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Objective To observe the effect of dipeptidyl peptidase 4 (DPP-4) silencing on lipopolysaccharide (LPS)-induced pyroptosis in alveolar macrophages, and to explore its possible mechanism. Methods MH-S alveolar macrophage cell lines (MH-S cells for short) in the logarithmic growth phase were randomly divided into the Control siRNA group (transfected with Control siRNA), DPP-4 siRNA group (transfected with DPP-4 siRNA), Control siRNA+LPS group (transfected with Control siRNA and then were added with LPS), and DPP-4 siRNA+LPS group (transfected with DPP-4 siRNA and then were added with LPS), respectively. The cell morphology of each group was observed under an inverted microscope, the proliferative viability of cells was assessed by CCK-8 method, the cytotoxicity of cells was determined by lactate dehydrogenase (LDH) cytotoxicity assay kit (expressed as LDH release), and the cell death proportion was detected by Calcein-AM/PI double staining method (expressed as PI positive cell rate）. The relative protein expression levels of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), cysteinyl aspartate specific proteinase p20 (Caspase-1 p20), N-Gasdermin D (GSDMD-N) and inflammatory cytokines interleukin-18 (IL-18) and interleukin-1β (IL-1β) in pyroptosis pathway were detected by Western blotting (WB）. MH-S cells in the logarithmic growth phase were randomly divided into the Control siRNA+LPS group (transfected with Control siRNA and then were added with LPS), DPP-4 siRNA + LPS group (transfected with DPP-4 siRNA and then were added with LPS), Control siRNA+SB203580+LPS group (transfected with Control siRNA and then were added with p38 inhibitor SB203580 and LPS), and DPP-4 siRNA+SB203580+LPS group (transfected with DPP-4 siRNA and then were added with p38 inhibitor SB203580 and LPS）. The activation of p38 and the expression levels of pyroptosisrelated proteins were detected by WB. Results There was no pyroptosis in cells of the Control siRNA group. A small number of cells showed pyroptosis in the DPP-4 siRNA group. A large number of cells showed pyroptosis in the Control siRNA + LPS group and the DPP-4 siRNA + LPS group, and the pyroptosis manifestation was more obvious in the DPP-4 siRNA + LPS group. The cell proliferation activity decreased successively in the Control siRNA group, the DPP-4 siRNA group, the Control siRNA + LPS group, and the DPP-4 siRNA + LPS group. The LDH release amount, the PI positive cell rate, and the relative expression levels of NLRP3, ASC, Caspase-1 p20, GSDMD-N, IL-18, and IL-1β proteins in cells all increased successively； significant difference was found between groups (all P<0. 05）. Compared with the DPP-4 siRNA + LPS treatment group, the relative expression levels of p-p38/p38, p-NF-κB/NF-κB, NLRP3, Caspase-1 p20, and GSDMD-N proteins decreased in the Control siRNA + LPS treatment group, the Control siRNA + SB203580 + LPS treatment group, and the DPP-4 siRNA + SB203580 + LPS treatment group, and the decrease was more significant in the Control siRNA + SB203580 + LPS treatment group and the DPP-4 siRNA + SB203580 + LPS treatment group (all P<0. 05）. Conclusion DPP-4 silencing can promote LPS-induced pyroptosis of MH-S cells, which may be related to the initiation of NLRP3 inflammasome formation and the release of inflammatory cytokines by promoting phosphorylation of p38 and NFκB, thereby regulating the Caspase-1-mediated classical pyroptosis pathway. [ABSTRACT FROM AUTHOR]

