ArticleBioMed research international2015
Thaliporphine derivative improves acute lung injury after traumatic brain injury.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Aquaporins: a novel perspective in the treatment of lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Protective effects of Stephania pierrei tuber-derived oxocrebanine against LPS-induced acute lung injury in mice.Inflammopharmacology · 2023Article
- Association between Traumatic Subarachnoid Hemorrhage and Acute Respiratory Failure in Moderate-to-Severe Traumatic Brain Injury Patients.Journal of clinical medicine · 2022Article
- Aquaporin 4 in Traumatic Brain Injury: From Molecular Pathways to Therapeutic Target.Neurochemical research · 2022Review
- The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review.Frontiers in medicine · 2022Review
- An inflammatory pulmonary insult post-traumatic brain injury worsens subsequent spatial learning and neurological outcomes.The journal of trauma and acute care surgery · 2019Article
- Mild Traumatic Brain Injury in Mice Beneficially Alters Lung NK1R and Structural Protein Expression to Enhance Survival after Pseudomonas aeruginosa Infection.The American journal of pathology · 2019Article
- Dai-Huang-Fu-Zi-Tang alleviates pulmonary and intestinal injury with severe acute pancreatitis via regulating aquaporins in rats.BMC complementary and alternative medicine · 2017Article
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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