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Biomedical subjects

B X Zeng

Publications and source records attributed to B X Zeng.

6 recordsLinked to original sources
PubMed2006

Protective effects of propofol on lipopolysaccharide-activated endothelial cell barrier dysfunction.

BACKGROUND: Propofol has been widely used in intravenous anesthesia. It possesses antioxidant and immunomodulating effects. This study aimed to investigate whether propofol may attenuate lipopolysaccharide (LPS)-induced endothelial cell barrier dysfunction and the possible mechanisms of such modulation. METHODS: Cultured human umbilical vein endothelial cells (HUVECs) were used to assess the following treatments: (i) no additives (negative control), (ii) LPS alone (1 and 10 microg/ml), (iii) propofol alone (20 microg/ml), (iv) intralipid (a solvent of propofol) alone (20 microg/ml), (v) LPS (10 microg/ml) combination with propofol (4 and 20 microg/ml) and (vi) LPS (10 microg/ml) combination with intralipid (20 microg/ml). Changes of cell permeability and filamentous actin (F-actin) were determined. Expression of nitrotyrosine proteins and activity of nuclear factor kappaB (NF-kappaB) were analyzed by Western blot and immunocytochemistry. Expression of endothelial nitric-oxide synthase (eNOS) and inducible nitric-oxide synthase (iNOS) were analyzed by reverse transcriptase-polymerase chain reaction. RESULTS: LPS markedly increased the permeability of endothelial cells, the formation of peroxynitrite and depolymerization of F-actin in HUVECs. LPS also significantly increased mRNA of iNOS, protein level of NF-kappaB and decreased mRNA of eNOS (P < 0.05). Propofol at both concentrations (4 and 20 microg/ml) significantly inhibited the LPS-induced increase in cell permeability and alteration in F-actin organization. Propofol also reduced the LPS-enhanced iNOS mRNA and NF-kappaB protein levels whilst it increased eNOS mRNA expression (P < 0.05). CONCLUSION: This study demonstrated that propofol, both at therapeutic concentrations and 5 times therapeutic concentrations, inhibited NF-kappaB activation in LPS-stimulated endothelial cells and was found to protect endothelial cells against LPS-induced barrier dysfunction.

Actins↗
PubMed2005

Rosiglitazone, an agonist of peroxisome proliferator-activated receptor gamma, reduces pulmonary inflammatory response in a rat model of endotoxemia.

OBJECTIVE: The effect of rosiglitazone, a potent peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonist, on pulmonary inflammation in endotoxemia was investigated. MATERIALS AND METHODS: Male Wistar rats were given either lipopolysaccharide (LPS, 6 mg/kg i.v.) or saline, pretreated with rosiglitazone (0.3 mg/kg i.v.) or its vehicle (dimethyl sulphoxide) 30 min before LPS. The selective PPAR-gamma antagonist GW9662 (0.3 mg/kg i.v.) was given 20 min before rosiglitazone. Wet/dry weight (W/D) ratio, myeloperoxidase (MPO) activity, malondialdehyde (MDA) as well as TNF-alpha and CINC-1 concentrations were measured in lung tissues 4 h after LPS injection. Expression of ICAM-1, NF-kappaB p65 and PPAR-gamma were also determined by immunohistochemistry or Western blot analysis. RESULTS: Rosiglitazone pretreatment significantly attenuated the increases in W/D ratio, MPO activity and MDA levels, and reduced pulmonary overproduction of TNF-alpha and CINC-1 as well as expression of ICAM-1 following endotoxemia. Rosiglitazone also inhibited the nuclear localization of NF-kappaB and up-regulated the expression of PPAR-gamma protein. The specific PPAR-gamma antagonist GW9662 abolished the effect of rosiglitazone. CONCLUSION: These findings suggest that PPAR-gamma agonists might be used as therapeutic agents in the therapy of inflammatory lung injury related to endotoxemia.

Anilides↗
PubMed2004

Protective effects of early treatment with propofol on endotoxin-induced acute lung injury in rats.

BACKGROUND: To investigate the effects of propofol administration on acute lung injury in endotoxin-induced shock in rats. METHODS: Seventy-six male Wistar rats were randomly assigned to one of five groups: (i) saline control; (ii) endotoxin alone (receiving lipopolysaccharide (LPS) 8 mg kg(-1) i.v.); (iii) pretreatment with propofol 1 h before LPS; (iv) simultaneous treatment with propofol and LPS; (v) post-treatment with propofol 1 h after LPS. During the 5 h after LPS injection, survival rates were recorded. Lung tissue was sampled to measure values of nitrite/nitrates (NO(2-)/NO(3-)) and tumour necrosis factor (TNF)-alpha in bronchoalveolar lavage (BAL) fluid, and wet-to-dry lung weight ratio, pulmonary permeability index, BAL protein and expression of inducible nitric oxide synthase (iNOS) and nitrotyrosine (NT). RESULTS: Compared with the endotoxaemic group, both the pre- and simultaneous treatment groups showed significantly improved 5 h survival rates, and attenuated endotoxin-induced increased BAL fluid NO(2-) /NO(3-) and TNF-alpha, iNOS mRNA and NT expression in lung tissue, and decreased pulmonary microvascular permeability. These beneficial effects were blunted in the post-treatment group. CONCLUSIONS: These findings indicate that early administration of propofol may provide protective effects against endotoxin-induced acute lung injury.

Anesthetics, Intravenous↗
PubMed2001

Subcellular expression of UGT1A6 and CYP1A1 responsible for propofol metabolism in human brain.

AIM: To observe the subcellular expression of UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P-450 1A1 (CYP1A1) mRNA in the human brain and investigate the effect of brain on extrahepatic metabolism of propofol. METHODS: Fifteen patients scheduled for craniotomy under propofol anesthesia were selected. Brain tis sue was taken and blood samples from the radial artery and the internal jugular vein were drawn simultaneously. PCR technique was used to detect UGT1A6 and CYP1A1 mRNA in the microsomes and mitochondria. Enzymatic activities were assayed. Blood propofol and propofol-glucuronide concentrations were measured with HPLC and GC, respectively. RESULTS: UGT1A6 mRNA was located mainly in the microsomes, and CYP1A1 mRNA was mainly in the mitochondria. The higher blood concentration of propofol and lower blood concentration of propofol-glucuronide were observed from the radial artery than from the internal jugular vein, respectively. The Km of UGT1A6 and CYP1A1 was (0.74 +/- 0.21) mmol and (548 +/- 50) mmol, respectively. The Vmax was (536 +/- 98) nmol . h-1 . mg-1 and (37 +/- 5) nmol . h-1 . mg-1, respectively. CONCLUSION: The human brain is an important organ for extrahepatic metabolism of propofol. The metabolism occurs within microsomes and mitochondria in brain.

Adult↗
PubMed2000

[A new generation of pulmonary function measuring system].

A system for measuring the pulmonary function was reported. The System consists of Fleisch flow transducer, a pressure transducer an amplifier, A/D converter, and a 486 computer. It can measure the indices of respiratory function under tidal breathing, the indices of tidal breathing flow volume loop and the dynamic indices of passive respiration.

Humans↗