Objective To detect the protective effect of sufentanil preconditioning on hepatic ischemia-reperfusion injury in rats and the role of c-Jun N-terminal kinase signal pathway in the mech-enism.Methods One hundred and sixty-two SD rats(in either gender,weighing 250-300 g)were ran-domly divided into seven groups:Sham-operated group (group S,n = 30 ),ischemia-reperfusion group (group IR,n =30),sufentanil preconditioning group (group SF1:1 μg/kg,n =30;group SF5:5 μg/kg,n =30;group SF10:10 μg/kg,n =30),SP600125 group (group SP,n =30),and dimethyl sulphoxide control group (group DMSO,n =6),different doses of sufentanil was administered 30 min before hepatic ischemia in group SF1,SF5 and SF10.Blood and liver samples were collected from each group at 0(T1 ),1 (T2 ),2 (T3 ),4 (T4 ),and 6 (T5 )hours after reperfusion.Serum alanine amin-otransferase (ALT)and aspartate aminotransferase (AST)were measured by an automatic biochemi-cal analyzer.Malondialdehyde (MDA)and superoxide dismutase (SOD)in liver tissue was measured. Liver sample was stained with HE to observe the hepatic pathological changes.Immunohistochemical method was used to determine the expression of JNK and western blotting was used to detect the ex-pression of P-JNK.Results Compared with group S,levels of AST,ALT increased significantly in group IR,SF1,SF5,SF10 at T1-T5 and in group SP,DMSO at T3 (P <0.05 ).Compared with group IR,levels of AST,ALT decreased significantly in group SF1,SF5,SF10 at T1-T5 and in group SP at T3 (P <0.05).Compared with group S,levels of MDA,SOD increased significantly in group IR,SF1, SF5,SF10 at T1-T5 and in group SP,DMSO at T3 (P < 0.05 ).Compared with group IR,levels of MDA,SOD decreased significantly in group SF1,SF5,SF10 at T1-T5 and in group SP at T3 (P <0.05).Compared with group SF1 and SF5,levels of MDA,SOD decreased significantly in SF10 at T4 . Compared with T1 ,the expression of p-JNK in group IR increased significantly at T3 (P < 0.05 ). Compared with group S,the expression of p-JNK in groups IR,SF1,SF5,SF10,SP,DMSO increased significantly at T3 (P < 0.05 ).Compared with group IR,the expression of p-JNK in groups SF1, SF5,SF10,SP decreased significantly and that in groups SF5,SF10 were less than that in group SF1 (P <0.05 ).The expression of p-JNK in group SF10 was less than that in group SF5 (P < 0.05 ). Conclusion Sufentanil preconditioning can reduce the hepatic ischemia-reperfusion injury and the dos-age of 10 μg/kg was the most effective.The protective mechanisms may inhibit JNK pathway and re-duce the expression of JNK.

Objective To evaluate the effects of isoflurane postconditioning on angiogenesis during cerebral ischemia-reperfusion ( I∕R) in rats and the role of Shh signaling pathway. Methods Thirty-two clean-grade healthy male Sprague-Dawley rats, aged 6-8 weeks, weighing 220-280 g, were divided into 4 groups ( n=8 each) by a random number table method:sham operation group ( Sham group) , I∕R group, isoflurane postconditioning group ( ISO group) , and isoflurane postconditioning plus Shh signaling pathway specific inhibitor cyclopamine group ( ISO+CYC group) . Cerebral ischemia was produced by inserting a 3-0 nylon thread with a rounded tip into the internal jugular vein. The nylon thread was threaded cranially until resistance was met. Occlusion was maintained for 1. 5 h followed by 24 h reperfusion. Neurological deficit was scored at 24 h of reperfusion. Rats were then sacrificed, and brains were removed for determination of cerebral infarct volume ( by TTC) and expression of glioma-associated oncogene homolog 1 ( Gli1) , vascu-lar endothelial growth factor ( VEGF) and transmembrane phosphoglycoprotein protein ( CD34) in cerebral cortex (by Western blot) and for examination of the pathological changes (by Nissl staining). Results Compared with Sham group, the neurological deficit score and cerebral infarct volume were significantly in-creased, and the expression of Gli1, VEGF and CD34 in the cerebral cortex was up-regulated in I∕R and ISO groups ( P <0. 05) . Compared with I∕R group, the neurological deficit score and cerebral infarct vol-ume were significantly decreased, and the expression of Gli1, VEGF and CD34 in the cerebral cortex was up-regulated ( P<0. 05) , and the pathological changes of brain tissues were significantly attenuated in ISO group, and no significant change was found in the parameters mentioned above in ISO + CYC group ( P>0. 05) . Compared with ISO group, the neurological deficit score and cerebral infarct volume were signifi-cantly increased, and the expression of Gli1, VEGF and CD34 in the cerebral cortex was down-regulated in ISO+CYC group ( P<0. 05) . Conclusion The mechanism by which isoflurane post-conditioning attenuates cerebral I∕R injury is related to activating Shh signaling pathway and promoting angiogenesis in rats.

