ObjectiveTo investigate the effects of Zuoguiwan on osteoclast activation induced by breast cancer and its mechanism. MethodsTo simulate breast cancer-induced osteoclastic bone metastasis， RAW264.7 cells were cultured in conditioned medium containing 50% supernatant of MDA-MB-231 breast cancer cells. The dosages of Zuoguiwan used in the experiment were sera containing 5% and 10% Zuoguiwan. Tartrate-resistant acid phosphatase （TRAP） staining was used to detect osteoclast activation. Enzyme-linked immunosorbent assay （ELISA） was used to measure Cathepsin K secretion from RAW264.7 cells. Real-time quantitative polymerase chain reaction （PCR） was used to detect the mRNA expression levels of osteocalcin （OCN） and bone sialoprotein （BSP）. Immunoprecipitation was employed to detect the interaction between Runt-related transcription factor 2 （Runx2） and core binding factor β subunit （CBF-β）. Western blot was used to assess the protein expression of Runx2， phosphorylated Runx2 （p-Runx2）， extracellular signal-regulated kinases 1/2 （ERK1/2）， p-ERK1/2， p38 mitogen-activated protein kinase （MAPK）， p-p38 MAPK， and CBF-β. ResultsCompared with the blank group， the MDA-MB-231 cell supernatant group showed a significant increase in TRAP-positive cell counts and Cathepsin K secretion. Meanwhile， the expression levels of p-Runx2， Runx2-CBF-β interaction， BSP and OCN mRNA， p-p38 MAPK， and p-ERK1/2 proteins were significantly decreased （P<0.01）. Compared with the MDA-MB-231 cell supernatant group， Zuoguiwan-containing sera significantly reduced TRAP-positive cell counts and Cathepsin K secretion （P<0.01）， significantly increased p-Runx2， BSP and OCN mRNA expression， as well as p-p38 MAPK and p-ERK1/2 protein levels， and promoted the interaction between Runx2 and CBF-β （P<0.01）. No significant change in Runx2 expression was observed. Compared to the blank group， the BVD-523 group showed significantly lower expression of p-p38 MAPK and p-ERK1/2 proteins （P<0.01）. Compared with the BVD-523 group， both low and high concentration Zuoguiwan-containing sera groups showed significantly higher p-p38 MAPK expression （P<0.01）， and the high concentration Zuoguiwan group also exhibited a significant increase in p-ERK1/2 expression （P<0.01）， while no statistical difference was found in the low-dose group. ConclusionZuoguiwan inhibits osteoclast activation by inducing phosphorylation of the key transcriptional regulator Runx2 in intra-osteoclast bone formation， and this process is closely associated with the activation of the p38 MAPK/ERK signaling pathway.

Objective To explore the factors affecting the prognosis of patients with symptomatic severe intracranial artery stenosis after interventional therapy,and to construct a nomogram prediction model accordingly.Methods The clinical data of 121 patients with symptomatic severe intracranial artery stenosis,who received interventional treatment at the First People's Hospital of Zhengzhou from June 1,2021 to October 31,2024,were retrospectively analyzed.The general data,characteristics of vascular lesions,treatment-related factors and prognosis of patients were collected.According to the modified Rankin scale(mRS)score,the patients were divided into good prognosis group(mRS score ≤2 points)and poor prognosis group(mRS score＞2 points).The clinical data were compared between the two groups.Multivariate logistic regression analysis was used to identify and determine independent factors affecting patient's outcomes,to construct a nomogram prediction model and to validate this model.Results Among the 121 patients,31(25.61％)had poor prognosis and 90(74.38％)had good prognosis.The postoperative 3-month mRS score was lower than preoperative mRS score value(P＞0.05).There were significant differences in hypertension history,stenosis site,stenosis degree,collateral circulation state,interventional therapeutic mode,cholesterol level,platelet count,lesion length and preoperative NIHSS score(P＜0.05)between the poor prognosis group and the good prognosis group.Multivariate analysis showed that hypertension history,stenosis degree,collateral circulation status,cholesterol level,platelet count,lesion's length and preoperative NIHSS score were the independent influencing factors for the prognosis of patients with symptomatic severe intracranial artery stenosis.The predicted AUC of the nomogram model was 0.931(95％ CI=0.873-0.989),and the calibration curve showed that the predicted value was in good agreement with the actual value.Conclusion Hypertension history,stenosis degree,collateral circulation status,cholesterol level,platelet count,lesion length and preoperative NIHSS score are the important influencing factors for the prognosis of patients with symptomatic severe intracranial artery stenosis.The nomogram prediction model constructed in this study shows a high accuracy in predicting the prognosis of patients,and it can provide important reference for clinical decision-making.

