In many pathogens infection,especially virus,antibody-dependent enhancement(ADE) can aggravate the infection and lead to severe diseases.In this immunopathological phenomenon,virus-specific antibodies enhance the entry of virus into monocytes,macrophages and granulocytic cells and even the replication of virus through different mechanism.This phenomenon has been reported in numerous pathogens including virus,bacteria and parasite and the mechanisms of ADE vary from different species.Further study of ADE can promote the vaccine research and development to make the most use of vaccine and prevent human body from pathogens,which will be helpful to control the spread of pathogens including Zika virus.In the present review,we review the research progress of ADE mechanism in recent years,including antibodies mediating,receptors mediating,complement mediating,viral proteins mediating and cellular mediating ADE.In addition,dengue virus,human immunodeficiency virus,Coxsackie virus,Ebola virus,Zika virus and other pathogens will be illustrated respectively.This review provides insights on the different mechanism of ADE in different pathogens.

ObjectiveTo investigate the effects of postconditioning with electric vagal stimulation on myocardial ischemia-reperfusion (I/R) injury in rats.MethodsSixty male SD rats weighing 250-350 g were randomly divided into 3 groups (n ＝ 20 each):group sham operation (group S); group myocardial I/R (group I/R) and group electric vagal stimulation postconditioning (group POES).Myocardial I/R was induced by occlusion of left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion in groups I/R and POES.In group POES right cervical vagus nerve trunk was stimulated for 30 min with continuous electric rectangular pulses (2 ms,10 Hz) starting from 15 min of myocardial ischemia.The voltage of the pulses was adjusted to decrease HR by 10％ of the baseline HR before stimulation.MAP,HR and RPP (MAP× HR) were recorded before (baseline) and at 1 and 10 min of ischemia and 30,60 and 120 min of reperfusion.Arterial blood samples were collected from 10 rats in each group at 120 min of reperfusion for determination of serum concentrations of cTnI,CK-MB,TNF-a,high mobility group box 1 protein (HMGB1),ICAM-1,IL-1,IL-6 and IL-10 (by ELISA).The animals were then sacrificed and myocardial infarct size was measured by Evans blue and TTC staining.Another 10 rats were sacrificed at 120 min of reperfusion for determination of myocardial contents of TNF-α,HMGB1,ICAM-1,IL-1,IL-6 and IL-10 (by ELISA).ResultsI/R induced myocardial infarct,significantly increased serum concentrations of cTnI,CK-MB,TNF-α,HMGB1,ICAM-1,IL-1 and IL-6 and significantly increased myocardial contents of TNF-α,HMGB1,ICAM-1,IL-1,IL-6 and IL-10 in both ischemic and non-ischemic regions in group I/R as compared with group S.Electric vagal stimulation significantly decreased myocardial infarct size and serum concentrations of cTnI,CK-MB,TNF-α,HMGB1,1CAM-1,IL-1 and IL-6 in group POES compared with group I/R.Myocardial contents of TNF-α,HMGB1,ICAM-1,IL-1 and IL-6 were significantly decreased while myocardial IL-10 content was increased in both ischemic and non-isehemic regions in groups POES compared with group I/R.ConclusionPostconditioning with electric vagal stimulation can attenuate myocardial I/R injury by inhibiting inflammatory response in rats.

