through the expression of nitric oxide synthase (NOS) and heme oxygenase (HO). METHOD: Cirrhotic (n=20) and non-cirrhotic (n=20) livers were obtained from patients who had undergone surgery. The mRNA and protein expressions of the various isoforms of NOS and HO were examined using competitive PCR, Western Blot and immunohistochemistry. RESULTS: There was no significant change in either inducible NOS (iNOS) or neuronal NOS (nNOS) expressions while endothelial NOS (eNOS) was up-regulated in cirrhotic livers. Concomitantly, caveolin-1, an established down-regulator of eNOS, was up-regulated. Inducible HO-1 and constitutive HO-2 were found to show increased expression in cirrhotic livers albeit in different localizations. CONCLUSION: The differences of NOS expression might be due to their differing roles in maintaining liver homeostasis and/or involvement in the pathology of cirrhosis. Sheer stress within the hypertensive liver may induce increased expression of eNOS. In turn, caveolin-1 is also increased. Whether this serves as a defense mechanism against further cirrhosis or is a consequence of cirrhosis, is yet unknown. The elevated expression of HO-1 and HO-2 suggest that CO may compensate in its role as a vasodilator albeit weakly. It is possible that CO and NO have parallel or coordinated functions within the liver and may work antagonistically in the pathophysiology of portal hypertension.
机译：目的：门脉高压症是肝硬化的常见并发症。肝内压力可以通过几种方式升高。影响脉管系统的异常结构，血管收缩器的增加以及从内脏内脏到门脉系统的循环增加都可能是造成这种情况的原因。因此，内源性血管扩张药可能能够缓解高血压。因此，我们旨在通过表达一氧化氮合酶（NOS）和血红素加氧酶（HO）来研究内源性血管扩张剂，一氧化氮（NO）和一氧化碳（CO）的水平。方法：从接受手术的患者中获取肝硬化（n = 20）和非肝硬化（n = 20）肝脏。使用竞争PCR，Western Blot和免疫组织化学检查NOS和HO各种同工型的mRNA和蛋白质表达。结果：肝硬化性肝组织中的内皮型NOS（eNOS）上调，诱导型NOS（iNOS）或神经元NOS（nNOS）的表达均无明显变化。随之而来的是，已经建立的eNOS下调蛋白caveolin-1被上调。发现诱导型HO-1和组成型HO-2在肝硬化肝中显示增加的表达，尽管在不同的位置。结论：NOS表达的差异可能是由于它们在维持肝脏稳态和/或参与肝硬化病理过程中的不同作用。高血压肝脏内的纯粹压力可能诱导eNOS表达增加。反过来，caveolin-1也增加了。尚不清楚这是否是预防进一步肝硬化的机制或是肝硬化的结果。 HO-1和HO-2的高表达表明，尽管CO可能微弱，但CO可以补偿其作为血管扩张剂的作用。一氧化碳和一氧化氮可能在肝内具有平行或协调的功能，并且可能在门脉高压的病理生理学中起相反的作用。

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