Objective To observe the polarization of alveolar macrophages and the activation of JNK/AP-1 signaling pathway in mice transfected with dipeptidyl peptidase-4 (DPP-4) siRNA or (and) added with c-Jun N-terminal kinase (JNK) inhibitor (SP600125) . Methods Mouse alveolar macrophages (MH-S) were cultured in vitro and randomly grouped into： control group (transfected with empty siRNA), siDPP-4 group (transfected with DPP-4 siRNA), lipopolysaccharide (LPS) group (transfected with empty siRNA+ LPS), siDPP-4+LPS group (transfected with DPP-4 siRNA+ LPS), LPS+SP600125 group (transfected with empty siRNA+ LPS combined with SP600125), and siDPP-4+LPS+ SP600125 group (transfected with DPP-4 siRNA+ LPS combined with SP600125), respectively. The expression levels of M1 and M2 polarization markers CD86 and CD206 proteins and the phosphorylation of JNK and activator protein-1 (AP-1) transcription proteins (c-Jun and c-Fos) in macrophages were detected by Western blotting, the mRNA levels of M1 markers [CD86, tumor necrosis factor (TNF) -α, iNOS, IL-1β] and M2 markers [CD206, arginine kinase-1 (ARG-1), IL-4, IL-10] in macrophages were detected by RT-qPCR, and M1 proinflammatory factor NO and intracellular reactive oxygen species (ROS) production in macrophage supernatant were detected by nitric oxide (NO) assay kit and immunofluorescence, respectively. Results Compared with the control group, the production of M1 proinflammatory factors NO and ROS, and the expression levels of M1 polarization markers (CD86 protein and CD86, TNF-α, iNOS, IL-1β mRNA) increased, and the expression levels of M2 polarization markers (CD206 protein and CD206, ARG-1, IL-4, IL-10 mRNA) decreased in the LPS group (all P<0. 05) . Compared with the LPS group, the production of M1 proinflammatory factors NO and ROS, and the expression levels of M1 polarization markers (CD86 protein and CD86, TNF- α, iNOS, IL-1β mRNA) increased, and the expression levels of M2 polarization markers (CD206 protein and CD206, ARG-1, IL-4, IL10 mRNA) decreased in the siDPP-4+LPS group (all P<0. 05) . Compared with the LPS group, the relative expression levels of p-JNK/JNK, p-c-Jun/c-Jun and p-c-Fos/c-Fos protein phosphorylation increased in the siDPP-4 +LPS group (all P< 0. 05) . Compared with the siDPP-4+LPS group, the relative expression levels of p-JNK/JNK, p-c-Jun/c-Jun, p-c-Fos/cFos protein phosphorylation decreased in the siDPP-4+LPS+SP600125 group (all P<0. 05) . Conclusions Transfection of DPP-4 siRNA can promote the M1 polarization of mouse alveolar macrophages induced by LPS, inhibit the M2 polarization of alveolar macrophages, and increase the phosphorylation expression of JNK, c-Jun and c-Fos proteins. Addition of JNK inhibitor may reduce the increase in phosphorylation expression of JNK, c-Jun and c-Fos proteins caused by transfection of DPP-4 siRNA. The mechanism of DPP-4 siRNA transfection promoting M1 polarization in mouse alveolar macrophages induced by LPS may be related to the activation of JNK/AP-1 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the application of magnetic resonance imaging (MRI) diffusion tensor imaging (DTI) in the assessment of white matter injury (WMI) and neurodevelopmental prognosis of preterm infants. Methods A total of 149 preterm infants were included, all of whom underwent head MRI+DTI examination, and the values of fractional anisotropy (FA) and apparent diffusion coefficient (ADC) were collected. According to the examination results, preterm in‐ fants were divided into the WMI group (40 cases) and nWMI group (109 cases). For further analysis, the WMI and nWMI groups were classified based on postmenstrual age (PMA) during MRI+DTI examination (33-34 weeks group, 35-36 weeks group, and ≥37 weeks group). We compared FA and ADC values between WMI and nWMI groups. The Gesell Develop‐ mental Scale was used