Objective:To evaluate the role of uncoupling protein 2 in dexmedetomidine-induced alleviation of myocardial ischemia-reperfusion (I/R) injury in diabetic mice.Methods:SPF C57BL/6 male mice, aged 6-8 weeks, weighing 20-25 g, in which the model of type 2 diabetes mellitus was established by high-fat feeding combined with intraperitoneal injection of streptozotocin, were used in this study. Ninety diabetic mice were divided into 5 groups ( n=18 each) by a random number table method: sham operation group (S group), myocardial I/R group, myocardial I/R+ UCP2 inhibitor genipin group (I/R+ G group), myocardial I/R+ dexmedetomidine group (I/R+ D group) and myocardial I/R+ dexmedetomidine+ UCP2 inhibitor genipin group (I/R+ DG group). Myocardial I/R injury model was established by ligating the left anterior descending coronary artery of diabetic mice for 60 min followed by 120 min of reperfusion. Dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D group. Genipin 100 mg/kg was intraperitoneally injected at 14 h prior to ischemia, and dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D+ G group. The concentrations of cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 in serum were detected by enzyme-linked immunosorbent assay at 120 min of reperfusion. The myocardial tissue was obtained for determination of the myocardial infarct size, the level of reactive oxygen species (ROS) (by flow cytometry), and the expression of UCP2, nuclear factor kappa B (NF-κB) inhibitory protein α (IκBα), phosphorylated IκBα (p-IκBα), NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) (by Western blot) and for observation of the morphological structure of the myocardial tissue. The cardiac function was evaluated by echocardiography at 24 h of reperfusion. Results:Compared with group S, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α, IL-6 and IL-10 were increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the stroke volume (SV), ejection fraction (EF), and left ventricular fractional shortening (FS) were decreased ( P<0.05), and the myocardial structure was severely damaged in group I/R. Compared with group I/R, the percentage of myocardial infarct size and level of ROS were significantly decreased, the concentrations of cTnI, TNF-α and IL-6 were decreased, the concentration of IL-10 was increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were decreased, the SV, EF and FS were increased ( P<0.05), and the pathological damage was significantly attenuated in group I/R+ D. Compared with group I/R+ D, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α and IL-6 were increased, the concentration of IL-10 was decreased, the expression of UCP2 was down-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the SV, EF and FS were decreased ( P<0.05), and the pathological damage was aggravated in group I/R+ D+ G. Conclusions:Dexmedetomidine may ameliorate myocardial I/R injury by up-regulating UCP2 expression in the myocardium and inhibiting mitochondrial ROS-mediated inflammatory responses in diabetic mice.

