Cerebral ischemia/reperfusion (I/R) injury manifests as progressive motor and cognitive dysfunction, primarily attributed to neuronal apoptosis. However, there is a lack of neuroprotective drugs targeting neuronal apoptosis in ischemic stroke. In this study, utilizing bioinformatics analysis, we hypothesized that TRPV1 could serve as a novel molecular target implicated in neuronal apoptosis during cerebral ischemia/reperfusion (I/R) injury. To validate our hypothesis in vivo, we employed mouse models of I/R injury induced by transient middle cerebral artery occlusion (tMCAO). Importantly, pre-injecting capsazepine (CPZ), a TRPV1 antagonist, significantly suppressed apoptotic pathway activity in neurons. Additionally, we investigated the regulatory role of CDK5, a well-known neuronal-specific kinase, in modulating the internalization and functionality of TRPV1 ion channels. Our findings revealed an augmented interaction between TRPV1 and CDK5 during cerebral ischemia/reperfusion (I/R) injury. The administration of the TAT-T407 interference peptide, derived from the phosphorylation site of TRPV1 for CDK5, resulted in a reduction of neuronal apoptosis within ischemic regions following cerebral ischemia/reperfusion (I/R) injury. This intervention significantly diminished cerebral infarct volume and improved neurological function. In summary, disrupting the TRPV1/CDK5 interaction through TAT-T407 peptides provides protection against neuronal apoptosis and cognitive decline, suggesting an innovative therapeutic strategy for ischemic stroke treatment.

Ischemic stroke is a devastative nervous system disease associated with high mortality and morbidity rates. Unfortunately, no clinically effective neuroprotective drugs are available now. In ischemic stroke, S100 calcium-binding protein b (S100b) binds to receptor for advanced glycation end products (Rage), leading to the neurological injury. Therefore, disruption of the interaction between S100B and Rage can rescue neuronal cells. Here, we designed a peptide, termed TAT-W61, derived from the V domain of Rage which can recognize S100b. Intriguingly, TAT-W61 can reduce the inflammatory caused by ischemic stroke through the direct binding to S100b. The further investigation demonstrated that TAT-W61 can improve pathological infarct volume and reduce the apoptotic rate. Particularly, TAT-W61 significantly improved the learning ability, memory, and motor dysfunction of the mouse in the ischemic stroke model. Our study provides a mechanistic insight into the abnormal expression of S100b and Rage in ischemic stroke and yields an invaluable candidate for the development of drugs in tackling ischemic stroke.

Abstract Ischemic stroke is a nervous system disease associated with high mortality and morbidity rates. Currently, there are no neuroprotective drugs for this disease. S100 calcium-binding protein b (S100b), which is abnormally expressed in the cerebrospinal fluid of patients, can bind to various other proteins and exacerbate the progression of stroke; receptor for advanced glycation end-products (Rage) is one of these proteins. To inhibit the occurrence of this interaction, a peptide (TAT-W61) based on the V-domain of S100b that interacts with Rage was produced. This study aimed to use TAT-W61 to reduce the levels of inflammation and apoptosis after ischemic stroke and to improve learning memory and motor dysfunction. In this study, S100b and Rage expression increased after ischemic stroke. Possible binding sites of S100b on Rage were mapped through molecular docking and polar–contact assays. In immunoprecipitation experiments, TAT-W61 inhibited the binding of S100b to Rage after ischemic stroke. TAT-W61 peptide, derived from Rage, could reduce the inflammatory and apoptotic response caused by ischemic stroke. It may also improve the infarct volume of the pathological injury and reduce the apoptotic rate. In particular, the TAT-W61 peptide could significantly improve learning, memory, and motor dysfunction in an ischemic stroke model. TAT-W61 peptide may help alleviate ischemic stroke injury.

