SIRT1 protects rat lung tissue against severe burn-induced remote ALI by attenuating the apoptosis of PMVECs via p38 MAPK signaling

被引:48
作者
Bai, Xiaozhi [1 ]
Fan, Lei [1 ]
He, Ting [1 ]
Jia, Wenbin [1 ]
Yang, Longlong [1 ]
Zhang, Jun [2 ]
Liu, Yang [1 ]
Shi, Jihong [1 ]
Su, Linlin [1 ]
Hu, Dahai [1 ]
机构
[1] Fourth Mil Med Univ, Xijing Hosp, Dept Burns & Cutaneous Surg, Xian 710032, Shaanxi, Peoples R China
[2] 205 Hosp Chinese Peoples Liberat Army, Dept Burn & Plast Surg, Jinzhou, Liaoning, Peoples R China
来源
SCIENTIFIC REPORTS | 2015年 / 5卷
基金
中国国家自然科学基金;
关键词
OXIDATIVE STRESS; ENDOTHELIAL-CELLS; VASCULAR-PERMEABILITY; RESVERATROL PROTECTS; OVINE MODEL; IN-VIVO; INJURY; SEPSIS; ANGIOGENESIS; MANAGEMENT;
D O I
10.1038/srep10277
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Silent information regulator type-1 (SIRT1) has been reported to be involved in the cardiopulmonary protection. However, its role in the pathogenesis of burn-induced remote acute lung injury (ALI) is currently unknown. The present study aims to investigate the role of SIRT1 in burn-induced remote ALI and the involved signaling pathway. We observed that SIRT1 expression in rat lung tissue after burn injury appeared an increasing trend after a short period of suppression. The upregulation of SIRT1 stimulated by resveratrol exhibited remission of histopathologic changes, reduction of cell apoptosis, and downregulation of pro-inflammatory cytokines in rat pulmonary tissues suffering from severe burn. We next used primary pulmonary microvascular endothelial cells (PMVECs) challenged by burn serum (BS) to simulate in vivo rat lung tissue after burn injury, and found that BS significantly suppressed SIRT1 expression, increased cell apoptosis, and activated p38 MAPK signaling. The use of resveratrol reversed these effects, while knockdown of SIRT1 by shRNA further augmented BS-induced increase of cell apoptosis and activation of p38 MAPK. Taken together, these results indicate that SIRT1 might protect lung tissue against burn-induced remote ALI by attenuating PMVEC apoptosis via p38 MAPK signaling, suggesting its potential therapeutic effects on the treatment of ALI.
引用
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页数:13
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