Objective To investigate the effects of emulsified isoflurane on apoptosis in human neuroblastoma cells and the role of c-Jun N-terminal kinase (JNK) in it.Methods The human neuroblastoma SHSY-5Y cells were seeded in 96-well plates or dishes and then randomly divided into 8 groups using a random number table:control group(group C,n=24),different concentrations of lipid emulsion groups(LE1 groups [n =24],LE2 group [n =24] and LE3 group [n =72]),different concentrations of emulsified isoflurane groups (EI1 group [n=24],El2 group [n=24] and EI3 group [n=72]),and emulsified isoflurane + JNK inhibitor SP600125 group (group EI-SP,n =24).At 24 h after the cells were plated,in LE1-3 groups,30％ lipid emulsion was added to the culture medium with the final concentrations of 0.395 6,0.791 2 and 1.582 4 μl/ml,respectively;in EI1-3 groups,8％ emulsified isoflurane was added with the final concentrations of 0.56,1.12 and 2.24 mmol/L,respectively;in group EI-SP,emulsified isoflurane was added with the final concentration of 1.12 mmol/L,and SP600125 was added at 1 h before addition of emulsified isoflurane with the final concentration of 10 μmol/L;the cells were cultured normally in group C.At 6,12 and 24 h of incubation in EI3 and LE3 groups,and at 24 h of incubation or culture in the other groups,the morphology of cells was detected,the cell viability was measured using methyl thiazolyl tetrazolium assay,and the expression of JNK,phosphorylated JNK (p-JNK) and cytochrome c (Cyt c) was detected by Western blot.Results Compared with group C,the cell viability was significantly decreased,and the expression of p-JNK and Cyt c was significantly up-regulated at 24 h of incubation in group EI2 and at 12 and 24 h of incubation in group EI3,the cell viability was significantly decreased (P＜0.05),and no significant change was found in the expression of p-JNK and Cyt c in group EI-SP,and no significant change was found in the cell viability and expression of p-JNK and Cyt c in LE1-3 and EI1 groups (P＞0.05).Compared with group EI1,the cell viability was significantly decreased,and the expression of p-JNK and Cyt c was significantly up-regulated at 24 h of incubation in EI2.3 groups (P＜0.05).Compared with group EI2,the cell viability was significantly decreased,and the expression of p-JNK and Cyt c was significantly up-regulated at 24 h of incubation in group EI3,and the cell viability was significantly increased,and the expression of p-JNK and Cyt c was significantly down-regulated in group EI-SP (P＜0.05).There was no significant difference in JNK expression between the eight groups (P＞0.05).Conclusion High concentrations of emulsified isoflurane can induce apoptosis in neurons only when applied for a long time,while low concentrations do not have the effect when applied for a short time.The mechanism by which emulsified isoflurane induces neuronal apoptosis is related to activation of JNK pathway.

Objective To explore the level of autophagy induced by oxygen glucose deprivation/reperfusion(OGD/R) injury in L02 cell.Methods L02 cells were cultured to establish the model of OGD/R injury and simulate clinical hepatic ischemia-reperfusion injury.The L02 cells were randomly divided into 5 groups : normal control group, oxygen-glucose deprivation 6 h/reperfusion 1,3,6,12 h group (OGD 6 h/R 1,3,6,12 h).Then observe the form changes of the L02 cells by optical microscope.The appreciation of the company's relative L02 cells was detected by MTT.The expression of autophagy related proteins such as Beclin-1, LC3 and p62 were evaluated by Western blot.Results Compared with the normal control group, the form damaged and the cells proliferation activity of L02 cells in the OGD/R group were gradually increased in a time-dependent manner.Compared with the normal control group, autophagy related proteins LC3 , Beclin-1 were increased at OGD 6 h/R 1 h.The expression of LC3 was gradually increased as the time went on and was increased gradually at OGD 6 h/R 6 h, reached a peak at OGD 6 h/R 12 h(P<0.01).The expression of Beclin-1 was gradually increased as the time went on and was increased gradually at OGD 6 h/R 6 h and OGD 6 h/R 12 h (P<0.01).The expression of p62 had no obvious change at OGD 6 h/R 1 h and OGD 6 h/R 3 h, began to increase sharply at OGD 6 h/R 6 h and reached a peak at OGD 6 h/R 12 h(P<0.01).Conclusion Our data suggests that oxygen-glucose deprivation/reperfusion may increase the level of autophagy and lead to autophagic cell death in L02 cell.