Background: Neuroinflammation plays a pivotal role in the pathogenesis of Central Nervous System (CNS) diseases. The phenolic glucoside gastrodin (GAS), has been known to treat CNS disorders by exerting anti-inflammatory activities. Our aim was to investigate the potential neuroprotective mechanisms of GAS on lipopolysaccharide (LPS)-induced mice. Methods: Male C57BL/6J mice were treated by LPS, before which GAS was adminisrated. The behavior tests such as forced swim test, tail suspension test, and elevated plus maze were performed to evaluate depressive-anxiety-like behaviors. A high-throughput sequencing (HTS) analysis was performed to screen out distinctive miRNAs which were validated using quantitative real-time PCR. Then, miRNA agomir or NC was injected stereotaxically into hippocampus of mice to explore the role of miRNA on GAS in response to LPS. Furthermore, Immunofluorescence and the hematoxylin and eosin (H&E) staining were employed to observe the cellular morphology. The protein levels of pro-inflammatory factors were evaluated by western blot. Finally, the target mRNA of miRNA was predicted using bioinformatics analysis. GO and KEGG enrichment analyses were conducted to clarify the potential function of target protein, which were visualized by bubble charts. Results: The behavioral data showed that mice in the LPS group had obvious depressive-anxiety-like behaviors, and 100 mg/kg GAS could improve these behavioral changes and alleviate the levels of pro-inflammatory cytokines in the hippocampus when mice were exposed to LPS for 6 h. Meanwhile, LPS-induced microglia and astrocyte activation in the CA1, CA2, CA3, and DG regions of the hippocampus were also reversed by GAS. Furthermore, miR-107-3p were screened out and verified for GAS in response to LPS. Importantly, miR-107-3p overexpression negatively abrogated the neuroprotective effects of GAS. Moreover, KPNA1 might be the target molecular of miR-107-3p. KPNA1 might regulate 12 neuroinflammation-related genes, which were mainly involved in cytokine−mediated signaling pathway. Conclusion: These results suggested that GAS might alleviate the LPS-induced neuroinflammation and depressive-anxiety-like behaviors in mice by downregulating miR-107-3p and upregulating the downstream target KPNA1. The indicates miR-107-3p may provide a new strategy for the treatment of CNS diseases.

目的 探讨环介导温扩增技术(Loop-mediate amplification,LAMP)检测呼吸道病原菌在临床中实际应用价值.方法 收集2018年3月-2019年4月徐州医科大学附属医院住院治疗的911例下呼吸道感染成人患者(＞18岁)的痰液标本,分别进行呼吸道病原菌核酸检测和痰培养,比较分析两种检测方法的检出结果.结果 利用LAMP法,在911份痰标本中肺炎克雷伯杆菌、金黄色葡萄球菌(金葡菌)、大肠埃希菌、铜绿假单胞菌、流感嗜血杆菌的检出率分别为1 1.2％、28.8％、51.8％、32.6％、15.9％,均高于传统痰培养方法的4.0％,8.2％,8.6％,17.7％,7.8％(P值均＜0.05).LAMP法对鲍曼不动杆菌、嗜麦芽窄食单胞菌的检出与培养法的一致性较高(Kappa值分别为0.791、0.699,P值均＜0.01).结论 利用LAMP法检测下呼吸道感染的病原体以混合检出为主,且以大肠埃希菌、铜绿假单胞菌、鲍曼不动杆菌和嗜麦芽窄食单胞菌的混合检出较多,相对于传统痰培养,有快速、敏感及病原体覆盖面广的优势.

Human cytomegalovirus (HCMV) infection in the respiratory tract leads to pneumonitis in immunocompromised hosts without available vaccine. Considering cytomegalovirus (CMV) mainly invades through the respiratory tract, CMV-specific pulmonary mucosal vaccine development that provides a long-lasting protection against CMV challenge gains our attention. In this study, N-terminal domain of GP96 (GP96-NT) was used as a mucosal adjuvant to enhance the induction of pulmonary-resident CD8 T cells elicited by MCMV glycoprotein B (gB) vaccine. Mice were intranasally co-immunized with 50 mu g pgB and equal amount of pGP96-NT vaccine 4 times at 2-week intervals, and then i.n. challenged with MCMV at 16 weeks after the last immunization. Compared with pgB immunization alone, co-immunization with pgB/pGP96-NT enhanced a long-lasting protection against MCMV pneumonitis by significantly improved pneumonitis pathology, enhanced bodyweight, reduced viral burdens and increased survival rate. Moreover, the increased CD8 T cells were observed in lung but not spleen from pgB/pGP96-NT co-immunized mice. The increments of pulmonary CD8 T cells might be mainly due to non-circulating pulmonary-resident CD8 T-cell subset expansion but not circulating CD8 T-cell populations that home to inflammation site upon MCMV challenge. Finally, the deterioration of MCMV pneumonitis by depletion of pulmonary site-specific CD8 T cells in mice that were pgB/pGP96-NT co-immunization might be a clue to interpret the non-circulating pulmonary-resident CD8 T subset expansion. These data might uncover a promising long-lasting prophylactic vaccine strategy against MCMV-induced pneumonitis.