Objective:To evaluate the role of NOD-like receptor protein 3 (NLRP3) inflammasome-mediated microglia activation in myocardial ischaemia-reperfusion-induced brain injury in mice.Methods:Fifty-two SPF healthy male wild-type C57BL/6 mice and 52 NLRP3 -/- mice, aged 8-10 weeks, were divided into 4 groups ( n=26 each) using a random number table method: wild type sham operation group (W-S group), wild type myocardial ischemia-reperfusion group (W-IR group), NLRP3 -/- sham operation group (NLRP3 -/--S group), and NLRP3 -/- myocardial ischemia-reperfusion group (NLRP3 -/--IR group). The myocardial ischemia-reperfusion-induced brain injury model was established by ligating the left anterior descending coronary artery for 45 min followed by 24 h of reperfusion in anesthetized mice. The cognitive function was evaluated using the modified Morris water maze test at 24 h of reperfusion. The mice were sacrificed after blood specimens were collected, and brain tissues were obtained for measurement of the blood-brain barrier permeability and water content, for microscopic examination of the pathological changes of brain tissues, and for determination of serum S-100β protein and neuron-specific enolase (NSE) concentrations, contents of interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α) in hippocampal tissues (by enzyme-linked immunosorbent assay), expression of NLRP3, apoptosis-associated speck-like protein (ASC), cleaved cysteine aspartate protease 1 (cleaved-caspase-1), gasdermin D (GSDMD), ionized calcium-binding adapter molecule 1 (Iba-1), and occludin in hippocampal tissues (by immunofluorescence and/or Western blot). The apoptosis rate of neurons and density of dendritic spine were calculated. Results:Compared with sham operation group, the escape latency was significantly prolonged, the number of crossing the original platform was decreased, and the time spent in the target quadrant was shortened, the concentrations of serum S-100β protein and NSE were increased, the blood-brain barrier permeability and brain water content were increased, the dendritic spine density in the hippocampal CA1 area was decreased, the contents of IL-1β, IL-6 and TNF-α were increased, the expression of NLRP3, ASC, cleaved-caspase-1, GSDMD and Iba-1 was up-regulated, and the expression of occludin was down-regulated ( P<0.05), and the pathological injury to brain tissues was found in ischemia-reperfusion group. Compared with W-IR group, the escape latency was significantly shortened, the number of crossing the original platform was increased, and the time spent in the target quadrant was prolonged, the concentrations of serum S-100β protein and NSE were decreased, the blood-brain barrier permeability and brain water content were decreased, the dendritic spine density in the hippocampal CA1 area was increased, the contents of IL-1β, IL-6 and TNF-α were decreased, the expression of NLRP3, ASC, cleaved-caspase-1, GSDMD and Iba-1 was down-regulated, and the expression of occludin was up-regulated ( P<0.05), and the pathological injury to brain tissues was alleviated in NLRP3 -/--IR group. Conclusions:NLRP3 inflammasome-mediated microglia activation is involved in myocardial ischaemia-reperfusion-induced brain injury in mice.

Objective:To evaluate the role of uncoupling protein 2 in dexmedetomidine-induced alleviation of myocardial ischemia-reperfusion (I/R) injury in diabetic mice.Methods:SPF C57BL/6 male mice, aged 6-8 weeks, weighing 20-25 g, in which the model of type 2 diabetes mellitus was established by high-fat feeding combined with intraperitoneal injection of streptozotocin, were used in this study. Ninety diabetic mice were divided into 5 groups ( n=18 each) by a random number table method: sham operation group (S group), myocardial I/R group, myocardial I/R+ UCP2 inhibitor genipin group (I/R+ G group), myocardial I/R+ dexmedetomidine group (I/R+ D group) and myocardial I/R+ dexmedetomidine+ UCP2 inhibitor genipin group (I/R+ DG group). Myocardial I/R injury model was established by ligating the left anterior descending coronary artery of diabetic mice for 60 min followed by 120 min of reperfusion. Dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D group. Genipin 100 mg/kg was intraperitoneally injected at 14 h prior to ischemia, and dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D+ G group. The concentrations of cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 in serum were detected by enzyme-linked immunosorbent assay at 120 min of reperfusion. The myocardial tissue was obtained for determination of the myocardial infarct size, the level of reactive oxygen species (ROS) (by flow cytometry), and the expression of UCP2, nuclear factor kappa B (NF-κB) inhibitory protein α (IκBα), phosphorylated IκBα (p-IκBα), NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) (by Western blot) and for observation of the morphological structure of the myocardial tissue. The cardiac function was evaluated by echocardiography at 24 h of reperfusion. Results:Compared with group S, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α, IL-6 and IL-10 were increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the stroke volume (SV), ejection fraction (EF), and left ventricular fractional shortening (FS) were decreased ( P<0.05), and the myocardial structure was severely damaged in group I/R. Compared with group I/R, the percentage of myocardial infarct size and level of ROS were significantly decreased, the concentrations of cTnI, TNF-α and IL-6 were decreased, the concentration of IL-10 was increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were decreased, the SV, EF and FS were increased ( P<0.05), and the pathological damage was significantly attenuated in group I/R+ D. Compared with group I/R+ D, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α and IL-6 were increased, the concentration of IL-10 was decreased, the expression of UCP2 was down-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the SV, EF and FS were decreased ( P<0.05), and the pathological damage was aggravated in group I/R+ D+ G. Conclusions:Dexmedetomidine may ameliorate myocardial I/R injury by up-regulating UCP2 expression in the myocardium and inhibiting mitochondrial ROS-mediated inflammatory responses in diabetic mice.