Non-ceding RNAs refer to a class of RNA molecules that do not have the function of coding proteins,mainly include microRNAs,long non-coding RNAs and cireular RNAs.Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection,which attacks the lung first.Recent studies have found that these non-coding RNAs,especially microRNAs,can regulate gene expression at various levels such as gene transcription,RNA maturation and protein translation,leading to the release and activation of proinflammatory and inflammatory mediators,the injury of vascular endothelial,and finally cause the lung injury.Researchers believe that non-coding RNAs appear to be not only diagnostic markers but also therapeutic targets for sepsis-induced acute lung injury.In this paper,the role and application of non-coding RNAs in sepsis-induced acute lung injury will be reviewed from their production and mechanism.

Objective To observe the effect and adverse reactions of ultrasound guided continuous femoral nerve block in postoperative analgesia after total knee arthroplasty(TKA) and to conduct the comparative study with traditional patient-controlled intravenous analgesia. Methods Forty patients undergoing elective unilateral knee replacement in this hospital from August 2015 to March 2016 were selected and divided into the group A and B, 20 cases in each group. The group A adopted ultrasound guided continuous femoral nerve block analgesia, while the group B adopted patient-controlled intravenous analgesia(PCA). The VAS score on postoperative 4,8,12,24,48 h were compared between the two groups, the VAS score of continuous passive motion on postoperative 24,48,72 h were compared between the two groups, the muscle strength grade and knee joint maximum passive flexion and extension on postoperative 2-6 d were compared between the two groups. Postoperative adverse reactions were observed. The levels of C-reactive protein(CRP) and interleukin- 6 (IL-6) were tested. The ultrasound monitoring of lower extremity deep vein thrombosis occurrence was performed and the changes of serum D -dimer was observed. Results The rest state VAS score at each time point in the group A was significantly lower that in the group B (P<0.05). The VAS score of continuous passive function exercise at postoperative 24,48,72 h in the group A was significantly lower than that in the group B (P<0.05). The passive flexion and extension mobility on postoperative 2,3,4 d in the group A was significantly higher than that in the group B(P<0.05). There was no signifi cant difference in muscle strength at each time point between the two groups (P>0.05). The number of PCA pressing times in the group A was less than that in the group B (P<0.05). The CRP level at postoperative 6 h in the group the A was lower than that in the group B (P<0.05). The IL-6 level after operation in the two group was higher than that before operation, but the intergroup had no significant difference (P>0.05). The lower extremity deep venous thrombosis formation detected by ultrasound had no significant difference between the two groups. The D-dimer level during perioperative period in the group A was lower than that in the group B (P<0.05). Conclusion Ultrasound guided continuous femoral nerve block used in postoperative analgesia in the patients undergoing knee arthroplasty has definite analgesic effect, can alleviate postoperative stress damage and incidence of postoperative complications, and is conducive to consolidate the operative curative effect.

Acute respiratory distress syndrome(ARDS) refers to non-cardiac respiratory failure caused by various internal and external factors in the lung, and is a common clinical critical illness.As in adults, lung-protective ventilation strategies combined with pharmacological support remain the mainstay of treatment for children with ARDS.A large number of clinical studies have been carried out on drug therapy, and some progress has been made.This article reviewed alveolar surfactants, hormones, nitric oxide, angiotensin converting enzyme 2, immune nutrition, etc., in order to provide references for subsequent treatment.

Objective To evaluate the effect of dezocine on cognitive function after sevoflurane anesthesia in a rat model of physiological stress.Methods Physiological stress was induced by applying repeated foot shock stimulation and confirmed by open field test.Thirty Spragne-Dawley rats with physiological stress,weighing 180-220 g,were divided into 3 groups (n=10 each) using a random number table:control group (group C),sevoflurane group (group S) and dezocine plus sevoflurane group (group D+S).Normal saline 0.5 ml was intraperitoneally injected at 6 h of oxygen inhalation in group C.Normal saline 0.5 ml was intraperitoneally injected at 6 h of 3.0％ sevoflurane inhalation in group S.Dezocine 3 mg/kg was intraperitoneally injected at 6 h of 3.0％ sevoflurane inhalation in group D+S.At 1,12,24 and 48 h after the end of intraperitoneal injection (T1-4),Morris water maze test was performed,and the time of staying at the original platform quadrant and frequency of crossing the original platform were recorded.The rats were sacrificed after the end of Morris water maze test,brains were removed and hippocampi were isolated for determination of nitric oxide synthase-1 (nNOS) expression (by Western blot) and nNOS positive cells (by immunohistochemistry).Results Compared with group C,the time of staying at the original platform quadrant was significantly shortened at T1,2,the frequency of crossing the original platform was reduced at T1,the expression of nNOS in hippocampus was down-regulated,and the number of nNOS positive cells in hippocampal CA1 region was reduced in group S (P＜0.05),and no significant change was found in the parameters mentioned above in group D+S (P＞0.05).Compared with group S,the time of staying at the original platform quadrant was significantly prolonged at T1,the frequency of crossing the original platform was increased at T1,2,the expression of nNOS in hippocampus was up-regulated,and the number of nNOS positive cells in hippocampal CA1 region was increased in group D+S (P＜0.05).Conclusion Dezocine can improve cognitive function after sevoflurane anesthesia in a rat model of physiological stress,and the mechanism may be related to up-regulating nNOS expression in hippocampi.