目的 探讨辛伐他汀对小鼠巨细胞病毒(MCMV)肺炎的保护作用.方法 30只雄性小鼠随机均分为三组:MCMV组和辛伐他汀组给予腹腔注射环磷酰胺80 mg/kg和MCMV悬液0.8 ml;辛伐他汀组加用辛伐他汀50 mg/kg灌胃,连续7d;对照组及MCMV组分别予以同体积的生理盐水灌胃.检测肺组织病理变化、Toll样受体2(TLR2)蛋白表达、IFN-γ和单核细胞趋化蛋白1(MCP-1)含量以及MCMV DNA含量.结果 对照组肺组织肺泡结构正常;MCMV组肺泡间质水肿,内有大量炎性细胞浸润,部分肺泡腔内有蛋白渗出,符合MCMV间质性肺炎的表现;辛伐他汀组间质性炎症浸润较MCMV组减轻.与对照组比较,MCMV组TLR2蛋白表达、IFN-γ和MCP-1含量以及MCMV DNA含量增加(P＜0.05);与MCMV组比较,辛伐他汀组TLR2蛋白表达、IFN-γ和MCP-1含量以及MCMV DNA含量下降(P＜0.05).结论 辛伐他汀对MCMV肺炎有保护作用,可能通过下调TLR2的表达、减少IFN-γ和MCP-1分泌以及抑制MCMV DNA的复制来发挥作用.

Objective To observe the changes in the expression chemokine receptor 3 (CXCR3) and lymphocyte subsets in patients with acute exacerbation and stable chronic obstructive pulmonary disease (COPD) and to elucidate their effect on COPD. Methods During January 2015 to June 2016, 43 cases of acute exacerbating of COPD patients, 43 sta-ble COPD patients, and 43 healthy people in our hospital were selected as the research objects. The expression levels of T lymphocyte subsets, B lymphocytes and CXCR3 in blood were measured and analyzed. Results Compared with the con-trol group, The levels of CD3+, CD4+, CD4+/CD8+of the T lymphocyte subsets and B lymphocyte subsets were signifi-cantly decreased in different COPD patients (P<0.05);while the expression levels of CXCR3 on the surfaces of CD4+and CD8+of the T lymphocyte subsets in peripheral blood of different COPD patients were increased significantly, and those of the acute exacerbating of COPD patients were significantly higher than the stable COPD patients (P<0.05). Conclusion The functions of the cellular immunity system and the humoral immunity system were dysbalanced appar-ently in patients with COPD acute exacerbating period. Lymphocyte subsets and their CXCR3 may have a significant ef-fect on the onset and development of COPD patients with acute exacerbations.

Objective To investigate the therapy and influencing factors for prognosis of ventilator-associated pneumonia(VAP) caused by multidrug-resistant organisms(MDROs).Methods 169 patients with VAP who were admitted to a hospital between January 2012 and December 2013 were included in analysis, 125 were in MDRO infection group and 44 in non-MDRO infection group.MDRO infection group was subdivided into MDR-A group(n=78, resistant to selected antimicrobial agents) and MDR-B group (n=47, sensitive to at least one kind of selected antimicrobial agent).Antimicrobial choice and prognosis between each group were analyzed and compared.Results 242 strains of pathogenic bacteria were isolated from airway secretion of VAP patients, 173(71.49％) were MDROs.The major pathogens causing VAP were Klebsiella spp.(n=66), Pseudomonas aeruginosa(n=64), Acinetobacter spp.(n=60), Staphylococcus aureus(n=27), and Escherichia coli (n=17), the percentages of MDROs of above pathogens were 68.18％, 50.00％, 91.67％, 88.89％, and 76.47％ respectively.The prognosis of MDRO infection group was poorer than that of non-MDRO infection group, MDR-A group had the worst prognosis(P<0.001).Persistent fever, leukocytosis, and progress of pulmonary inflammation in VAP patients suggested poor prognosis(all P<0.001);antimicrobial use in patients with effective therapy was higher than those in a worsened condition before onset, at the beginning of onset, and after culture of specimens(all P<0.001), while coma, early-onset VAP and multiple bacterial infection had no prognostic significance in patients with VAP(all P>0.05).Conclusion There is high incidence of MDRO infection in patients with VAP, effective antimicrobial therapy can improve the prognosis.