Objective To investigate the effects of postconditioning with α7 nicotinic acetylcholine receptor (α7nAChR) agonist and ischemia on myocardial ischemia-reperfusion (IR) injury in rats. Methods Fifty adult male SD rats weighing 290-320 g were randomly divided into 5 groups ( n = 10 each): Ⅰ sham operation group, Ⅱ IR group, Ⅲ ischemic postconditioning group, Ⅳ α7nAChR agonist postconditioning group and Ⅴpostconditioning with α7nAChR agonist and ischemia group. Myocardial I/R was induced by ligation of anterior descending branch of left coronary artery for 30 min followed by 1 80 min of reperfusion. In group] the anterior descending branch was only exposed but not ligated. In group Ⅲ the hearts were subjected to 3 episodes of 10 second ischemia at 10 second intervals at the end of 30 min ischemia before 180 min reperfusion, Intraperitoneal PNU282987 2.4 mg/kg was injected at the end of 30 min ischemia before 180 min reperfusion in group Ⅳ and Ⅴ .Blood samples were taken from right internal jugular vein at 180 min of reperfusion. Then the rats were killed and hearts removed to determine the concentrations of serum cardiac troponin-I (cTnI), TNF-α and high-mobility group box 1 (HMGB1) by ELISA. The infarction size was measured by Evans blue and triphenyltetrazolium chloride staining. Results The infarction size was significantly larger in the other groups and concentrations of serum cTrI, TNF-α and HMGB1 were significantly higher in group Ⅱ than in group Ⅰ ( P ＜ 0.05). The infarction size was significantly smaller and concentrations of serum cTnI, TNF-α and HMGBI were significantly lower in group Ⅲ, Ⅴ than in group Ⅱ (P ＜ 0.05). The infarction size was significantly smaller in group Ⅴ and concentrations of serum cTnI, TNF-α and HMGB1 were significantly lower in group Ⅳ and Ⅴ than in group Ⅲ (P ＜0.05). The infarction size was significantly smaller and concentrations of serum cTnI, TNF-α and HMGB1 were significantly lower in group Ⅴ than in group Ⅳ ( P ＜ 0.05 ). Conclusion Postconditioning with α7nAChR agonist and ischemia can reduce myocardial I/R injury and the efficacy is better than that of α7nAChR agonist postconditioning or ischemic postconditioning alone.

Objective To investigate the role of cyclooxygenase-2(COX-2)and mitochondrial adenosine tuiphosphate sensitive potassium channels (mito-KATP channels) in sufentanil preconditioning-induced delayed cardiopreteetion against myocardial ischemia-reperfnsion (I/R) injury in rats. Methods Seventy-two adult male Wistsr rats weighing 250-300 g were randomly divided into 6 groups ( n =12 each). Group Ⅰ,Ⅱ,Ⅲ were preconditioned with intraperitoneal (IP) normal saline (NS) 1 ml/kg while group Ⅳ,Ⅴ,Ⅵ with IP sufentanil 20 μg/kg at 24 h before myocardial ischemia. Group Ⅱ and Ⅴ were given IP NS-398 ( COX-2 inhibitor) 5 mg/kg at 30 rain before myocardial ischemla while group Ⅲ and Ⅵ were given intravenous 5-HD (mito-KATP channelblocker) 10 mg/kg at 10 min before ischemia or before being killed. Six animals in each group underwent 45 min myocardial ischemia followed by 120 min reperfusion, while the other six animals in each group were killed immediately before ischemia for determination of myocardial COX-2 expression and myocardial PGF2 and PGF1α content. Myocardial ischemia was induced by occlusion of left anterior descending branch (LAD) of coronary artety for 45 rain followed by 120 min reperfusion. MAP and HR were recorded immediately before ischemia (T0), at 15, 30, 45 rain of ischemia (T1-3) and at 30, 60, 90, 120 vain of reperfusion (T4-7). Heart rate-blood pressure product (RPP) was calculated. Arterial blood samples were obtained at T0.3 and T7 for measurement of plasma CK-MB activity. The animals were killed at the end of 120 nan reperfusion. The hearts were removed for determination of myocardial infarct area (IA) and area at risk (AAR). LA/AAR was calculated. Results There was no significant difference in HR, MAP and RPP at all time points among the 6 groups. Preconditioning with sufentanil significantly decreased plasma CK-MB activity at T3 and T7 and IA/AAR in group Ⅳ as compared with group Ⅰ.Myocardial COX-2 expression was up-regulated and PGE2 and PGF1α, contents were elevated by sufentanil preconditioning in group Ⅳ as eomared with control group (Ⅰ). In group Ⅴ and Ⅳ preconditioning with NS-398/5-HD significantly increased plasma CK-MB concentration and IS/AAB as compared with group Ⅳ, indicating involvement of COX-2 and mito-KATP channels in the sufentanil-induced delayed cardioprotection.The myocardial PGE2 and PGF1α contents were significantly reduced in group Ⅴ as compared with group Ⅳ. There was no significant difference in the myocardial COX-2 expression among group Ⅳ, Ⅴ and Ⅵ. Conclusion Both COX-2 and mito-KATP channels are involved in sufentanil preconditioning-induced delayed cardiopmtection.