Objective To investigate the protective effect of propofol (Pro) in combination with ligustrazin (Lig) on the liver against ischemia-reperfusion (I/R) injury and the mechanisms involved.Methods Fifty male SD rats weighing 240-280 g were randomly divided into 5 groups of 10 animals each: group Ⅰ received sham operation (sham); group Ⅱ I/R; group Ⅲ Pro + I/R; group Ⅳ Lig + I/R and group Ⅴ Pro + Lag + I/R. The animals were anesthetized with intraperitoneal pentobarbital 20 mg?kg-1 . Liver ischemia was produced by clamping the hepatic hilum for 30 min, then the clamp was removed for 60 min reperfusion. In group Ⅲ propofol was infused at 20 mg?kg-1 ?h-1 starting from 20 min before ischemia until hepatic hilum was clamped. In group Ⅳ a bolus of ligustrazin 60 mg?kg-1 was given i.v. 20 min before ischemia. In group Ⅴ propofol was infused and a bolus of ligustrazin was given i.v. as in group Ⅲ and Ⅳ 20 min before hepatic ischemia. Blood samples were taken at the end of 60 min reperfusion for determination of serum activities of ALT, AST and LDH and meanwhile a liver specimen was obtained for determination of MDA content, SOD and XOD activities and for electron microscopic examination. Results Serum ALT and AST activities were significantly higher in group Ⅱ , Ⅲ , Ⅳ and Ⅴ than in group Ⅰ (sham) (P

Objective To explore the general anesthetic EI on the rat fetal neural stem cell proliferation(NSCs) and the role played by JNK in the influence. Methods The cultured rat fetal NSCs were randomly divided into 6 groups (n=8 each):normal group (group N);fat milk group (group F);EI groups(including 8. 12,9. 80,12. 04 mmol/L EI) , 9. 80 mmol/L EI group+20 μmol/L SP600125 group ( group EISP) . After incubated for 12 hours, the cellular effects of EI and cell viability were evaluated by MTT reduction assay. The apoptotic rate of the rat NSCs were determined by flow cytometry, and the expression of protein Caspase-3 was observed by Western blot. Results There was no statistical difference in cell viability, apoptotic rate and protein expression of Caspase-3 in group N and group F. EI group had higher cell apoptotic rate(P<0. 01), protein expression of Caspase-3 (P<0. 05 ) , but lower cell viability than group N ( P<0. 01 ) . And significant differences were found between three do-ses of EI groups (P<0. 05). Compared with EI group, lower cell apoptotic rate (P<0. 01), protein expression of Caspase-3 but higher cell viability were observed in group EISP ( P<0. 05 ) . Conclusion JNK plays an important role in EI-induced cytotoxicity possibly in a dose-dependent manner.