AIM:To investigate the effects of simvastatin on the expression of Toll-like receptor 2 ( TLR-2 ) , interferon-γ(IFN-γ) and monocyte chemoattractant protein-1 (MCP-1) in lung tissues of mice with mouse cytomegalovirus ( MCMV) pneumonia and to explore the possible mechanism .METHODS:Male BALB/c mice (6~8 weeks old, n=40) were randomly divided into 5 groups: normal control (NC) group, MCMV infection group, simvastatin group 1 (SMV1 group), simvastatin group 2 (SMV2 group), and simvastatin group 3 (SMV3 group).The mice in SMV1, SMV2 and SMV3 groups were gavaged with simvastatin (50 mg· kg-1 · d-1 for 7 d) 7 d before, on the same day of and 3 d after in-traperitoneal injection of MCMV , while the mice in normal control group and MCMV infection group were gavaged with the same volume of normal saline .HE staining was used to observe the pathological changes of lung tissues in mice .Total tis-sue protein was extracted from the lung homogenates to detect the expression of TLR-2 by Western blot and immunohisto-chemical staining .Real-time PCR was used to analyse the content of MCMV DNA .The levels of IFN-γand MCP-1 were measured by enzyme-linked immunosorbent assay (ELISA).RESULTS:Compared with NC group, the pathological chan-ges of the lung tissues of the mice in MCMV group showed alveolar interstitial edema , alveolar wall widening and a large number of inflammatory cells .The expression of TLR-2 in the lung tissues of the mice in model group was increased signifi-cantly.The content of MCMV DNA was increased , and the expression of IFN-γand MCP-1 was also increased significant-ly.Compared with the mice in MCMV group , the pathological changes of the lung tissues of simvastatin groups showed that the inflammatory cells were decreased .The expression of TLR-2 was down-regulated.The content of MCMV DNA was de-creased, and the levels of IFN-γand MCP-1 were also decreased significantly .At the same time, the expression of TLR-2 and the content of MCMV DNA in SMV1 group were less than those in SMV2 and SMV3 groups (P<0.05), and no statis-tically significant difference between SMV 2 and SMV3 groups was observed .CONCLUSION:Simvastatin down-regulates the TLR-2 signaling pathway , and reduces the expression of TLR-2 and replication of MCMV DNA , thus attenuating the pathological damage of the lung tissue .Early intervention with simvastatin plays an important role in preventing the infection of MCMV and reducing the inflammation .

Objective To study the risk factors of AECOPD patients complicated with pulmonary embolism, in order to improve the diagnostic rate of PE in patients with COPD.Methods 117 AECOPD patients from January 2012 to December 2015 who were examined by CT pulmonary angiography were selected in this study, including 58 cases of PE.Their clinical data were retrospectively analyzed, and multivariate regression analysis was used to find the risk factors of PE in AECOPD.Results Single factor analysis showed that the following factors were significantly different between the PE positive group and the PE negative group:?D-dimmer, PO2, edema of lower extremity, DVT, diameter of pulmonary artery, the ratio of pulmonary artery to ascending aorta diameter and the ratio of pulmonary artery to descending aorta diameter.Multiple regression analysis showed that D-dimmer (OR=1.287, 95%CI: 1.008-1.643, P<0.05), the ratio of pulmonary artery to ascending aorta diameter (OR=2.924E3, 95%CI: 2.212-3.866E6, P<0.05) and diameter of pulmonary artery (OR=1.821, 95%CI: 1.675-1.999, P<0.05) were the risk factors.When the cut-off point of D-dimmer was 1.245ug/mL, the sensitivity and specificity of COPD with PE were 60.3% and 72.9%.When the cut-off point of the ratio of pulmonary artery to ascending aorta diameter was 0.903, the sensitivity and specificity of COPD with PE were 69% and 72.9%.When the cut-off point of diameter of pulmonary artery was 33.845 millimeter, the sensitivity and specificity of COPD with PE were 60.3%and 69.5%.Conclusion Patients with AECOPD admitted to hospital should be considered for the presence of PE if they have the risk factors of D-dimmer>1.245ug/mL, the ratio of pulmonary artery to ascending aorta diameter>0.903 or the diameter of pulmonary artery>33.845 millimeter.