Objective To compare the effects of ischemic preconditioning versus ischemic postconditioning on myocardial ischemia-reperfusion (I/R)-induced inflammatory response in rats. Methods Forty male SD rats weighing 290-320 g were randomly divided into 4 groups ( n = 10 each): Ⅰ group sham operatin (group S); Ⅱ group I/R; Ⅲ group ischemic preconditioning (group IPC) and Ⅳ group ischemic postconditioning (group IPOC).Myocardial I/R was induced by 30 min ligation of left anterior descending branch (LAD) of coronary artery followed by reperfusion. In group IPC myocardial I/R was preceded by 3 cycles of ischemia followed by reperfusion (each lasting 5 min) while in group IPOC 3 cycles of I/R (each lasting 10 s) was started at the end of 30 min myocardial ischemia. MAP, HR and RPP ( MAP × HR) were recorded before (baseline) and at 1 and 20 min of ischemia and 60, 120 and 180 min of reperfusion. Venous blood samples were collected at 30 and 180 min of reperfusion for determination of serum concentrations of TNF-α, IL-6, high-mobility group box 1 (HMGB1) and cTnI. The animals were sacrificed at 180 min of reperfusion and the myocardial infarct size was measured. Results Myocardial I/R significantly decreased MAP and RPP and increased myocarcial infarct size, serum concentrations of TNF-α, IL-6,HMGB1 and cTnI in group I/R as compmed with group S. Ischemic pre- and postconditioning significantly increased MAP and reduced myocardial infarct size and I/R-induced increase in serum TNF-α, HMGB1 and cTnI concentrations in group Ⅲ and Ⅳ as compared with group Ⅱ (I/R). The myocardial infarct size was significantly larger and the serum concentrations of TNF-α, IL-6 and HMGB1 were significantly higher in ischemic postconditioning group than in the preconditioning group. Conclusion Ischemic preconditioning is more effective in attenuating the myocardial I/R-induced inflammatory response than the ischemic postconditioning.

ObjectiveTo evaluate the effects of combined vagus nerve electric stimulation postconditioning and limb remote ischemic postconditioning on myocardial ischemia-reperfusion (I/R) injury in rats.Methods One hundred male SD rats aged 8 weeks weighing 250-350 g were randomly allocated into 5 groups ( n =20 each):sham operation group (group S); I/R group; vagus nerve electric stimulation postconditioning group (group POES) ; limb remote ischemic postconditioning group (group RP) and vagus nerve electric stimulation postconditioning + limb remote ischemic postconditioning group (group POES-RP).Myocardial I/R was induced by occlusion of left anterior descending branch (LAD) of coronary artery for 30 min followed by 120 min reperfusion in groups I/R,POES,RP and POES-RP.In groups POES and POES-RP,right cervical vagus nerve trank was stimulated for 30 min with continuous electric rectangular pulses (2 ms,10 Hz) starting from 15 min of myocardial ischemia.The voltage of the pulses was adjusted to decrease HR by 10％ of the baseline HR before stimulation.In groups RP and POES-RP the animals underwent 10 min ischemia of bilateral hind limbs starting from 20 min of myocardial ischemia.Arterial blood samples were collected from 10 rats in each group at 120 min of reperfusion for determination of serum concentrations of cTnI,CK-MB,TNF-α,high mobility group box 1 protein (HMGB1),intercellular adhesion molecule-1(ICAM-1),IL-1,IL-6 and IL-10 (by ELISA).The animals were then sacrificed and myocardial infarct size was measured by Evans blue and TTC staining.Another 10 rats were sacrificed at 120 min of reperfusion for determination of myocardial contents of TNF-α,HMGB-1,ICAM-1,IL-1,ID6 and IL-10 (by ELISA).ResultsI/R induced myocardial infarct and significantly increased serum concentrations of cTnI,CK-MB,TNF-α,HMGBi,ICAM-1,IL-1 and IL-6 and increased myocardial contents ofTNF-α,HMGB1,ICAM-1,IL-1,IL-6 and IL-10 in both ischemic and non-ischemic regions in group I/R as compared with group S.Vagus nerve electric stimulation postconditioning,limb remote ischemic postconditioning and vagus nerve electric stimulation postconditioning + limb remote ischemic postconditioning significantly decreased myocardial infarct size and serum concentrations of cTnI,CK-MB,TNF-α,HMGB1,ICAM-1,IL-1 and IL-6 and decreased myocardial contents of TNF-α,HMGB1,ICAM-1,IL-1,IL-6 in groups POES,RP and POES-RP as compared with group I/R.Compared with group I/R,myocardial IL-10 content in both ischemic and non-ischemic regions was significantly increased in groups POES and POES-RP.Compmared with group POES,myocardial infarct size,serum concentrations of cTnI,CK-MB,TNF-α,ICAM-1 and myocardial contents of ICAM-1 and IL-6 in ischemic region were significantly decreased,while myocardial content of IL-10 in non-ischemic region was increased in group POES-RP.Compared with group RP,myocardial infarct size,serum concenuations of cTnI,CK-MB,TNF-α,HMGB1,ICAM-1,IL-1,IL-6 and myocardial contents of TNF-α,ICAM-1,IL-1 and IL-6 in ischemic region were significantly decreased,myocardial content of IL-10 in ischemic region was increased and HMGB1,ICAM-1,IL-1 and IL-6 contents were decreased,IL-10 content was increased in myocardial of ischemic region in group POES-RP.ConclusionMyocardial I/R injury is attenuated and myocardial protection is enhanced by combination of vagus nerve electric stimulation postconditioning and limb remote ischemic postconditioning in rats by inhibiting inflammatory response in rats.