Objective To investigate the effect of sevoflurane preconditioning on lung compliance and oxygenation index during one lung ventilation( OLV) . Methods In this study, sixty patients, ASAⅠorⅡ, scheduled for pul-monary surgeries were enrolled, and randomly divided into two groups:sevoflurane preconditioning group(n=30) and total intravenous group( n=30 ) . For preconditioning, patients in sevoflurane preconditioning group were ad-ministrated with one minimal alveolar concentration(1MAC) sevoflurane for 30 min after general anesthesia induc-tion and then followed with total intravenous anesthesia. While in total intravenous group, only intravenous anes-thetic agents were administrated for maintenane of anesthesia after induction. The indexes of hemodynamics, pulse oximeter( SpO2 ) , plateau pressure( Pplat) and lung compliance( Cdyn) were recorded at the following time points:before anesthesia( T0 ) , after anesthesia induction at laternal position TLV 30 min( T1 ) ,30 min after OLV( T2 ) , 60 min after OLV( T3 ) and recovering TLV 20 min( T4 ) . Arterial blood samples were taken to measure partial pressure of carbon dioxide( PaCO2 ) , partial pressure of oxygen( PaO2 ) , pH, oxygenation index( PaO2/FiO2 ) at the follow-ing time points: T1 , T2 , T3 , T4 . Results Compared with T1 , the oxygenation index and lung compliance de-creased significantly at T2 ,T3 ( P<0. 05 ); compared with total intravenous group, the lung compliance was obvi-ously higher than that in sevoflurane preconditioning group at T2,T3(P<0. 05). There were no significantly differ-ences in the oxygenation index between total intravenous group and sevoflurane preconditioning group at all time points. Conclusion Compared with total intravenous anesthesia with propofol , sevoflurane preconditioning can im-prove lung compliance, but does not make contribute to improve oxygenation index.

0.05).The CSFP before and after opening dura mater was obviously lower than the baseline value (P0.05).The total dose of propofol in group T was smaller than in group C.CONCLUSION:Target controlled infusion of propofol is better than continuous pump injection in lowering the ICP during neurological surgery.

Objective To investigate the effect of peroxisome proliferator-activated receptor α agonist Wy14643 on mechanical ventilation-induced lung injury in rats.Methods Thirty-two healthy male SD weighing 250-300 g were randomly divided into 4 groups(n = 8 each): group Ⅰ control(group C);group Ⅱ mechanical ventilation(group V)and group Ⅲ,Ⅳ pretreated with different doses of Wy14643(group W1 ,W2).The animals were anesthetized with intraperitoneal 3% pentobarbital 30 mg/kg and tracheostomized.The femoral artery and external jugular vein were cannulated for blood sampling and drug administration.Group C received no mechanical ventilation.In group V,W1 and W2 the animals were mechanically ventilated for 2 h(VT 40 ml/kg,RR40 bpm,I:E=1:2,FiO2 21%).In group W1 and W2 Wy14643 1 and 3 mg/kg were administered iv at 1 h before mechanical ventilation.Arterial blood samples were collected at 1 and 2 h of mechanical ventilation for determination of PaO2/FiO2.Serum SOD activity and MDA concentration were measured at the end of 2 h mechanical ventilation.The animals were then killed and the lungs removed for microscopic examination,lung lavage and W/D lung weight ratio.The MIP-2 and TNF-α concentrations in BALF were measured.Results Two hour mechanical ventilation significantly decreased serum SOD activity and increased serum MDA concentration,W/D lung weight ratio and TNF-α and MIP-2 concentrations in BALF as compared with group C.Wy14643 pretreatment significantly attenuated these mechanical ventilation-induced changes in group W1 and W2 in a dose-dependent manner.Conclusion Wy14643 can attenuate mechanical ventilation induced lung injury in rats and it is related to the dose.

