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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.)

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.)

Objective To observe the neuroprotective effect of hyperoside （HYP） pretreatment on mice with cerebral ischemia-reperfusion injury induced by middle cerebral artery occlusion （MCAO），and to explore its possible mechanism from the aspect of blood-brain barrier （BBB）. Methods Eighty-four male ICR mice were randomly divided into four groups： Sham group， HYP group， MCAO group， and MCAO+HYP group. Before operation， mice in the HYP group and MCAO+HYP group were administered HYP intragastrically at a dose of 50 mg/kg. MCAO method was used to establish the cerebral ischemia-reperfusion injury models in the MCAO and MCAO+HYP groups. Only the neck blood vessels were separated without any other treatment in the Sham and HYP groups. All experimental mice were executed at 24 h after reperfusion. The neurological deficit and infarct volume were evaluated by Longa， Bederson and TTC staining， respectively. Immunohistochemical staining was applied to observe the pathological changes of hippocampal CA1 region， and we counted the positive cells of NeuN， GFAP and PECAM. The expression levels of ZO-1 and Claudin5 were assessed by Western blotting. Results The Longa score， Bederson score and infarct volume of the MCAO and MCAO+HYP groups were higher than those of Sham and HYP groups， and those of MCAO group were higher than those of MCAO+HYP group （all P<0. 05）. Compared with the MCAO group， MCAO+HYP group had significantly decreased neuronal cell death and decreased activation of astrocytes and vascular endothelial cells in the hippocampal CA1 region. The number of NeuN positive cells in MCAO+HYP groups was higher than that in MCAO groups， while the number of GFAP and PECAM positive cells in the MCAO+HYP group was lower than that in the MCAO group （P<0. 05）. The expression levels of ZO-1 and claudin5 protein were higher in the MCAO+HYP group than in MCAO group （both P<0. 05）. Conclusion HYP pretreatment has neuroprotective effect on mice with cerebral ischemia reperfusion injury and its mechanism might be related to maintaining the integrity of BBB. [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.)

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　筛选口腔鳞状细胞癌（鳞癌）组织中跨膜四超家族成员 1 蛋白 (TM4SF1) mRNA，观察 TM4SF1 在 口腔鳞癌组织中的表达变化，并探讨其临床意义。方法　从 GEO 公共数据库 (https://www.Ncbi. nlm. nih. gov / GSE9844)。下载口腔鳞癌基因表达谱及相关临床数据(研究号分别为 GSE13601、GSE19089、GSE74530、GSE78060、GSE9844 ）。从这 5 个 TM4SF1 探针中获得标准化均差 (SMD) 和中间表达值。利用 GEO 数据库的 GEO2RE 工具对 口腔鳞癌和癌旁黏膜组织中TM4SF1 mRNA 进行筛选和分析。采用免疫组织化学SP 法检测口腔鳞癌组织及其癌 旁黏膜组织中TM4SF1 蛋白，并探讨 TM4SF1 蛋白与患者临床病理资料之间的关系。结果　筛选出口腔鳞癌组织 中存在TM4SF1 mRNA，且其表达水平高于癌旁黏膜组织 (P<0.05)。M4SFI 蛋白主要定位于口腔鳞癌细胞膜中， 其在口腔鳞癌组织中阳性表达量高于癌旁黏膜组织 (P<0.05)。TM4SFI 蛋白在Ⅲ ～ Ⅳ期口腔鳞癌患者中的阳性 表达量高于Ⅰ ～ Ⅱ期患者 (P<0.05)，但与其他临床病理资料如民族、年龄、性别、吸烟、饮酒、血型、分级、肿瘤大 小、淋巴结转移无关。结论　口腔鳞癌组织中筛选出的 TM4SF1 mRNA 表达升高；TM4SF1 蛋白在口腔鳞癌组织中 呈高表达，与口腔鳞癌临床分期有关，可能参与口腔鳞癌的发生、发展。 [ABSTRACT FROM AUTHOR]

目的观察IgA 肾病( IgAN) 患者肾组织中鞘氨醇激酶1 ( SphKl) 、α－平滑肌肌动蛋白( α-SMA) 的表达变 化，分析SphKl 表达与 α-SMA 及肾功能指标的相关性。方法IgAN 患者18 例，穿剌取病肾组织纳入实验组； 同期 行手术治疗的肾癌患者5 例，取病理证实的癌旁正常肾组织纳入对照组。采用免疫组化法检测两组肾组织中的 SphKl 、α-SMA，采用Image Pro Plus 图像分析软件分析光密度值表示蛋白相对表达噩。采用Pearson 相关分析法分 析SphKl 与 α-SMA 表达、24 h 尿蛋白、血肌酐、尿索氮水平的相关性。结果实验组肾组织中SphKl 、α-SMA 相对 表达量分别为34.73 口37、44. 47 土8 . 51 ，对照组分别为18. 65 土2 . 30、19. 85 士2 . 96 ， 实验组SphKl 、α-SMA 相对表 达量均高于对照组(P 均<0 . 05) 。实验组SphKl 表达与α-SMA 表达、24 h 尿蛋白、血肌酐水平呈正相关( r 分别为 0. 61 、0. 70、0. 5 1, P 分别为0. 007、0. 001 、0. 029) ;SphKl 表达与尿索氮水平无直线相关关系(r = 0. 13,P = 0. 600) 。 结论IgAN 患者肾组织中SphKl 、α-SMA 商表达，且SphKl 表达与α-SMA 表达、24 h 尿蛋白、血肌酐水平存在相关 性。SphKl 可能参与了IgAN 的发病，并与肾脏损害程度有关。 [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.)

目的观察雷公藤多苷灌胃对大鼠糖尿病肾病的治疗作用,并探讨其作用机制。方法将45只Wistar大鼠随机分为正常组、对照组和实验组,各15只。对照组和实验组予以链脲佐菌素55 mg/kg腹腔内注射建立糖尿病肾病大鼠模型,正常组给予同等剂量的生理盐水腹腔注射。建模成功后,实验组大鼠给予雷公藤多苷1.8g/(kg·d)灌胃,1次/d;正常组及对照组给予同等剂量的生理盐水灌胃,1次/d。三组大鼠自由饮水进食,不给予任何降糖处理。三组大鼠灌胃前(治疗前)及灌胃12周后(治疗后)分别检测其血糖、24小时尿蛋白、血清肌酐和尿素氮。同时于灌胃12周末处死大鼠,检测其肾皮质结缔组织生长因子(CTGF)。结果实验组和对照组大鼠治疗前24小时尿蛋白、血清肌酐和尿素氮水平高于正常组(P均<0.05);实验组大鼠治疗后24小时尿蛋白、血清肌酐和尿素氮水平较治疗前降低(P均<0.05),且低于对照组治疗后(P均<0.05)。正常组、实验组和对照组治疗后大鼠肾皮质CTGF相对表达量分别为0.18±0.03、0.52±0.07、0.69±0.08,实验组、对照组与正常组相比,实验组与对照组相比,P均<0.05。治疗后实验组大鼠24小时蛋白尿与肾组织中CTGF表达水平呈正相关(r=0.54,P<0.05)。结论雷公藤多苷灌胃对大鼠糖尿病肾病有明显的治疗作用,可能通过下调糖尿病大鼠肾脏CTGF表达抑制蛋白尿、保护肾功能。 [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.)