Objective:To evaluate the role of NOD-like receptor protein 3 (NLRP3) inflammasome-mediated microglia activation in myocardial ischaemia-reperfusion-induced brain injury in mice.Methods:Fifty-two SPF healthy male wild-type C57BL/6 mice and 52 NLRP3 -/- mice, aged 8-10 weeks, were divided into 4 groups ( n=26 each) using a random number table method: wild type sham operation group (W-S group), wild type myocardial ischemia-reperfusion group (W-IR group), NLRP3 -/- sham operation group (NLRP3 -/--S group), and NLRP3 -/- myocardial ischemia-reperfusion group (NLRP3 -/--IR group). The myocardial ischemia-reperfusion-induced brain injury model was established by ligating the left anterior descending coronary artery for 45 min followed by 24 h of reperfusion in anesthetized mice. The cognitive function was evaluated using the modified Morris water maze test at 24 h of reperfusion. The mice were sacrificed after blood specimens were collected, and brain tissues were obtained for measurement of the blood-brain barrier permeability and water content, for microscopic examination of the pathological changes of brain tissues, and for determination of serum S-100β protein and neuron-specific enolase (NSE) concentrations, contents of interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α) in hippocampal tissues (by enzyme-linked immunosorbent assay), expression of NLRP3, apoptosis-associated speck-like protein (ASC), cleaved cysteine aspartate protease 1 (cleaved-caspase-1), gasdermin D (GSDMD), ionized calcium-binding adapter molecule 1 (Iba-1), and occludin in hippocampal tissues (by immunofluorescence and/or Western blot). The apoptosis rate of neurons and density of dendritic spine were calculated. Results:Compared with sham operation group, the escape latency was significantly prolonged, the number of crossing the original platform was decreased, and the time spent in the target quadrant was shortened, the concentrations of serum S-100β protein and NSE were increased, the blood-brain barrier permeability and brain water content were increased, the dendritic spine density in the hippocampal CA1 area was decreased, the contents of IL-1β, IL-6 and TNF-α were increased, the expression of NLRP3, ASC, cleaved-caspase-1, GSDMD and Iba-1 was up-regulated, and the expression of occludin was down-regulated ( P<0.05), and the pathological injury to brain tissues was found in ischemia-reperfusion group. Compared with W-IR group, the escape latency was significantly shortened, the number of crossing the original platform was increased, and the time spent in the target quadrant was prolonged, the concentrations of serum S-100β protein and NSE were decreased, the blood-brain barrier permeability and brain water content were decreased, the dendritic spine density in the hippocampal CA1 area was increased, the contents of IL-1β, IL-6 and TNF-α were decreased, the expression of NLRP3, ASC, cleaved-caspase-1, GSDMD and Iba-1 was down-regulated, and the expression of occludin was up-regulated ( P<0.05), and the pathological injury to brain tissues was alleviated in NLRP3 -/--IR group. Conclusions:NLRP3 inflammasome-mediated microglia activation is involved in myocardial ischaemia-reperfusion-induced brain injury in mice.

