Evaluation of Ethanol on Gastric Epithelial Restoration in Vitro

Ethanol exerts damaging effects on gastric mucosa and delays ulcer healing. To investigate the effect of ethanol on the wound repairing process, we used a wound repair model using primary cultured gastric mucosal cells. A confluent monolayer gastric mucosal cell sheet consisting mainly of mucous cells was wounded to make a cell-free area of constant size. Cell-free area was restored with time after wounding and monitored every 12 hr using a computer image analyzer to observe epithelial cell restoration quantitatively in the presence and absence of ethanol (2.0%). It was found that, although the control wound was completely repaired in 36 to 48 hr, the group treated with 2.0% ethanol showed a significant delay of repair. In the control, 5-bromodeoxyuridine-positive cells appeared around the wound in 24 to 36 hr. In contrast, the group treated with 2.0% ethanol showed no 5-bromodeoxyuridine-positive cells during the experiment. In conclusion, 2.0% ethanol retarded the repair of gastric mucosal restoration by inhibiting the initial gastric cell migration, followed by inhibition of proliferation of cells.     

双歧三联活菌胶囊联合降脂化浊汤对非酒精性脂肪性肝炎患者肠黏膜屏障的保护作用

目的 探讨双歧三联活菌胶囊联合降脂化浊汤对非酒精性脂肪性肝炎患者肠黏膜屏障的保护作用。方法 选取门诊治疗的NASH患者90例,随机分为中西医组(n=45例)和西医组(n=45例)。西医组患者予以双歧三联活菌胶囊630mg/次,2次/d,温水口服;中西医组患者在西医组治疗基础上予以疏肝降脂汤,加水煎煮至200ml,分早晚两次口服,两组均连用12周。检测并比较两组患者治疗前后肝功能指标、血清内毒素、D-乳酸和二胺氧化酶(DAO)水平的变化。结果 治疗12周后,两组ALT、AST和γ-GT以及血清内毒素、D-乳酸和DAO水平较前均明显下降(P<0.05或P<0.01),且中西医组下降值较西医组更明显(P<0.05)。结论 双歧三联活菌胶囊联合疏肝降脂汤治疗NASH的疗效较显著,能降低血清内毒素、D-乳酸和DAO水平,减少或抑制内毒素血症产生,降低肠黏膜通透性,修复受损肠粘膜屏障,使得肝功能逐渐恢复正常。     

结肠炎大鼠炎症黏膜提取液对骨髓间质干细胞增殖和表面分化抗原的影响

背景:动物实验和临床试验均表明间质干细胞(MSCs)对受损肠道组织有一定修复作用,然而目前尚不清楚肠道炎症微环境对MSCs移植治疗炎症性肠病(IBD)有何影响。目的:通过体外实验观察结肠炎大鼠模型肠道炎症黏膜提取液对骨髓MSCs增殖和表面分化抗原的影响。方法:以全骨髓贴壁法分离和原代培养大鼠MSCs并行传代扩增。取三硝基苯磺酸(TNBS)结肠炎大鼠模型肠道炎症黏膜提取液(0、1、2、3 ml)与MSCs共培养,倒置相差显微镜观察各组细胞贴壁和生长情况,绝对计数法绘制细胞生长曲线,流式细胞术检测细胞表面分化抗原表达。结果:全骨髓贴壁法可成功分离MSCs,所获细胞CD29、CD44表达阳性,CD105表达低度阳性,CD34、CD45表达阴性。3 ml炎症黏膜提取液处理组MSCs接种6 h后见细胞贴壁,36 h开始克隆性增生,此后细胞增殖速度较空白对照组明显加快,第6 d即达100%融合,但表面分化抗原表达与空白对照组相比无明显变化。结论:结肠炎大鼠炎症黏膜提取液可促进骨髓MSCs增殖,但对细胞表面分化抗原无明显影响。     