Objective To evaluate the protective effects of fentanyl postconditioning and remote limb ischemic postconditioning (RLIP) against myocardial ischemia-reperfusion (I/R) injury in rats. Methods Thirty-nine male SD rats aged 8 weeks weighing 250-350 g were randomly allocated into 5 groups: Ⅰ group sham operation (group S, n = 5); Ⅱ group I/R ( n = 7); Ⅲ group fentanyl postconditioning (group F, n= 9); Ⅳ group RLIP (group R, n = 9) and group Ⅴ fentanyl postconditioning + RLIP (group F-R, n = 9). The animals were anesthetized with intraperitoneal 3% pentobarbital 50 mg/kg, intubated and mechanically ventilated. Myocardial I/R was induced by occlusion of anterior desending branch of left coronary artery for 30 min followed by 180 min reperfusion. Fentanyl 30 μg/kg was injected iv at 15 min of myocardial ischemia in group F and F-R In group R and F-R the animals underwent 10 min ischemia of bilateral hind limbs starting from 15 min of myocardial ischemia. HR and MAP were recorded at 5,60,120 and 180 min of reperfusion and rate-pressure product( RPP, HR × MAP) were calculated. At the end of 180 min reperfusion, arterial blood samples were obtained for measurement of the activities of plasma lactate dehydrogenase (LDH) and creatine kinase isoenzyme MB (CK-MB), and the concentration of serum cardiac troponin Ⅰ (cTnI). The animals were then sacrificed. The infarct size was evaluated by double staining with Evans blue and triphenyl tetrazolium chloride. Results Myocardial I/R significantly increased plasma LDH and CK-MB activities and serum cTnI concentration and decreased HR,MAP and RPP as compared with group S.Fentanyl postconditioning and RLIP both decreased plasma CK-MB activity, serum cTnI concentration and infarct size and increased HR, MAP and RPP in group F, R and F-R as compared with group I/R. Plasma CK-MB activity,serum cTnI concentration and RPP were significantly lower and infarct size was smaller in group F-R than in group F. The infarct size was significantly smaller and MAP and RPP were higher in group F-R than in group R.Conclusion Fentanyl postconditioning can provide a myocardial protection against I/R injury. Myocardial protection is enhanced by combination of fentanyl postconditioning and RLIP.

