Resolvin D1 reduces deterioration of tight junction proteins by upregulating HO-1 in LPS-induced mice
Resolvin D1 reduces deterioration of tight junction proteins by upregulating HO-1 in LPS-induced mice
复制标题
Resolvin D1 通过上调 LPS 诱导的小鼠中的 HO-1 来减少紧密连接蛋白的恶化
DOI：
10.1038/labinvest.2013.80
复制
发表时间：
2013-07
影响因子：
5
通讯作者：
Xie W, Wang H, Wang L, Yao C, Yuan R, Wu Q.
中科院分区：
文献类型：
--
作者：
Xie W, Wang H, Wang L, Yao C, Yuan R, Wu Q.
急性肺损伤（ALI）和急性呼吸窘迫综合征（ARDS）的特点是肺通透性增加，死亡率高。Resolvin D1（RvD 1）具有较强的抗炎和促消退活性，可减轻ALI动物模型的肺水肿。然而，RvD 1对肺水肿的保护作用的机制仍然未知。本研究旨在探讨RvD 1对脂多糖（LPS）诱导的急性肺损伤（ALI）模型中紧密连接蛋白破坏导致通透性水肿的影响及其机制。以湿干比和伊文思蓝浸润评估肺水肿程度;免疫荧光染色和western blot检测紧密连接蛋白（TJ）occludin和紧密连接蛋白-1（ZO-1）表达;真实的时间PCR检测肺组织mRNA表达; TUNEL法检测肺屏障细胞凋亡。小鼠吸入LPS后24 h，肺湿干比和Evans蓝浸润表明RvD 1预处理可减轻肺水肿和肺毛细血管通透性。此外，RvD 1减弱LPS诱导的TJ蛋白ZO-1和occludin的降解显着。我们发现RvD 1增加血红素氧合酶-1（HO-1）的表达有助于保护TJ的恶化。此外，我们发现RvD 1可以减少LPS诱导的小鼠肺细胞凋亡。总之，RvD 1具有减轻肺水肿和恢复肺毛细血管通透性的能力，并且至少部分地通过上调HO-1表达来减少LPS诱导的小鼠ALI中TJ的破坏。
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is characterized by increased pulmonary permeability with high mortality. Resolvin D1 (RvD1), which has potent anti-inflammatory and pro-resolving activity, can attenuate pulmonary edema in the animal model of ALI. However, the mechanism underlying the protection of RvD1 on pulmonary edema is still unknown. Here we explore the effects and mechanism of RvD1 on the disruption of tight junction protein that results in the permeability edema in a model of lipopolysaccharide (LPS)-induced ALI. The severity of pulmonary edema was assessed by wet-to-dry rate and Evans blue infiltration; expressions of tight junction (TJ) proteins occludin and zona occludin-1 (ZO-1) were examined by immunofluorescence staining and western blot; mRNA in lung tissue was studied by real time-PCR; the TUNEL kit was performed for the detection of apoptosis of pulmonary barrier. Twenty-four hours after LPS inhalation by mice, wet-to-dry rate and Evans blue infiltration indicated that pretreatment with RvD1 relieved the pulmonary edema and pulmonary capillary permeability. Moreover, RvD1 attenuated the LPS-induced deterioration of TJ protein ZO-1 and occludin significantly. And we found that RvD1 increased heme oxygenase-1 (HO-1) expression contributed to the protection on the deterioration of TJs. In addition, we found that RvD1 could reduce pulmonary cellular apoptosis in LPS-induced mice. In conclusion, RvD1 possesses the ability that relieves the pulmonary edema and restores pulmonary capillary permeability and reduces disruption of TJs in LPS-induced ALI of mice, at least in part, by upregulating HO-1 expression.
登录
查看更多内容
影响因子：
3.4
作者：
Capaldo, Christopher T.;Nusrat, Asma
通讯作者：
Nusrat, Asma
DOI：
10.1084/jem.192.8.1197
发表时间：
2000-10-16
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Serhan CN;Clish CB;Brannon J;Colgan SP;Chiang N;Gronert K
通讯作者：
Gronert K
影响因子：
4
作者：
C. M. Itallie;James M. Anderson
通讯作者：
C. M. Itallie;James M. Anderson
影响因子：
8.8
作者：
通讯作者：
--
影响因子：
7.8
作者：
Simionescu, N;Simionescu, M;Palade, G E
通讯作者：
Palade, G E