HMGB1 与claudin-1 在重症急性胰腺炎肠黏膜屏障损伤中的表达及意义

目的：探讨高迁移率族蛋白B1（HMGB1）与claudin-1在重症急性胰腺炎（SAP）肠黏膜屏障损伤时的表达改变及意义。方法：将24只雄性Wistar大鼠随机均分为假手术组,SAP模型组（模型组）,SAP模型+HMGB1 抑制剂丙酮酸乙酯（EP）处理组（EP处理组）。SAP模型采用5%牛磺胆胆酸钠逆行胰管注射法,EP处理组于造模后2 h尾静脉注射EP溶液。各组大鼠于术后24 h处死,测定血浆淀粉酶（AMY）,内毒素（LPS）,血浆二胺氧化酶（DAO）水平;观察肠黏膜的病理学变化;免疫组织化学法观察肠黏膜claudin-1蛋白的表达;RT-PCR法检测肠组织HMGB1和claudin-1 mRNA的表达。结果：与假手术组比较,模型组大鼠血浆AMY,LPS和DAO水平均明显升高（均P<0.05）;小肠黏膜屏障受损,上皮细胞间紧密连接破坏;肠黏膜claudin-1蛋白表达降低,肠组织HMGB1 mRNA表达升高,claudin-1 mRNA的表达降低。与模型组比较,EP处理组肠组织HMGB1 mRNA表达降低,claudin-1蛋白与mRNA表达升高,各损伤指标均明显改善。结论：SAP肠黏膜屏障损伤可能与肠组织HMGB1表达升高,从而下调紧密连接蛋白claudin-1的表达有关;HMGB1抑制剂EP对SAP肠黏膜屏障损伤具有保护作用。

     

黏膜方对IgA肾病大鼠异常糖基化IgA1及肾间质纤维化的干预及机制研究

目的:研究血清和肾组织中的异常糖基化IgA1水平与IgA肾病的间质纤维化程度的相关性;阐明黏膜方治疗IgA肾病的作用机制。方法:采用口服牛血清白蛋白、四氯化碳皮下注射和尾静脉注射脂多糖免疫复合法建立IgA肾病大鼠模型,随机分为正常组、模型组、中药组(黏膜方)及西药组(福辛普利钠)、中西医结合组(黏膜方+福辛普利),观察治疗后各组血清和肾组织异常糖基化的IgA1水平、血清IgA-纤维连接蛋白(IgA-FN)、肾组织转化生长因子-β1(TGF-β1)和α-平滑肌肌动蛋白(α-SMA)及其mRNA的表达量。结果:血清IgA-FN,中药组及中西医结合组低于模型组(P<0.001);血清异常糖基化IgA1量,中药组及西药组均低于模型组(P<0.05);肾组织中的异常糖基化IgA1水平,模型组高于正常组(P<0.05),各治疗组低于模型组(P<0.05);肾组织中TGF-β1mRNA及蛋白表达量模型组均显著高于正常组(P<0.01),各治疗组TGF-β1mRNA及蛋白表达均低于模型组(P<0.05);模型组α-SMAmRNA高于正常组(P<0.05),各治疗组低于模型组(P<0.001),模型组α-SMA蛋白表达阳性面积高于正常组(P<0.001),中西医结合组和西药组阳性面积低于模型组(P<0.05);肾组织α-SMAmRNA及蛋白表达与血清及肾组织中异常糖基化IgA1呈正相关(P<0.005);肾组织TGF-β1mRNA与血清及肾组织异常糖基化IgA1呈正相关(P<0.005)。结论:血清中异常糖基化IgA1与肾间质纤维化程度密切相关,黏膜方能减轻实验性IgAN大鼠血清及肾脏异常糖基化的IgA1水平,改善肾间质纤维化。     

Mucosal secretion changes during radiotherapy in the oral cavity

Mucositis in the oral cavity is a serious complication during radiation therapy for head and neck cancer, causing local discomfort and pain. In severe cases, hospitalization and interruption of radiotherapy may be necessary. The pathogenesis of this mucositis is not clear. With the purpose of getting more understanding of the pathogenesis of the mucositis, we examined the mucosal secretion from ten patients during radiotherapy with an imprint technique. In the secretion we studied the cellular composition and cellular function. In eight of ten treated patients the numbers of granulocytes increased in the secretion after 2 weeks of radiation therapy. The granulocytes, however, did not show any signs of phagocytosis. The patients all developed mucositis. We propose that the granulocytes in the secretion might play an important role in the development of mucositis during radiotherapy.     

