Green tea extract modulates actin remodeling via Rho activity in an in vitro multistep carcinogenic model.

Alteration of actin polymerization and loss of actin filaments is a marker of cellular dedifferentiation and early malignant transformation. To study this phenomenon, an in vitro human urothelial model consisting of two cell lines, HUC-PC and MC-T11, were incorporated into the study design. These two cell lines have different malignant transformation potential. The effect of green tea extract (GTE), a potential anticancer agent, on actin remodeling was investigated. Upon exposure to the carcinogen 4-aminobiphenyl (4-ABP), the untransformed HUC-PC undergoes malignant transformation whereas the transformed MC-T11 progresses from noninvasive to invasive tumor. GTE induces actin polymerization in MC-T11 cells in a dose-responsive manner, but this effect is less obvious in the untransformed, more differentiated HUC-PC cells, which natively have higher actin polymerization status. In contrast, GTE antagonizes carcinogen 4-ABP induced actin depolymerization and stress fiber disruption in HUC-PC cells. In MC-T11 cells, GTE inhibits 4-ABP induced motility by increasing cell adhesion and focal adhesion complex formation. The effect of GTE on actin remodeling seems to be mediated by the stimulation of small GTP-binding protein Rho activity, because C3 exoenzyme, a specific inhibitor for Rho, blocks GTE-mediated Rho activation and stress fiber formation in MC-T11 cells. This study shows that GTE exerts an effect on cytoskeletal actin remodeling and provides further support for the use of GTE as a chemopreventive agent.     

百令胶囊对实验性糖尿病大鼠肾脏的保护作用

目的：探讨百令胶囊对实验性糖尿病大鼠肾脏的保护作用。方法：SD大鼠45只，分为正常对照组、糖尿病对照组及糖尿病治疗组。各糖尿病组以四氧嘧啶腹腔内注射制成糖尿病模型。治疗组大鼠给予给予百令胶囊0．2g／kg／天灌胃，每天1次，共12周。取肾脏行光镜和电镜检查，并进行图像分析，同时行血糖、血脂、肾功能、24h尿蛋白排泄量、肾重／体重、肾组织糖基化产物测定。统计学处理采用方差分析。结果与糖尿病对照组比较，治疗组大鼠血TG、TC、肾重／体重、24h尿蛋白排泄量以及肾脏组织蛋白糖基化产物水平均有不同程度的降低（P〈0．05）。与正常对照组比较，光镜检查显示糖尿病对照组大鼠肾小球截面积明显增大（P〈0．01），系膜区基质增生扩大；肾小球硬化明显，平均肾小球硬化指数明显增加（P〈0．01）；电镜显示大鼠肾小球基底膜显著的不均匀增厚，并伴有广泛的肾小管上皮细胞的髓样变性及胞浆空泡化变性。治疗组上述病变明显减轻（P〈0．01）。结论：百令胶囊显著改善糖尿病大鼠肾脏结构，防止系膜区扩大和基底膜增厚，具有显著地抗肾小球纤维化的作用。     

高速离心法在中药口服制剂工艺中的应用

综述了高速离心法在中药口服液、颗粒剂及胶囊剂等口服制剂工艺中的应用.高速离心技术具有保留有效成分、提高制剂稳定性、缩短生产周期、降低生产成本等优点,值得推广.     

顶空气相色谱法测定盐酸依匹斯汀中溶剂残留

建立顶空气相色谱法分析盐酸依匹斯汀中溶剂残留.采用DB-1大口径毛细管柱,以正丙醇为内标进行定量.甲醇、乙醚、三氯甲烷、四氢呋喃的线性范围分别为7.9 ～ 317.0μg·ml-1 (r=0.9996),0.7～35.5μg·ml-1(r=0.9998),1.5～73.5μg·ml-1 (r=0.9992),0.9～44.4μg·ml-1(r=0.9994),回收率分别为101.64%,97.18%,99.32%,101.12%,RSD分别为1.97%,1.10%,2.40%,0.84%.本方法简单、准确、灵敏度高、重现性好.     

