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BioMed Research International
Volume 2015 (2015), Article ID 729831, 10 pages
Research Article

Thaliporphine Derivative Improves Acute Lung Injury after Traumatic Brain Injury

1Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
2Division of Orthodontics & Dentofacial Orthopedics and Pedodontics, Department of Dentistry, Tri-Service General Hospital, Taipei 114, Taiwan
3Division of Neurosurgery, Department of Surgery, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 23142, Taiwan
4School of Medicine, Tzu Chi University, Hualien 97004, Taiwan
5Teaching Department of Medicine, China Medical University, Taichung 40402, Taiwan
6Department of Physiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan

Received 30 August 2014; Revised 13 November 2014; Accepted 13 November 2014

Academic Editor: Anastasia Kotanidou

Copyright © 2015 Gunng-Shinng Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Acute lung injury (ALI) occurs frequently in patients with severe traumatic brain injury (TBI) and is associated with a poor clinical outcome. Aquaporins (AQPs), particularly AQP1 and AQP4, maintain water balances between the epithelial and microvascular domains of the lung. Since pulmonary edema (PE) usually occurs in the TBI-induced ALI patients, we investigated the effects of a thaliporphine derivative, TM-1, on the expression of AQPs and histological outcomes in the lung following TBI in rats. TM-1 administered (10 mg/kg, intraperitoneal injection) at 3 or 4 h after TBI significantly reduced the elevated mRNA expression and protein levels of AQP1 and AQP4 and diminished the wet/dry weight ratio, which reflects PE, in the lung at 8 and 24 h after TBI. Postinjury TM-1 administration also improved histopathological changes at 8 and 24 h after TBI. PE was accompanied with tissue pathological changes because a positive correlation between the lung injury score and the wet/dry weight ratio in the same animal was observed. Postinjury administration of TM-1 improved ALI and reduced PE at 8 and 24 h following TBI. The pulmonary-protective effect of TM-1 may be attributed to, at least in part, downregulation of AQP1 and AQP4 expression after TBI.