目的 观察热毒宁对鼠巨细胞病毒(MCMV)感染小鼠肺组织干扰素-γ(IFN-γ)和白介素-4(IL-4)细胞因子水平的影响及其抗MCMV作用机制.方法 40只BALB/c鼠随机分5组,每组8只,A为空白对照组,B为免疫低下对照组,C为MCMV肺炎模型组,D为热毒宁治疗组,E为更昔洛韦治疗组.HE染色观察小鼠肺组织的病理改变,荧光定量PCR检测肺组织MCMV DNA的变化,酶联免疫试验(ELISA)法检测肺组织中IFN-γ和IL-4的变化.结果 1)与A组相比,C组肺组织病理染色显示肺泡壁内有大量炎性细胞浸润,肺泡壁增宽,部分肺泡腔内有蛋白渗出;MCMV DNA含量升高,肺组织中炎症因子IFN-γ和IL-4明显增多(P＜0.05);2)与C组相比,给予药物干预后,D、E组肺组织病理改变较前减轻,MCMV DNA含量降低,炎性因子IFN-γ和IL-4明显下降(P＜0.05);而D、E两组相比差异无统计学意义(P＞0.05).结论 热毒宁干预后,肺组织的病理改变较前减轻,抑制CMV DNA的复制,IFN-γ和IL-4明显下降;此效应可能是通过抑制CMV的复制周期并干预下游细胞因子从而发挥抗病毒作用.

Objective To investigate the changes in the content of serum C reaction protein ( CRP) and interleukin-1β( IL-1β) , nerutropil ( N) percentage and pulmonary function ( FEV1%) and their significance in the acute and remission stages of chronic obstruction pulmonary disease ( COPD) patients.Methods A total of 45 COPD patients and 30 healthy subjects were included into the current study.Blood samples were collected at the acute and remission stages (Day 7) of COPD patients as well as 30 healthy subjects to determine the levels of serum CRP, IL-1βand N.Mean-while, FEV1%was detected.Results COPD patients at the acute stage produced remarkably higher serum CRP posi-tive rate and the levels of CRP, N and IL-1βthan those at the remission stage and the controls.COPD patients at the a-cute stage showed significantly lower FEV1%than those at the remission stage and the controls.The level of CRP was negatively associated with FEV1%, but positively associated with the amount of IL -1β.Conclusions The level of CRP is obviously increased in the acute exacerbation stage of COPD patients, and which was negatively related with FEV1%, but positive related with inflammatory factors.The level of CRP can be adopted as a sensitive indicator of the severity of COPD.