Objective To evaluate the roles of PI3K/Akt and JAK/STAT signal transduction pathways in reduction of myocardial ischemia/reperfusion (I/R) injury by postconditioning with α subunit-containing nicotinic acetylcholine receptor (α7nAChR) agonist in rats.Methods Sixty Sprague-Dawley rats,weighing 290-320 g,were randomly divided into 4 groups (n =15 each):I/R group,ischemic preconditioning group (IPC group),ischemic postconditioning group (IPOC group) and postconditioning with specific α7nAChR agonist PNU282987 group ( PNU group ).Myocardial I/R was produced by 30 min occlusion of left anterior descending coronary artery followed by 180 min reperfusion in the 4 groups.The animals were subjected to 3 cycles of 5 min myocardial ischemia and 5 min reperfusion before 30 min myocardial ischemia in IPC group.The animals underwent 3 cycles of 10 s myocardial ischemia at 5 s intervals before 180 min reperfusion in group IPOC.PNU282987 2.4 mg/kg was injected intraperitoneally immediately before the reperfusion.At 60 min of reperfusion,5 rats in each group were sacrificed and the hearts were removed to determine the expression of Akt and STAT3 mRNA,phosphorylated Akt (p-Akt) and phosphorylated STAT3 (p-STAT3) in myocardial tissues.The left 10 rats in each group were sacrificed at 180 min of reperfusion and the hearts were removed to measure the infarct size.Results Compared with I/R group,the expression of STAT3 mRNA and p-Akt was significantly up-regulated in IPC group,and the expression of p-Akt and p-STAT3 was significantly up-regulated in IPOC group ( P ＜ 0.05).The infarct size was significantly reduced in IPC,IPOC and PNU groups compared with I/R group ( P ＜ 0.05 ).Conclusion The mechanism by which α7nAChR agonist postconditioning reduces myocardial I/R injury is not related to PI3K/Akt and JAK/STAT signal transduction pathways in rats.

Objective To investigate the role of reactive oxygen species (ROS) in the reduction of myocardial ischemia-reperfusion (I/R) injury by fentanyl postconditioning and remote limb ischemic postconditioning in rats.Methods Sixty-three male Sprague-Dawley rats,aged 8 weeks,weighing 250-350 g,were equally and randomly allocated into 7 groups:sham operation group (group S),group I/R,fentanyl postconditioning group (group F),remote limb ischemic postconditioning group (group R),ROS scavenger N-(2-Mercaptopropionyl) glycine (MPG) group (group M),MPG + fentanyl postconditioning group (group MF),and MPG + remote limb ischemic postconditioning group (group MR).Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 180 min of reperfusion.In group S the anterior descending branch was only exposed but not ligated.MPG 5 mg/kg was infused intravenously from 5 min before ischemia to 15 min of reperfusion in groups M,MF and MR,while the equal volume of normal saline was given in the other four groups.In groups F and MF,fentanyl 30 μg/kg was injected intravenously at 15 min of myocardial ischemia.In groups R and MR,the animals underwent 10 min ischemia of bilateral hind limbs starting from 15 min of myocardial ischemia.Arterial blood samples were taken at 180 min of reperfusion to determine the serum cardiac troponin I (cTnI) concentration.The rats were then sacrificed.The infarct size was measured by TTC.Results Compared with group S,the serum cTnI concentration and infarct size were significantly increased in the other six groups (P ＜0.05).Compared with group I/R,no significant change was found in the serum cTnI concentration and infarct size in M group,and the serum cTnI concentration and infarct size were significantly decreased in F and R groups (P ＜ 0.05).There was no significant difference in the serum cTnI concentration and infarct size between MF group and F group (P ＞ 0.05).The serum cTnI concentration was significantly higher and the infarct size was larger in group MR than in group R (P ＜ 0.05).Conclusion ROS is involved in the reduction of myocardial I/R injury by remote limb ischemic postconditioning in rats,but not in the myocardial protection provided by fentanyl postconditioning.

Objective: To investigate the effect of exercise intervention on sleep quality of female college students with anxiety, and to further explore the mediating effect of negative emotions in this association. Methods: Seventy female college students were randomly divided into experimental group (34 patients) and control group(36 patients). The experimental group received eight-week aerobic exercise and yoga training. The control group received no training. Sleep Quality Scale, Negative Emotion Scale and Anxiety Self-rating Scale were used to assess the level of sleep and negative emotion before and after exercise intervention. Results: After exercise intervention, sleep quality (4.31±1.26), anxiety (36.41±7.32) and negative emotion (2.37±0.50) in the experimental group significantly improved(P<0.01), no similar changes were found in the control group(P<0.05). By examining the mediating effects, negative emotions played a partial mediating role in the association between exercise and sleep quality(t=6.77, P<0.01). Conclusion Exercise intervention significantly improved the quality of sleep and negative emotion among female college students with anxiety. Negative emotions play a partial role in the positive effect of exercise on sleep quality.