ABSTRACT
<p><b>OBJECTIVE</b>To observe the dynamic expression of transmembrane (TM)-tumor necrosis factor (TNF)-alpha and secreted (S)-TNF-alpha in the development of endotoxic shock and explore the actions and mechanism of TM-TNF-alpha in liver of the rat with endotoxic shock.</p><p><b>METHODS</b>Endotoxic shock in rats was induced by intravenous injection of dead gram negative bacteria E. Coli; the kinetics of TM-TNF-alpha on peritoneal macrophages and S-TNF-alpha in serum of these rats were determined. Pretreatment with TNF alpha converting enzyme antisense oligonucleotide (5 mg/kg) 30 minutes before rats were administrated dead bacteria inhibited enzymatic cleavage of TM-TNF-alpha into S-TNF-alpha. Six hours after bacteria injection, TM-TNF-alpha and S-TNF-alpha were also detected respectively. The pathological injury in the livers of rats with endotoxin shock was examined, and artery pressure was constantly measured.</p><p><b>RESULTS</b>The kinetics of TM-TNF-alpha expression in the development of endotoxic shock was different from that of S-TNF-alpha expression in serum. The expression of TM-TNF-alpha began to increase on the surface of peritoneal macrophages and liver within 30 min, after bacteria challenge and peaking within a period of 4.5 hours followed by a gradual decrease to a relatively high level which was maintained for at least 24 hours. The TACE antisense oligonucleotide pretreated rats showed remarkable increase in TM-TNF-alpha expression by peritoneal macrophages and liver (P < 0.001), and their arterial blood pressure were maintained within normal levels and there were no detectable pathological changes in their livers.</p><p><b>CONCLUSIONS</b>These findings suggested that TM-TNF-alpha may be a potent endogenous regulator involved in anti-inflammatory responses to maintain normal arterial pressure and protect liver tissue from pathological injury in during endotoxin shock. This study confirmed the important role of TNF-alpha in endotoxic shock which is not only of important theoretical significance, but also of practical interest in providing experimental basis for clinical treatment of endotoxin shock.</p>
Subject(s)
Animals , Rats , Chemical and Drug Induced Liver Injury , Disease Models, Animal , Endotoxins , Toxicity , Liver Diseases , Metabolism , Membrane Proteins , Bodily Secretions , Oligonucleotides, Antisense , Pharmacology , Rats, Wistar , Shock, Septic , Metabolism , Tumor Necrosis Factor-alpha , Bodily SecretionsABSTRACT
AIM: To explore the effects of 5-HT and electrolytes on the airway remodeling in guinea pigs with bronchial asthma.METHODS: 70 guinea pigs were divided into 7 groups: control group,model group,continued model group,5-HT group,anti-5-HT group,high Mg~(2+) group,low Mg~(2+) group.Remodeling model was established with ovalbumin.RESULTS: ① In model group,5-HT of serum and thickness of airway walls were significantly increased compared with control group(P
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The effect of ahalysantinfarctasum (AFT) on acute hypoxic pulmonary hypertension of dogs was examined. The'decrease in pulmonary vascular resistance and a dose dependent attenuation of acute hypoxic pulmonary vasoconstriction by AFT were found. AFT did not alter systemic vascular resistance. PaO_2 and PaCO_2 6-keto-PGF_(1?) increased significantly, however after the intravenous infusion of AFT, TXB_2 did not change. It is suggested that AFT may attenuate hypoxic pulmonary vasoconstriction by tnducing the synthesis or release of PG I to nreyent nulmonary hypertension
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the normal control group (Pthe continued asthma model group (P
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AIM: To investigate the effect of compoun d poria prescription (CPP), a Chinese medicine, on weight, blood glucose, blood fa t and microcirculation in nutrition obesity rats and attempt to look for a new a pproach for obesity prevention and cure. METHODS: 30 Wistar rats were divided into normal food raised gro up (group A), high energy food raised group (group B), and high energy food comb ined with CPP raised group (group C). The changes of weight, blood glucose, bloo d lipid and microcirculation were detected, respectively. RESULTS: After CPP treatment in experimental obesity rats, the a v erage weight reduced from (313.00?17.29) g to (217.50?17.50) g (P