THE ROLE OF NITRIC OXIDE AND EICOSANOIDS IN LUPUS NEPHRITIS

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者的研究机构。 本研究的目的是探讨一氧化氮和反应性中间产物在狼疮性肾炎（LN）中的作用。 一氧化氮（NO）是一种在血液中发现的短寿命分子，可引起炎症。 狼疮患者产生异常数量的这种分子，并且认为NO至少部分负责打开导致肾脏损伤的炎症。 具体来说，NO可能会增加肾脏中称为类花生酸的有害物质的水平，并降低其保护性物质的水平。 目前尚不清楚的是，LN中异常高水平的NO是否最终导致LN中的炎症或类花生酸的改变，或者它们是否仅仅是已经存在的炎症的标志物。 NO如何导致狼疮损伤或改变类花生酸水平也不清楚。 这项研究旨在通过在狼疮活动和不活动期间跟踪狼疮患者一年以上来回答其中一些问题，以了解疾病活动是否与NO，活性氧中间体和传统炎症标志物水平有关。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The purpose of this study is to examine the role of nitric oxide and reactive intermediate production in lupus nephritis (LN). Nitric oxide (NO) is a short-lived molecule found in the blood that turns on inflammation. Lupus patients produce abnormal amounts of this molecule, and it is thought that NO is at least partly responsible for turning on the inflammation that causes damage to the kidneys. Specifically, NO may increase the level of harmful and reduce the level of protective substances in the kidney called eicosanoids. What remains unclear is whether the abnormally high levels of NO in LN are ultimately responsible for the inflammation or alterations in eicosanoids in LN or whether they are merely markers for already existing inflammation. How NO causes damage in lupus or alters the levels of eicosanoids is also unclear. This study is designed to answer some of these questions by following lupus patients over one year during periods of lupus activity and inactivity to see if disease activity relates to levels of NO, reactive oxygen intermediates, and traditional markers of inflammation.