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Objective To evaluate the effects of penehyclidine hydrochloride on the oxidative stress and cell apoptosis during endotoxin-induced acute lung injury (ALI) in neonatal rats.Methods Forty 7-day-old Wistar rats weighing 12-18 g were randomly divided into 3 groups (n=10 each) using a random number table: penehyclidine hydrochloride group (group PHC), acute lung injury (group AKI) and normal saline group (group NS).The ALI model was induced with intraperitoneal endotoxin 5.0 mg/kg in groups PHC and ALI.In group PHC, penehyclidine hydrochloride 2.0 mg/kg was injected intraperitoneally at 1 h before ALI respectively, while the equal volume of normal saline was administered in groups NS and ALI.At 4 h after endotoxin injection,the rsts were sacrificed.The lungs were collected to determine the wet/dry (W/D) lung weight ratio.The expression of SOD was detected by xanthine oxidase method.The expression of MDA was detected by sulfuretted barbitone method.Levels of cytochrome C (Cyt-C) and Caspase-3 were determined with immunohistochemical method (IHC), and cell apoptosis (by TUNEL).Apoptotic index was calculated.Results Compared with group NS, the W/D ratio and the contents of MDA were significantly increased, the contents of SOD were significantly decreased in groups ALI and PHC (P＜0.05).Compared with group ALI, the W/D ratio and the contents of MDA were significantly decreased, the contents of SOD were significantly increased in group PHC (P＜0.05).Compared with group NS, the contents of Cyt-C, Caspase-3, and apoptotic index were significantly increased in groups ALI and PHC (P＜0.05).Compared with group ALI, the contents of Cyt-C, Caspase-3, and apoptotic index were significantly decreased in group PHC (P＜0.05).Conclusion Penehyclidine hydrochloride ameliorates endotoxin-induced ALI by inhibiting oxidative stress and cell apoptosis in neonatal rats.
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Objective To investigate the effect of sevoflurane anesthesia on the cognitive function and phosphorylation of tau in hippocampal neurons in amyloid precursor protein (APP) transgenic mice.Methods Male APP gene mutation mice,weighing 18-22 g,aged 8-12 weeks,were used in the study.Forty-four APP positive mice were randomly divided into 2 groups (n =10 each):sevoflurane group (group AS,n =28) and control group (group AC,n =16).Forty-four APP negative mice were randomly divided into 2 groups:sevoflurane group (group S,n =28) and control group (group C,n =16).Animals in groups S and AS inhaled 3％ sevoflurane for 4 h.While in groups C and AC,animals inhaled pure oxygen for 4 h.Morris water maze was performed 24 h after sevoflurane or pure oxygen inhalation.The phosphorylation of tau at Ser262 and Ser396 was detected by Western blot on 1 day after pure oxygen inhalation (T1) in groups AC and C,and on 1,3 and 7 days after sevoflurane inhalation in groups AS and S.Results Compared with group C,the escape latency was significantly prolonged and the duration of staying at the original platform quadrant was shortened in groups S and AC,and the phosphorylation of tau at Ser262 in group S and phosphorylation of tau at Ser262 and Ser396 in group AS were increased (P ＜0.05).Compared with group S,the escape latency was significantly prolonged,the duration of staying at the original platform quadrant was shortened and the phosphorylation of tau at Ser262 and Ser396 was increased in group AS (P ＜ 0.05).Compared with group AC,the escape latency was significantly prolonged,the duration of staying at the original platform quadrant was shortened and the phosphorylation of tau at Ser262 and Ser396 was increased in group AS (P ＜ 0.05).Conclusion Sevoflurane anesthesia can aggravate the impairment of cognitive function in APP positive mice and the increase in the phosphorylation of tau at Ser262 and Ser396 is involved in the mechanism.
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ObjectiveTo investigate the effect of sevoflurane preconditioning on heme oxygenase-1 (HO-1) expression in lung tissues during one lung ventilation (OLV) in rats.MethodsTwenty-four male SD rats weighing 220-250 g were randomly divided into 4 groups ( n =6 each):control group (group C) ; two lung ventilation group (group T); OLV group (group O) and sevoflurane preconditioning+ OLV group (group SO).The animals were anesthetized with intraperitoneal pentobarbital sodium 40 mg/kg.In group T,the animals were tracheal intubated and bilateral lungs were ventilated for 1 h (VT 10 ml/kg,RR 60 bpt/min,I∶E 1∶2) and PETCO2 was maintained at 35-50 mm Hg.In groups O and SO,the animals were tracheal intubated and OLV was performed for 1 h (VT 5 ml/kg,RR 80 bpt/min,I:E 1:2) and PETCO2 was maintained at 35-50 mm Hg.In group SO,2.4％sevoflurane was inhaled for 30 min before OLV and then washed out by inhalation of oxygen for 15 min.The left lung tissues were removed in groups C and T,and the bilateral lung tissues were removed in groups.O and SO for microscopic examination and determination of wet/dry lung weight ratio (W/D ratio) and expression of HO-1 (by Western blot).Results Compared with group C,W/D ratio was significantly increased and the expression of HO-1 was up-regulated in left lung tissues in group T and in bilateral lung tissues in groups O and SO ( P ＜0.05).Compared with group T,W/D ratio was significantly increased and the expression of HO-1 was up-regulated in bilateral lung tissues in group O and in right lung tissues in group SO ( P ＜ 0.05).Compared with group O,W/D ratio was significantly decreased,the expression of HO-1 was up-regulated (P ＜ 0.05) and the pathological changes were reduced in bilateral lung tissues in group SO.ConclusionThe mechanism by which sevoflurane preconditioning reduces OLV-induced lung injury is related to up-regulation of HO-1 expression.
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Objective To investigate the effect of fructose-1,6-diphosphate (FDP) pretreatment on myocardial connexin43 (Cx43) in a rat model of acute myocardial ischemia.Methods Thirty-six male 8-12 week old SD rata weighing 220-280 g were randomly divided into 3 groups (n=12 each):group Ⅰ sham operation (group S);group Ⅱ ischemia(group Ⅰ)and group Ⅲ FDP+ischemia(group F).The animals were anesthetized with intraperitoneal 10%chloral hydrate 40 mg/100 g,tracheostomized and mechanically ventilated.Acute myocardial ischemia was induced by occlusion of left anterior descending coronary artery for 30 min.Myocardial ischemia was;verified by elevation of S-T segment on ECG.In group F FDP 100 mg/kg was injected iv at 10 min before ischemia.Arrhythmia was recorded within 30 min after occlusion and the severity of arrbythmia was aggesged.The hearts were removed after 30 min myocardial ischemia.The Left ventricle area (LVA),myocardial infarct area (IA) and area at risk (AAR) were measured and AAR/LVA and IA/AAR ratios were calculated.The expression of myocardial Cx43 protein was determined by immuno-histochemestry and analysis of mean optical density.Results The severity of arrhythmia was significantly higher in group F and I than in gropu S.while lower in group F than in group I(P<0.05).The IA,IA/AAR ratio was significantly lower in group F than in group I.The myocardial Cx43 protein expression was down-regulated in group I and F as compared with group S.and was significantly lower in group I than in group F.Conclusion FDP pretreatment can protect myocardium against acute ischemia by up-regulation of myocardial Cx43 expression.