Objective:To investigate the clinicopathological and genetic features of confined placental mosaicism (CPM) and its effect on fetal intrauterine growth.Methods:Fourteen CPM cases of Haidian Maternal and Children Health Hospital were collected from May 2018 to March 2022. Clinicopathological examination on placental specimens and molecular genetic analysis were performed.Results:The age of the parturient women ranged from 27 to 34 years, with an average age of (30.0±3.54) years. The gestational weeks ranged from 35 +1 to 41 +2 weeks. There were 4 premature births and 10 term births, among which 6 were female and 8 were male fetuses. Nine cases (9/14) had adverse pregnancy outcomes, including 7 cases of fetal growth restriction. The weight of CPM placenta decreased, with 6 cases below the 10th percentile of weight standards and 5 cases between the 10th and 25th percentile. All 14 CPM placental specimens showed morphological changes of perfusion dysfunction to varying degrees, with mainly placental-maternal vascular malperfusion followed by placental-fetal vascular malperfusion. The mosaic chromosomes in different CPM cases varied, with 16-trisomy/monosomy mosaicism being the most common followed by 7-trisomy and 21-trisomy/monosomy mosaicism. The mosaic proportion was unequal in different parts of the same CPM placenta, with the mosaic proportion of umbilical cord, fetal membranes, fetal surface, maternal surface, and edge ranging from 1% to 70%. Conclusions:The mosaic chromosomes in different CPM cases vary, and the mosaic proportion is unequal in different parts of the same CPM placenta. The pathological morphology is mainly manifested as perfusion dysfunction, which can lead to adverse pregnancy outcomes such as fetal growth restriction and preterm birth.

Objective:To analyze the depressive symptoms of physical and mental workers and the impact of their behavior and lifestyle on their depressive symptoms.Methods:In August 2022, a cross-sectional study design was adopted to select 553 workers as research subjects using cluster sampling. General demographic information, health-related behaviors and lifestyles were collected, and their depressive symptoms were evaluated using the Chinese version of the Patient Health Questionnaire 9 (PHQ-9). The differences in general demographic information, health-related behaviors and lifestyles between physical and mental workers were analyzed, and logistic regression was used to analyze the influencing factors of depressive symptoms in occupational populations.Results:Among the 553 subjects, 317 were physical workers (57.32%) and 236 were mental workers (42.68%). Statistically significant differences were observed between the two groups in terms of education level, monthly income, smoking rate, regular physical exercise rate and appropriate sleep time rate ( P<0.05). The score and the detection rate of depression symptoms among physical workers were (9.67±2.75) points and 20.82% (66/317), respectively, which were higher than those of mental workers [(8.34±2.18) points, 12.71% (30/236) ] ( t=6.13, χ 2=6.20, P<0.05). The results of logistic regression analysis showed that smoking, regular physical exercise, appropriate sleep time and mental work were influencing factors of depressive symptoms among the occupational population ( OR=1.592, 95% CI: 1.316-1.825; OR=0.659, 95% CI: 0.416-0.830; OR=0.502, 95% CI: 0.257-0.717; OR=0.839, 95% CI: 0.522-0.967; P<0.05) . Conclusion:The depressive symptoms of physical workers are more serious than those of mental workers. Low education level, not frequently participating in physical exercise, smoking and sleep disorder are potential risk factors that affect the depressive symptoms of the occupational population.