Objective To investigate whether Wnt/β-catenin signaling pathway mediating the neuroprotection of isoflurane post-conditioning in hippocampal neurons damage induced by ischemia/reperfusion injury in rats.Methods According to the randomized principle, 60 male Sprague-Dawley rats were randomly divided into five groups (12 rats in each group):sham group (group S), model group (group M), ISO+model group (group MI), ISO+model+DKK-1 group (group MDI) and model+DKK-1 group (group MD).A rat model of middle cerebral artery occlusion (MCAO) was established with 90 min ischemia followed by 24 hreperfusion.Group S was only exposed to one side of the internal carotid artery without fishing line.Isoflurane post-conditioning groups (group MI, MDI) were immediately treated with 1.5％isoflurane for 60 min at the onset of reperfusion.DKK-1 (5μg/kg) was injected intracerebroventricularly 30 min before the model established in group MDI and group MD.After reperfusion for 24 h, Longa score method was used for neurological deficit score.HE staining and Tunel fluorescence was employed to observe the morphological changes of neurons.Immunohistochemistry and Western Blot were applied to detect the expression of target protein in CA1 region.Results Compared with group S, the neurobehavioral score, the number of apoptosis and the expression of Bax and GSK-3βprotein in group M all increased (P<0.05), while the expression ofβ-catenin and Bcl-2/Bax ratio decreased (P<0.05) ;Compared with group M, the neurobehavioral score, the number of apoptosis and the expression of Bax protein were significantly decreased (P<0.05), while the expression of Bcl-2, β-catenin protein and the Bcl-2/Bax ratio were significantly increased (P<0.05) in group MI.Compared with group MI, the neurobehavioral score, the number of apoptosis, Bax and GSK-3βprotein in group MDI were significantly increased (P<0.05), while the Bcl-2, β-catenin protein expression, and Bcl-2/Bax ratio were significantly decreased (P<0.05).Conclusion Isoflurane post-conditioning may protect the hippocampus neurons against cerebral ischemic reperfusion-induced damage via the way that the Wnt/β-catenin signaling pathway regulates the expression levels of Bcl-2 and Bax proteins in rats.

Objective : To investigate the effect of paederosidic acid methyl ester (PAME) on postoperative learning and memory impairment in mice and its mechanism. Methods : C57BL/6J male mice were randomly divided into Sham group , operation group , operation + PAME group ( PAME group) , operation + NADPH oxidase 4(Nox4) adeno⁃associated virus overexpression group (Nox4 overexpression group) , operation + Nox4 adeno⁃associated virus no⁃laden group ( AAV no⁃load group) , and operation + PAME + Nox4 overexpression group ( PN group) . Exploratory laparotomy was performed. PAME(20 mg/kg) was administered by continuous gavage for 7 days after operation , and adeno⁃associated virus was injected into the hippocampus 28 days before operation. Morris water maze test and conditioned fear test were used to detect the learning and memory ability of mice. The expression of Nox4 protein was observed by immunofluorescence. The protein expressions of Nox4 , long chain acyl CoA synthetase 4 (ACSL4) and glutathione peroxidase 4 (GPX4) were detected by Western blot. Reactive oxygen species (ROS) and iron content were determined by spectrophotometry. Results : Compared with the Sham group , the learning and memory ability of the operation group , the Nox4 overexpression group and the AAV no⁃load group decreased , the protein expression of Nox4 and ACSL4 increased , the protein expression of GPX4 decreased , and the ROS and iron content increased. After PAME treatment , the postoperative learning and memory ability of mice was improved , and Nox4 and ferroptosis in hippocampal neurons were alleviated. Conclusion Conclusion PAME treatment can improve the learning and memory ability of postoperative mice , which may be related to the inhibition of hippocampal Nox4⁃mediated ferroptosis.