Objective To evaluate the effects of pretreatment with different doses of phosphocreatine on hepatic ischemia-repeffusion (I/R) injury in rats.Methods.Thirty male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 5 groups (n =6 each):sham operation group (group S),hepatic I/R group (group I/R),and pretreatment with different doses of phosphocreatine groups (groups P1-3).Hepatic I/R was induced by 90 min occlusion of the hepatic artery and portal vein entering the middle and left lobes of the liver followed by 4 h reperfusion in anesthetized rats.Phosphocreatine 50,150 and 450 mg/kg were injected via the tail vein at 60 min before ischemia in groups P1-3,respectively.In groups S and I/R,the equal volume of normal saline was given instead.Blood samples were taken from the abdominal aorta at 4 h of reperfusion for determination of plasma alanine aminotransferase (ALT),aspartate aminotransferase (AST),TNF-α and IL-1β concentrations.The rats were then sacrificed and the livers were removed for determination of myeloperoxidase (MPO) activity (by ELISA),intercellular adhesion molecule-1 (ICAM-1) expression (by immunohistochemistry),and cell apoptosis (by TUNEL) and for microscopic examination (by electron microscopy).Results The MPO activity in liver tissues,plasma ALT and AST activities,TNF-α and IL-1β concentrations and the number of apoptotic cells were significantly higher in groups I/R and P1-3 than in group S,while lower in groups P1-3 than in group I/R (P ＜ 0.05).The parameters mentioned above were decreasedin turn in groups P1-3 (P ＜ 0.05).Conclusion Phosphocreatine pretreatment can attenuate the hepatic I/R injury in rats in a dose-dependent manner and inhibition of the inflammatory responses is involved in the mechanism.

Objective To evaluate the effects of dexmedetomidine on dreaming during general anesthesia in pediatric patients.Methods A total of 400 pediatric patients of both sexes,aged 5-12 yr,with body mass index of 15.2-18.1 kg/m2,of American Society of Anesthesiologists physical status Ⅰ,undergoing elective orthopedic surgery under general anesthesia,were randomly divided into control group (group C,n=200) and dexmedetomidine group (group D,n =200) according to the computer-generated random numeral order and numeral parity.Dexmedetomidine was infused intravenously in a loading dose of 0.5 μg/kg over 10 min before induction of anesthesia followed by infusion of 0.5 μg · kg-1 · h-1 until 30 min before the end of surgery in group D,while the equal volume of normal saline was given instead of dexmedetomidine in group C.The pediatric patients who regained consciousness and recovered orientation in post-anesthesia care unit were interviewed for dreaming using a modified Brice questionnaire,and the dream (emotion,hearing and behaviours in dreams,memories for dreams) was evaluated using a 5-point Likert scale.Results Compared with group C,the incidence of dreaming was significantly decreased,the memory score was decreased (P＜0.05),and no significant change was found in emotion,hearing and behaviour scores in dreams in group D (P＞0.05).Conclusion Dexmedetomidine can decrease the development of dreaming during general anesthesia and produces no effect on the content of dreams (most are pleasant) in pediatric patients.

Objective To evaluate the effect of propofol preconditioning on endoplasmic reticulum stress induced by hypoxia-reoxygenation (H/R) in HEPG2 cells.Methods HEPG2 cells were randomly divided into 4 groups using a random number table:control group (group C),propofol group (group P),H/R group and H/R + propofol preconditioning group (group PP).In group C,the cells were cultured routinely for 42 h.In group H/R,after being cultured routinely for 6 h,the cells were exposed to 1％ O2 + 5％ CO2 + 94％ N2 for 12 h followed by 12 h reoxygenation.In group PP,the cells were cultured for 6 h in the culture medium containing propofol 10 μmol/L (final concentration),and then H/R was induced.The cell viability was detected by MTT assay.The expression of immunoglobulin heavy chain-binding protein (BIP),C/EBP homologous protein (CHOP) and activated caspase-3 was determined by Western blot.The expression of BIP,CHOP and caspase-3 mRNA was determined by RT-PCR.Results Compared with group C,the cell viability was significantly decreased,and the expression of BIP,CHOP and activated caspase-3 protein and mRNA was up-regnlated in H/R and PP groups,and no significant changes were found in the parameters mentioned above in group P.Compared with group H/R,the cell viability was significantly increased,and the expression of BIP,CHOP and activated caspase-3 protein and mRNA was down-regulated in PP group.Conclusion Propofol preconditioning can promote the cell proliferation and attenuate H/R injury to HEPG2 cells through inhibiting endoplasmic reticulum stress.