Your browser doesn't support javascript.
loading
Propofol inhibits burn injury-induced hyperpermeability through an apoptotic signal pathway in microvascular endothelial cells
Tian, K.Y.; Liu, X.J.; Xu, J.D.; Deng, L.J.; Wang, G..
  • Tian, K.Y.; Guangdong Academy of Medical Sciences. Guangdong General Hospital. Department of Anesthesiology. Guangzhou. CN
  • Liu, X.J.; Guangdong Academy of Medical Sciences. Guangdong General Hospital. Department of Anesthesiology. Guangzhou. CN
  • Xu, J.D.; Guangdong Academy of Medical Sciences. Guangdong General Hospital. Department of Anesthesiology. Guangzhou. CN
  • Deng, L.J.; Guangdong Academy of Medical Sciences. Guangdong General Hospital. Department of Anesthesiology. Guangzhou. CN
  • Wang, G.; Guangdong Academy of Medical Sciences. Guangdong General Hospital. Department of Anesthesiology. Guangzhou. CN
Braz. j. med. biol. res ; 48(5): 401-407, 05/2015. graf
Article in English | LILACS | ID: lil-744380
ABSTRACT
Recent studies have revealed that an intrinsic apoptotic signaling cascade is involved in vascular hyperpermeability and endothelial barrier dysfunction. Propofol (2,6-diisopropylphenol) has also been reported to inhibit apoptotic signaling by regulating mitochondrial permeability transition pore (mPTP) opening and caspase-3 activation. Here, we investigated whether propofol could alleviate burn serum-induced endothelial hyperpermeability through the inhibition of the intrinsic apoptotic signaling cascade. Rat lung microvascular endothelial cells (RLMVECs) were pretreated with propofol at various concentrations, followed by stimulation with burn serum, obtained from burn-injury rats. Monolayer permeability was determined by transendothelial electrical resistance. Mitochondrial release of cytochrome C was measured by ELISA. Bax and Bcl-2 expression and mitochondrial release of second mitochondrial-derived activator of caspases (smac) were detected by Western blotting. Caspase-3 activity was assessed by fluorometric assay; mitochondrial membrane potential (Δψm) was determined with JC-1 (a potential-sensitive fluorescent dye). Intracellular ATP content was assayed using a commercial kit, and reactive oxygen species (ROS) were measured by dichlorodihydrofluorescein diacetate (DCFH-DA). Burn serum significantly increased monolayer permeability (P<0.05), and this effect could be inhibited by propofol (P<0.05). Compared with a sham treatment group, intrinsic apoptotic signaling activation - indicated by Bax overexpression, Bcl-2 downregulation, Δψm reduction, decreased intracellular ATP level, increased cytosolic cytochrome C and smac, and caspase-3 activation - was observed in the vehicle group. Propofol not only attenuated these alterations (P<0.05 for all), but also significantly decreased burn-induced ROS production (P<0.05). Propofol attenuated burn-induced RLMVEC monolayer hyperpermeability by regulating the intrinsic apoptotic signaling pathway.
Subject(s)


Full text: Available Index: LILACS (Americas) Main subject: Cross Infection / Equipment Contamination Limits: Humans Country/Region as subject: South America / Brazil Language: English Journal: Braz. j. med. biol. res Journal subject: Biology / Medicine Year: 2015 Type: Article / Project document Affiliation country: China Institution/Affiliation country: Guangdong Academy of Medical Sciences/CN

Similar

MEDLINE

...
LILACS

LIS


Full text: Available Index: LILACS (Americas) Main subject: Cross Infection / Equipment Contamination Limits: Humans Country/Region as subject: South America / Brazil Language: English Journal: Braz. j. med. biol. res Journal subject: Biology / Medicine Year: 2015 Type: Article / Project document Affiliation country: China Institution/Affiliation country: Guangdong Academy of Medical Sciences/CN