Thaliporphine Derivative Improves Acute Lung Injury after Traumatic Brain Injury

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.

Dai-Huang-Fu-Zi-Tang alleviates pulmonary and intestinal injury with severe acute pancreatitis via regulating aquaporins in rats

“…Towne JE demonstrated that the expression levels of AQP-1 and AQP-5 decreased in lungs with pulmonary edema (PE) following viral infection [ 15 ]. PE usually occurs in the Traumatic Brain Injury (TBI)-induced ALI patients, and aquaporins (AQPs), particularly AQP1 and AQP4, maintain water balances between the epithelial and microvascular domains of the lung [ 16 ]. Sakai et al study reported that the genes of AQP4 and AQP8 were mainly expressed in the murine colon [ 17 ].…”

Association between Traumatic Subarachnoid Hemorrhage and Acute Respiratory Failure in Moderate-to-Severe Traumatic Brain Injury Patients

“…The second mechanism is probably caused by a catecholamine surge. Catecholamine surge is a sudden and dramatic increase in serum levels of the catecholamines adrenaline and noradrenaline and causes the vasoconstriction of peripheral vessels, which may eventually lead to neurogenic pulmonary edema, resulting in ARF [ 2 , 24 , 25 , 26 , 27 , 28 , 29 , 30 ]. It often occurs if the hypothalamic–pituitary axis is injured post diffused brain injury indicated by severe traumatic SAH.…”

Erythropoietin-Derived Peptide Protects Against Acute Lung Injury After Rat Traumatic Brain Injury

“…Total RNA was isolated and reverse transcribed into cDNA by using RNAprep Pure Tissue Kit (TIANGEN Biotech, Beijing, China) and Quantscript RT Kit (TIANGEN Biotech, Beijing, China), then qRT-PCR was carried out according to the manufacturer’s protocol (TIANGEN Biotech, Beijing, China). The relative gene expression was detected by qRT-PCR using the standard 2 -ΔΔCT method [24]. Each sample was run in triplicate.…”