鼻中隔矫正术后鼻黏膜缝合的临床应用研究

目的探讨鼻内镜下鼻中隔矫正术后行鼻中隔黏膜缝合的应用效果。方法将120例行鼻中隔偏曲矫正患者随机分为黏膜缝合组和鼻腔填塞组各60例,比较两组患者在术后鼻部疼痛、头痛、流泪、吞咽困难、睡眠障碍的视觉模拟评分（VAS）及并发症情况。结果在术后鼻部疼痛、头痛、流泪、吞咽困难、睡眠障碍这5个方面,黏膜缝合组的VAS评分均明显低于鼻腔填塞组,差异有统计学意义（P〈0.05）。结论鼻中隔偏曲矫正术后行鼻黏膜缝合术,不需要对鼻腔进行填塞,术后痛苦小,也避免了鼻中隔血肿等并发症的发生,具有更好的临床效果。     

Epidermoid Cyst Arising in the Buccal Mucosa: Case Report and Literature Review

Epidermoid cysts are benign subcutaneous lesions, and the large majority of these cysts affect the floor of the mouth; however, the buccal mucosa is not the usual site of occurrence. To date, only 5 articles have been published with 6 cases of epidermoid cysts arising in the buccal mucosa. Therefore, the aim of this study was to describe the clinical, histopathological and immunohistochemical features of a case of an epidermoid cyst located in the buccal mucosa. To our knowledge, this is the first report of an oral epidermoid cyst describing an intense foreign body gigantocellular inflammatory reaction against epithelial keratin component. Although the usual diagnosis for epidermoid cysts is based on histopathological findings, this case report addresses novel information regarding the immunohistochemical pattern which may be found in these lesions.     

肥大细胞在急性应激性肠黏膜屏障损伤中的作用机制

背景：应激所致肠黏膜屏障损伤的机制以及肥大细胞（MC）在其中的作用尚未明确。目的：探讨肠黏膜MC（IMMC）在急性应激性肠黏膜屏障损伤中的作用机制。方法：Sprague—Dawley（SD）大鼠随机分为正常对照组（N组）、应激组（S组）,S组给予急性冷束缚应激建立模型,按照应激结束后处死时间进一步分为S2h、S4h、SSh、S16h、S24h组。取回肠末端观察组织病理学改变,以Chiu’S评分评估肠黏膜组织损伤程度,以甲苯胺蓝染色计数IMMC,以透射电镜观察肠黏膜组织和IMMC超微结构,以ELISA法检测肠黏膜组织组胺含量。结果：S组的Chiu’S评分均显著高于N组（P〈0．05）,呈先升后降的趋势,以S8h组最高。S2h、S4h组的IMMC计数显著高于N组（P〈0．05）,S8h、S16h、S24h组IMMC计数与N组相比差异无统计学意义（P〉0．05）。IMMC计数与Chiu’S评分无相关性（P〉0．05）。S组肠黏膜超微结构破坏明显,IMMC胞质大量脱颗粒。S2h、S4h、S8h组的肠黏膜组织组胺含量较N组显著降低（P〈0．05）,呈逐渐下降趋势。S16h、S24h组组胺含量与N组相比差异无统计学意义（P〉0．05）。肠黏膜组织组胺含量与Chiu’S评分呈负相关（P=0．03）。结论：急性应激状态下,IMMC脱颗粒释放炎性介质是导致肠黏膜屏障损伤的重要机制。