to evaluate the development of 39 preterm infants at 6 months of corrected age. Among them, there were 18 cases of adaptive behavioral development retardation, 16 cases of individual-social behavior developmental retarda‐ tion, 21 cases of gross motor performance developmental retardation, 25 cases of fine motor behavior developmental retarda‐ tion and 19 cases of speech behavior developmental retardation. Spearman correlation was used to analyze the correlations between the FA and ADC values and the Gesell Developmental Scale. Results The FA values of each ROI in the nWMI group were higher than those of the WMI group at different corrected age (all P<0. 05). ADC values of periventricular white matter and genu of corpus callosum in the WMI group at the corrected age of 33-34 weeks were higher than those of the nW‐MI group (all P<0. 05). At the corrected age of 35-36 weeks, ADC values in genu of corpus callosum and posterior limbs of internal capsule in the WMI group were higher than those in the nWMI group (all P<0. 05). At the corrected age of ≥37 weeks, ADC values in semiovale center, periventricular white matter, genu of corpus callosum and posterior limbs of internal capsule in the WMI group were higher than those in the nWMI group (all P<0. 05). There was a negative correlation between the ADC value of periventricular white matter and Gesell Developmental Scale score in premature infants with gross motor de‐ velopment delay (r=-0. 594, P<0. 05). The ADC value of the forelimb of the internal capsule was negatively correlated with the Gesell Developmental Scale score in preterm infants with cognitive behavior developmental retardation (r=-0. 524, P< 0. 05). Conclusions FA values in anterior and posterior limbs of internal capsule and paraventricular white matter can re‐ veal WMI in preterm infants. ADC value of the periventricular white matter can reflect the development of gross motor. [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

转化生长因子-β1（TGF-β1）是目前最为有效的促肝纤维化因子之一，在介导和促进肝纤维化的发生发展 中发挥重要作用。在正常肝脏中，多种细胞如肝细胞、肝星状细胞（HSCs）可分泌潜伏形式的TGF-β1存储于TGF-β 池。当肝脏受到持续损伤时，TGF-β池中的 TGF-β1生物活性被激活后不仅可促进肝内多种细胞不断分泌 TGF-β1 和其他细胞因子，还可促进肝内多种细胞转分化为肌成纤维细胞导致细胞外基质增生和降解失衡。HSCs作为肝纤 维化启动和发展的中心，其分泌的TGF-β1作用于HSCs自身和肝细胞受体等其他细胞受体，同时TGF-β1在HSCs内 主要通过 Smad和 non-Smad信号通路使 HSCs作出相应应激反应，多种介质可对 TGF-β1或其信号通路上的蛋白产 生促进或抑制的作用，最终影响TGF-β1对HSCs的调控作用。 [ABSTRACT FROM AUTHOR]

目的: 观察超声引导下胸椎椎间孔阻滞治疗胸腹部带状疤疹后神经痛( PHN) 的效果。方法; 选择胸腹 部PHN 患者123 例，根据引导方式分为超声组52 例、X 线组71 例， 分别给予超声、X 线引导下胸椎椎间孔神经阻 滞治疗。对比两组治疗前、第1 次治疗后1 d、出院时视觉模拟法( VAS) 评分及住院时间、治疗次数、治疗过程中出 现的并发症。结果: 治疗前两组VAS 评分比较差异无统计学意义(P > 0. 05) ， 第1 次治疗后1 d、出院时两组VAS 评分均较治疗前降低(P 均< 0. 05) ， 第1 次治疗后1 小出院时两组间VAS 评分比较差异无统计学意义(P 均＞ 0. 05) 。两组住院时间、治疗次数比较差异无统计学意义( P 均＞ 0. 05) 。两组均未发生血气胸、全脊麻、硬膜外阻 滞、感染等不良反应。结论: 超声引导下椎间孔神经阻滞治疗胸腹部PHN 效果确切， 安全性高。 [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

目的观察甘草酸对缺血/再灌注大鼠心肌细胞凋亡的影响，并探讨其机制。方法将50只SD大鼠随 机分为假手术组、模型组及甘草酸低、中、高剂量组5组，各10只。后四组制备缺血/再灌注大鼠模型，假手术组只 穿线不结扎左冠状动脉降支，甘草酸低、中、高剂量组在缺血前半小时分别于股静脉注射30、60、90 mg/kg的甘草 酸，假手术组与模型组注射同体积生理盐水。取各组心肌组织，采用TUNEL染色法测算心肌细胞凋亡率，Western blotting法检测MKK/JNK信号通路蛋白[丝分裂原活化蛋白激酶4/7( MKK4/7)氨基末端激酶l/2/3(JNKl/ 2/3)、磷酸化MKK4/7 (P-MKK4/7)、磷酸化JNKl/2/3( p-JNKl/2/3)]及凋亡相关蛋白[天冬氨酸特异性半胱氨酸 蛋白酶(Caspase)8、B淋巴细胞瘤-2蛋白（Bcl-2)、Bcl-2相关X蛋白（Bax)、CaSpase-3 ]的表达，同时观察心肌组织病 理改变情况。结果与假手术组相比，模型组细胞凋亡率高，p-MKK4/7、p-JNKl/2/3、CaSpase-8、Bax、Caspase-3表 达高而Bcl-2表达低(P均<0.05) D与模型组相比，甘草酸中剂量组及甘草酸高剂量组细胞凋亡率低，p-MKK4/7、 p-JNKl/2/3、CaSpase-8、Bax、CaSpase-3表达低而Bcl-2表达高（P均<0.05 )。模型组较假手术组大鼠心肌组织中出 现较多变性坏死心肌细胞，有较多炎性细胞浸润;甘草酸低、中、高剂量组较模型组心肌细胞水肿程度轻且炎性细 胞少。结论甘草酸可减少缺血/再灌注大鼠心肌细胞凋亡及心肌组织损伤;其机制可能为抑制MKK/JNK信号 通路中MKK4/7和JNK1/2/3磷酸化，降低Caspase-8、Bax Xaspase-3表达，升高Bcl-2表达。 [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)