OBJECTIVE:To evaluate the association of obstructive sleep apnea hypopnea syndrome (OSAHS) with carotid atherosclerosis and the efficacy of continuous positive airway pressure (CPAP) treatment. METHODS:A total of 93 OSAHS patients diagnosed by polysomnography (PSG) were selected from Sleep Disorders Center at Affiliated Hospital of Xuzhou Medical College between March 2013 and December 2014. Based on the results of apnea-hypopnea index (AHI), they were divided into mild (n=22), moderate (n=37), and severe OSAHS group (n=34). Meanwhile, 28 healthy adult individuals matched for age and body mass index (BMI) were enrolled as the control group. The carotid intima-mesa thickness (IMT) was measured by color Doppler uhrasonography, and plasma levels of tumor necrosis factor-α (TNF-α), endothelin-1 (ET-1) and nitric oxide (NO) were determined by Enzyme-Linked Immunosorbent Assay (ELISA). The correlations between carotid IMT and plasma levels of TNF-α, ET-1 and NO were analyzed. A total of 24 patients with moderate to severe OSAHS underwent CPAP treatment and the carotid IMT, plasma levels of TNF-α, ET-1 and NO were compared before and after CPAP treatment. RESULTS:OSAHS patients had significant increase of carotid IMT with the increasing disease severity, and the carotid IMT in mild, moderate and severe OSAHS groups were all significantly higher than that in the control group ((0.73 ± 0.31), (0.86 ± 0.07), (1.07 ± 0.14) vs (0.65 ± 0.10) mm, all P<0.05). The plasma levels of TNF-α and ET-1 in mild to severe OSAHS group were significantly higher than those in controls ((17.45 ± 3.02), (23.81 ± 2.91), (35.16 ± 3.43) vs (12.53 ± 3.48) ng/L and (0.81 ± 0.13), (1.06 ± 0.21), (1.66 ± 0.30) vs (0.64 ± 0.12) ng/L, all P<0.05 ), whereas plasma levels of NO in the three OSAHS groups were significantly decreased compared with the control group ((35.46 ± 10.12), (29.32 ± 9.47), (20.16 ± 7.41) vs (45.43 ± 7.92) µmol/L, all P<0.05). Furthermore, there were significant differences in plasma levels of TNF-α, ET-1 and NO among the three OSAHS groups (all P<0.05). Carotid IMT was positively correlated with plasma TNF-α and ET-1 (r=0.56 and 0.51) and negatively correlated with plasma NO (r=-0.46) (all P<0.05). After 3 months of CPAP treatment, plasma levels of TNF-α and ET-1 in OSAHS patients were significantly reduced ((19.64 ± 5.28), (0.94 ± 0.21) vs (28.72 ± 5.36), (1.36 ± 0.36) ng/L), and plasma NO was markedly increased ((33.57 ± 6.32) vs (24.34 ± 4.46) µmol/L, all P<0.05). However, CPAP treatment did not have a significant effect on carotid IMT ((0.91 ± 0.21) vs (0.96 ± 0.14) mm), P>0.05). CONCLUSIONS:Systemic inflammation and vascular endothelial dysfunction may play an important role in pathogenesis and development of carotid artery atherosclerosis in OSAHS. Short-term CPAP therapy alleviates systemic inflammation and improves endothelial function, but does not influence the increased carotid IMT in OSAHS patients.

目的:观察Nogo-B在慢性阻塞性肺病(COPD)合并慢性肺源性心脏病患者血液中的变化,并分析其相关性及意义.方法:住院COPD患者77例,分为COPD组(38例)和COPD合并肺心病组(CP组,39例),另选取正常健康者20例作为正常组.分别检测血浆Nogo-B、NT-proBNP水平.结果:Nogo-B、NT-proBNP在COPD组[(22.41±6.62)pg/mL、(91.32±8.77) pg/mL]高于正常组[(7.02±2.55) pg/mL、(20.34±5.72)pg/mL];在CP组[(51.45±8.75)pg/mL、(506.28±14.91)pg/mL]高于COPD组,组间比较差异均有统计学意义(P＜0.01).Nogo-B与右室内径呈正相关(r=0.745,P＜0.01),与左室内径/右室内径(LV/RVD)呈负相关(r=-0.591,P＜0.01);Nogo-B与NT-proBNP呈正相关(r=0.725,P＜0.01),与PO2呈负相关(r=-0.415,P＜ 0.01).COPD继发肺心病ROC曲线示Nogo-B、NT-proBNP的曲线下面积为0.683、0.655(均P＜0.05).结论:Nogo-B在COPD继发肺心病的发生过程中起着重要作用;Nogo-B与NT-proBNP对COPD继发肺心病的评估有一定意义.

目的 研究复数菌肺部感染发生的相关因素及其对预后的影响.方法 收集江苏徐州医学院附属医院2012年1月 2013年12月住院患者的呼吸道分离菌阳性病例,分析比较肺部单一与多种病原菌感染因素及对预后和经济负担的影响.结果 复数菌肺部感染患者252例,以医院感染为主.与519例单一细菌感染比较,两组性别无差异(P＞0.05),复数菌感染患者年龄略高(P＜0.05),原发病主要以脑血管意外和脑外伤为多,与开放气道(气管插管或切开)、入住重症监护病房(ICU)及住院时间密切相关(P＜0.01),治疗总费用和药费均高于单一细菌感染.复数菌肺部感染时对患者预后影响最大,病情恶化或病死率高(P＜0.01).结论 复数菌肺部感染多发生于ICU住院患者,住院时间长,预后差,治疗费用高.加强呼吸道病原监控,避免发生复数菌肺部感染,对改善预后有重要意义.

