Partial liquid ventilation with var

Partial liquid ventilation with various types of perfluorocarbon (PFC) has been
shown to be beneficial in treating acute lung injury, a clinical outcome that may
involve the anti-inflammatory activity of PFC. FC-77 is a type of PFC with
relatively higher vapor pressure and evaporative loss than other PFCs during
partial liquid ventilation. Overproduction of nitric oxide (NO) by inducible
nitric oxide synthase (iNOS) has been proposed to play a crucial role in the
pathogenesis of inflammatory diseases. However, whether the iNOS/NO pathway is
affected by FC-77 is unknown. Thus, the aim of this study was to investigate
whether FC-77 inhibits iNOS expression and NO production in lipopolysaccharide
(LPS)-treated RAW 264.7 macrophages. We found that treatment with FC-77
significantly attenuated LPS-induced iNOS expression/activity and production of
NO and reactive oxygen species (ROS). FC-77 also attenuated LPS-induced
pro-inflammatory cytokine formation, but enhanced interleukin-10 production.
Furthermore, the LPS-induced degradation of cytosolic IkappaB-alpha and
activation of nuclear transcription factor-kappaB (NF-kappaB) were also inhibited
by FC-77. In conclusion, the present study is the first to demonstrate that FC-77
decreases LPS-induced NO production in macrophages, which may be associated with
the suppression of pro-inflammatory cytokines, and ROS production, as well as
NF-kappaB activation. These results also provide a novel explanation for its
anti-inflammatory activity.

結果 (中文) 1:

部分液体通气与各种类型的全氟化碳 (PFC) 已证明是有益的治疗急性肺损伤，一个可能的临床结果涉及的抗炎活性的 PFC FC-77 段是一新型的有源 PFC相对较高的蒸气压力和比其他全氟化碳过程中的蒸发损失部分液体通气。生产过剩的诱导型一氧化氮 (NO)提出了一氧化氮合酶 (iNOS) 在中发挥关键作用炎性疾病的发病机制。然而，iNOS/无通路受 FC 77 是未知的。因此，本研究的目的是探讨是否 FC-77 抑制 iNOS 的表达和 no 在脂多糖(LPS)-治疗原始 2.647 巨噬细胞。我们发现治疗与 FC 77大大减毒的 LPS 诱导 iNOS 的表达活性和生产不和活性氧 (ROS)。FC-77 也减毒 LPS 诱导炎性细胞因子的形成，但增强白细胞介素-10 的产生。此外，胞浆 IkappaB-α LPS 诱导降解和激活的核转录因子 （NF-活化因子受） 均有抑制作用通过 FC-77。总之，本研究是首次证明，FC 77减小 LPS 诱导 NO 在巨噬细胞，可能与相关的生产炎性细胞因子和活性氧的产生，抑制以及NF-活化因子受激活。这些结果也提供了一种新型的解释其抗炎活性。

結果 (中文) 3:

部分液体通气与不同类型的氟碳（PFC）已显示有利于治疗急性肺损伤，一个可能的临床结果涉及PFC FC-77的抗炎活性是一种PFC相对较高的蒸汽压力和蒸发损失比其他PFCs在部分液体通气。诱导性一氧化氮（NO）的产生一氧化氮合酶（iNOS）已经提出了在发挥着至关重要的作用炎症性疾病的发病机制。然而，无论是NO通路受FC-77是未知的。因此，本研究的目的是调查无论FC-77抑制脂多糖iNOS的表达和NO的产生（脂多糖）治疗的生264.7巨噬细胞。我们发现，治疗与FC-77能显著抑制LPS诱导的iNOS的表达/活动和生产NO和活性氧（活性氧）。FC-77也减轻LPS诱导的促炎性细胞因子的生成，但增强白介素-10。此外，LPS诱导的胞浆IKB-α的降解核转录因子κB（NF-κB）活性受到抑制通过FC-77。总之，目前的研究表明，FC-77第一降低脂多糖诱导的巨噬细胞NO的产生，这可能与相关联的抑制促炎性细胞因子，和活性氧的产生，以及NF-κB的活化。这些结果还提供了一个新的解释，其抗炎活性。