Effect of inflammation on endothelial cells induced by poly-L-lactic acid degradation in vitro and in vivo

Abstract

As a promising candidate, biodegradable Poly-L-lactic Acid (PLLA) has been extensively used in coronary artery stents. In our previous reports, PLLA stents implanted in porcine coronary arteries showed safety without stent thrombosis. However, inflammatory responses were observed, which needed further study. In this study, human aortic endothelial cells (HAEC) were treated with different volume percentages of extract of pre-degraded PLLA (extract of PLLA) in vitro, and the cell growth curve and morphological changes were examined. The expression of inflammatory cytokines such as NF-κB, VEGF and VCAM-1 were also observed by ELISA. In addition, PLLA stent was implanted in porcine coronary artery to examine morphological changes, functional marker eNOS and inflammatory responses. The extract of PLLA caused significant growth inhibition and release of NF-κB, VEGF and VCAM-1 in HAEC with volume percentage-dependence. Although re-endothelialization and expression of eNOS was observed, expression of NF-κB and lymphocytes surrounding PLLA were also found after PLLA stents were implanted in the artery. This study demonstrated the effects of inflammation on endothelial cells induced by PLLA degradation in vitro and showed the inflammation in vivo, suggesting that anti-inflammatory strategy is necessary for PLLA stent implantation in the artery.     

Cajal间质细胞的研究进展

Cajal间质细胞(interstitial cells of Cajal,ICC)是一类主要分布于胃肠道的间质细胞,是胃肠道的起搏细胞(pacemaker cell)和信号传导细胞,与肌细胞以及末梢神经元有着紧密的关系,具有激发和促进胃肠蠕动的作用.借助于电子显微镜技术,清楚观察到了ICC位置分布和内部精细结构;应用免疫荧光等生化技术,发现了其特殊表达的C-kit蛋白;利用电生理技术,得知多种胃肠动力障碍疾病也与其异常有关.多年来,学者逐渐在胃肠道、胆道、膀胱、子宫等部位发现了ICC的踪迹,并试图阐述其与某些疾病的发生机制.本文就ICC的起源、形态学、受体和功能、以及与其相关的疾病等作一综述.     

Albiflorin Attenuates Mood Disorders Under Neuropathic Pain State by Suppressing the Hippocampal NLRP3 Inflammasome Activation During Chronic Constriction Injury

BackgroundNeuropathic pain is a multifaceted and ubiquitous disease across the globe. Mood disorders, such as anxiety and depression, are frequently observed in patients suffering from neuropathic pain. Both neuropathic pain and comorbid mood disorders seriously impact quality of life. Accumulated evidence shows that activation of the NOD-like receptor protein 3 (NLRP3) inflammasome is involved in the neuroinflammatory pathogenesis of neuropathic pain, anxiety, and depression. However, the role of the NLRP3 inflammasome in the pathological process of anxiety and depression under the neuropathic pain state has not been fully described. Albiflorin, a monoterpene glycoside, may be a potential regulator of the NLRP3 inflammasome, but it is not clear whether albiflorin relates to NLRP3 inflammasome activation.MethodsWe used a systematic pharmacological method to confirm whether the activation of the NLRP3 inflammasome in the hippocampus was involved in the development of neuropathic pain associated with mood disorders and whether albiflorin could be an effective treatment for these symptoms.ResultsThe NLRP3 inflammasome contributed to the neuropathic pain and comorbid anxiety and depression-like behaviors induced by chronic constriction injury of the sciatic nerve, and albiflorin may relieve these symptoms via inhibition of the NLRP3 inflammasome activity. Moreover, albiflorin enhanced the translocation of the nuclear factor erythroid 2-related factor 2 into the nucleus and suppressed nuclear factor-kappa B activity in the hippocampus.ConclusionsAlbiflorin, as a potential therapeutic agent, might greatly improve the overall symptoms of neuropathic pain.