Objective Toexplore the expressions of interleukin-16 (IL-16), interferon-γ (IFN-γ), CXC chemokine receptor 3 (CXCR3), and CRP and their clinical significance in acute exacerbation chronic obstructive pulmonary disease by observing the changes in these factors in patients with AECOPD. Methods 103 patients with AECOPD and 20 healthy controls were collected. According to the 2013 GOLD guideline, all the patients with AECOPD were divided into4 groups(group A of 21 patients, B of 30, C of 27, andD of 25). Results As compared withthe control group, plasma concentrations of IL-16, IFN-γ, CXCR3. and CRP were significantly increased in the patients with AECOPD (P < 0.01), and as the severity of the disease was elevating, these expression levels were significantly increased.While the expression levels of IL-16, IFN-γ, CXCR3, and CRP levels were significantly reduced after treatment, but they were still higherthan those in the control group (P < 0.05). The expression levels of serum IL-16, IFN-γ, CXCR3, and CRP were significantly correlated in patients with AECOPD. Conclusions Expressions of IL-16, IFN-γ and CXCR3 are significantly increased in AECOPD, which is correlated with disease severity and decreased after treatment, suggesting that these three factors may be associated with the occurrence and development of COPD.

目的 探讨三七皂苷(panax notoginseng saponins,PNS)对人肺腺癌A549(hA549)细胞的致凋亡作用.方法 体外培养的hA549细胞,经不同浓度的PNS或联合应用磷脂酰肌醇3-激酶(PI3K)特异性抑制剂LY294002处理.采用MTT比色法检测肺腺癌A549细胞存活率,Hoechst33258荧光染色法检测其细胞形态学变化,流式细胞术检测细胞凋亡率,Western blot检测凋亡抑制基因Bcl-2、Bax和蛋白激酶B(Akt)蛋白的表达.结果 PNS能降低肺腺癌细胞的存活率,且其效应随剂量和作用时间的增加有增强的趋势;在PNS组可见细胞核出现固缩、边集和凋亡小体,并发现肺癌细胞凋亡率提高,细胞内Bax蛋白表达上调,Bcl-2、Akt蛋白表达下调.各浓度PNS组与空白对照组及溶剂对照组相比,差异均有统计学意义(P＜0.05);PNS与LY294002联合应用则具有协同作用,可进一步促进肺癌细胞的凋亡及其细胞内的Bax蛋白表达上调和Bcl-2及Akt蛋白表达下调,与单用PNS组相比差异具有统计学意义(P＜0.05).结论 PNS具有降低肺癌细胞存活率、诱导癌细胞凋亡的作用,并与PI3K特异性抑制剂LY294002具有协同作用,这可能与抑制PI3K/Akt信号通路、促进凋亡蛋白表达有关.

Objective To observe the changes of hypersensitive C-reactive protein (hs-CRP), Fibrinogen ( Fib) , N-terminal fragment of pro-brain natriuretic peptide ( NT-proBNP) in COPD patients complicated with pulmo-nary hypertension ( PH) . Methods 105 patients with COPD were enrolled in our hospital. 55 patients were classi-fied as the group A ( COPD without PH) and 50 patients as the group B ( COPD with PH) . Pulmonary pressure was assessed by Doppler echocardiography, FEV1% and FEV1/FVC by lung function test. The expression of hs-CRP, NT-proBNP and Fib and arterial blood gas analysis were measured. Results The levels of hs-CRP, Fib and NT-proBNP in the group B were significantly higher than in the group A (P<0. 05). The levels of PaCO2, hs-CRP, Fib and NT-proBNP were positively correlated with pulmonary pressure ( P<0. 05 ) . The levels of PaCO2 , hs-CRP and Fib were positively correlated with NT-proBNP (P<0. 05). Conclusion The levels of hs-CRP, Fib, NT-proBNP are positively related to PH in COPD patients, suggesting that systemic inflammation plays a role in the pathogenesis of PH in COPD.