Objective:To investigate the current status of literature reading report and clinical research ability among professional postgraduate students in pediatrics, and to provide a reference for cultivating high-quality pediatric talents.Methods:A total of 91 professional postgraduate students majoring in pediatrics were selected as research subjects from five affiliated hospitals of Zhengzhou University, and according to whether they participated in literature reading report, they were divided into participating group with 38 students and non-participating group with 53 students. The method of questionnaire combined with interview was used to investigate the implementation of literature reading report, the willingness to participate in literature reading report, and the current status of clinical research ability. SPSS 25.0 was used to perform the chi-square test and the Wilcoxon rank-sum test.Results:In the participating group, 60.53% (23/38) of the students thought that there was a significant improvement in clinical research ability after literature reading report, and in the non-participating group, 94.12% (48/51) of the students wanted to carry out literature reading report. Compared with the non-participating group, the participating group had significantly higher publication rate, project participation rate, academic exchange rate, and literature reading quantity ( P<0.05) and significantly better abilities of literature search and reading, professional English, and PPT presentation ( P<0.05), while there were no significant differences between the two groups in the scores of statistical analysis ability, project design ability, clinical thinking ability, and evidence-based medicine ability ( P>0.05). Conclusions:Literature reading report can promote the improvement in clinical research ability among professional postgraduate students in pediatrics, and it should be carried out regularly for a long time with adherence to the principle of clinical orientation and emphasis on the reading of methodology and statistics in literature.

Objective:To explore the molecular mechanism of dexmedetomidine(Dex)protecting ischemia/reperfusion(I/R)myocardium.Methods:Wild type mice were grouped into control(Control)group,sham operation(Sham)group,WT I/R group,WT Dex group,and Dectin-1 knock out mice were grouped into KO I/R group and KO Dex group in the in vivo study(n=6).TTC stain-ing was used to determine the myocardial infarction area(%)of the above six groups of mice.HE staining and pathological analyze was used to determine the myocardial injury.Serum TNF-α,IL-6 and IL-10 levels in mice were detected by ELISA.Flow cytometry(FCM)was used to count and sort of infiltrating M2 macrophages and neutrophils in myocardium.qPCR assay was used to determine the Dectin-1 mRNA expression in the above sorted cells.Results:TTC results showed that there was no myocardial infarction in the mice of Control group and Sham group.Compared with the WT I/R group,the infarct volume was significantly lower in WT Dex group,KO I/R group and KO Dex group(P<0.05).Compared with the KO I/R group,the infarct volume was reduced in KO Dex group(P<0.05).The results of HE staining showed that the myocardial fibers of the WT I/R group of mice were disorderly arranged,with a large number of broken myocardial fibers,while the myocardial fibers of the WT Dex group,KO I/R group and KO Dex group of mice had a little breakage,the structural damage was not significant,and the myocardial arrangement was relatively neat.The degree of myocardi-al injury of mice in KO Dex group were less than that in KO I/R group mice.ELISA results showed that compared with Sham group,the serum TNF-α and IL-6 levels of the mice in WT I/R group were significantly increased,and the IL-10 level was significantly de-creased.Compared with WT I/R group,serum TNF-α and IL-6 levels of the mice in WT Dex group and KO I/R group were significant-ly decreased,and IL-10 level was significantly increased.Compared with KO I/R group,the serum TNF-α and IL-6 levels of the mice in KO Dex group were significantly decreased,and the IL-10 level was significantly increased(P<0.05).FCM cell counting results showed that compared with Sham group,a large number of M2 macrophages and neutrophils were infiltrated in the myocardium of WT I/R group of mice(P<0.05).Compared with WT I/R group,the M2 macrophages and neutrophils infiltrated in the myocardium were significantly decreased in WT Dex group,KO I/R group and KO Dex group of mice(P<0.05).While there was no significant differ-ence between the KO I/R group and the KO Dex group mice(P>0.05).qPCR results showed that compared with Sham group,the ex-pression level of Dectin-1 mRNA in the myocardial infiltrated M2 macrophages and neutrophils were significantly up-regulated in WT I/R group of mice(P<0.05).While compared with WT I/R group,the expression level of Dectin-1 mRNA in Dex group of mice was sig-nificantly lower(P<0.05).Mice in KO I/R group and KO Dex group did not express Dectin-1.Conclusion:The protective mecha-nisms of Dex preconditioning on I/R injured myocardium involves reducing the infiltrating number of M2 macrophages and neutrophils in myocardium after I/R injury,which may be achieved by inhibiting the expression of Dectin-1.