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Interleukin-6, desmosome and tight junction protein expression levels in reflux esophagitis-affected mucosa

World Journal of Gastroenterology 2009年第29期15卷 3621-3630页

作者： Fei-Yue Li Yan Li Department of Digestive Diseases Central Hospitalof Daqing Youtian Daqing 163000 Heilongjiang ProvinceChina Department of Digestive Diseases Shengjing Hospitalof China Medical University Shenyang 110004 LiaoningProvince China

AIM： To investigate the correlation between the expression levels of interleukin （IL）-6 and proteins in tight junctions （TJs） in the esophageal mucosa of rats modeling different types of reflux esophagitis （RE）, and the ability of aluminum phosphate to protect against RE-induced mucosal damage via these proteins. METHODS： Male SPF Wistar rats aged 56 d were divided randomly into acid RE, alkaline RE, mixed RE, and control groups. Various surgical procedures were performed to establish rat models of acid RE. At 14 d after the procedure, some of the rats started aluminum phosphate treatment. Transmission electron microscopy （TEM） was used to observe the morphological features of TJs and desmosomes in the esophageal epithelium. Immunohistochemical methods and Western blotting were used to measure expression of claudin 1, occludin, ZO-1, JAM-l, DSG-1 and IL-6; reverse transcription polymerase chain reaction （RT- PCR） was used to measure expression of mRNA of claudin 1, occludin, ZO-1, JAM-1, DSG-1 and IL-6. RESULTS： At day 14 alter the procedures, an RE model was established in all subsequently sacrificed rats of groups A, B and C. By both gross and microscopic observation, the mucosa was damaged and thickened as the disease progressed. With TEM observation, a widened intercellular space was noticed, with significantly fewer desmosomes. Immunohistochemistry showed significantly higher levels of all proteins in all RE models compared to control rats at 3 d after operation （65.5% ± 25.6% vs 20.5% ± 2.1%, P 〈 0.05, respectively）. At 14 d after operation, along with continuing hyperplasia in the basal layer, the expression of TJ proteins in individual cells gradually decreased （12.4% ± 2.1% vs 20.5% ± 2.1%, P 〈 0.05, respectively）. Western blottings and RT-PCR showed a directly proportional increase in IL-6 levels in relation to TJ proteins, as compared to controls （0.878 ± 0.024 vs 0.205 ± 0.021 and 0.898±0.022 vs 0.205 ± 0.021, P 〈 0.05, respectively）. Upon treatment with

关键词： Reflux esophagitis Desmosome tightjunction Proteins Mucosa

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Scutellaria barbata attenuates diabetic retinopathy by preventing retinal inflammation and the decreased expression of tight junction protein

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International Journal of Ophthalmology(English edition) 2017年第6期10卷 870-877页

作者： Xi-Yu Mei Ling-Yu Zhou Tian-Yu Zhang Bin Lu Li-Li Ji The MOE Key Laboratory for Standardization of Chinese Medicines Shanghai Key Laboratory of Complex Prescription Institute of Chinese Materia Medica Shanghai University of Traditional Chinese Medicine Shanghai 201203 China

AIM： To observe the attenuation of ethanol extract of Herba Scutellaria barbata （SE） against diabetic retinopathy （DR） and its engaged mechanism. METHODS： C57BL/6J mice were intraperitoneally injected with streptozotocin （STZ, 55 mg/kg） for 5 consecutive days to induce diabetes, The diabetic mice were orally given with SE （100, 200 mg/kg） for lmo at lmo after STZ injection. Blood-retinal barrier （BRB） breakdown was detected by using Evans blue permeation assay. Real-time polymerase chain reaction （RT-PCR）, Western blot and immunofiuorescence staining were used to detect mRNA and protein expression. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum contents of tumor necrosis factor-e （TNF-a） and interleukin （IL）-II. RESULTS： SE （100, 200 mg/kg） reversed the breakdown of BRB in STZ-induced diabetic mice. The decreased expression of retinal claudin-1 and claudin-19, which are both tight junction （T J） proteins, was reversed by SE. SE decreased the increased serum contents and retinal mRNA expression of TNF-a and IL-113. SE also decreased the increased retinal expression of intercellular cell adhesion molecule-1 （ICAM-1）. SE reduced the increased phosphorylation of nuclear factor kappa B （NFKB） p65 and its subsequent nuclear translocation in retinas from STZ- induced diabetic mice. Results of Western blot and retinal immunofluorescence staining of ionized calcium-binding adapter molecule 1 （Ibal） demonstrated that SE abrogated the activation of microglia cells in STZ-induced diabetic mice. CONCLUSION： SE attenuates the development of DR by inhibiting retinal inflammation and restoring the decreased expression of TJ proteins including claudin-1 and claudin-19.

关键词： scutellaria barbata diabetic retinopathy tightjunction inflammation nuclear factor kappa B microglia

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