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| 1 | Potential beneficial effects of butyrate in intestinal and extraintestinal diseases显示文摘The multiple beneficial effects on human health of the short-chain fatty acid butyrate,synthesized from nonabsorbed carbohydrate by colonic microbiota,are well documented.At the intestinal level,butyrate plays a regulatory role on the transepithelial fluid transport,ameliorates mucosal inflammation and oxidative status,reinforces the epithelial defense barrier,and modulates visceral sensitivity and intestinal motility.In addition,a growing number of studies have stressed the role of butyrate in the prevention and inhibition of colorectal cancer.At the extraintestinal level,butyrate exerts potentially useful effects on many conditions,including hemoglobinopathies,genetic metabolic diseases,hypercholesterolemia,insulin resistance,and ischemic stroke.The mechanisms of action of butyrate are different;many of these are related to its potent regulatory effects on gene expression.These data suggest a wide spectrum of positive effects exerted by butyrate,with a high potential for a therapeutic use in human medicine. | Roberto Berni Canani Margherita Di Costanzo Ludovica Leone Monica Pedata Rosaria Meli Antonio Calignano | 2011 | World Journal of Gastroenterology2011，17，12： | 52 |
| 2 | Jianpi Qingchang decoction alleviates ulcerative colitis by inhibiting nuclear factor-κB activation显示文摘AIM To inve s t igat e t he t he r ape ut ic e f f e c t of Jianpi Qingchang decoction(JPQCD) on dextran sulfate sodium(DSS)-induced ulcerative colitis(UC) in mice.METHODS C57BL/c mice were injected intragastrically with 5% DSS instead of drinking water for 7 d, and their body weight, diarrhea severity and fecal bleeding were monitored, while the mice in the control group were treated with standard drinking water, without DSS. After 7 d, the DSS drinking water was changed to normal water and the DSS group continued with DSS water. The control and DSS groups were given normal saline by intragastric injection. The 5-aminosalicylic acid(5-ASA) group was treated orally with 5-ASA at a dose of 100 mg/kg daily. The JPQCD group was treated orally with JPQCD at a dose of 17.1 g/kg daily. On day 14, the colon length was measured, the colorectalhistopathological damage score was assessed, and protein levels of interleukin(IL)-1β, IL-8 and tumor necrosis factor-alpha(TNF-α) in colon supernatants were measured by enzyme-linked immunosorbent assay. m RNA expression of IL-1β, IL-8, TNF-α and nuclear factor-kappa B(NF-κB) was detected by realtime quantitative polymerase chain reaction. Western blotting was used to detect the protein expression of NF-κB and inhibitor of kappa B. RESULTS Acute inflammation occurred in the mice administered DSS, including the symptoms of losing body weight, loose feces/watery diarrhea and presence of fecal blood; all these symptoms worsened at 7 d. The colons of mice treated with DSS were assessed by histological examination, and the results confirmed that acute inflammation had occurred, as evidenced by loss of colonic mucosa and chronic inflammatory cell infiltration, and these features extended into the deeper layer of the colon walls. The expression levels of IL-1β, IL-8 and TNF-α in the DSS group were higher than those in the control group(P < 0.05), and the expression levels of IL-1β, IL-8 and TNF-α in the JPQCD and 5-ASA groups were lower than those in the DSS group after treating with JPQCD and 5-ASA. Comparing with the DSS group, the mR NA level of IL-1β, IL-8, TNF-α and NF-κB was significantly reduced by 5-ASA and JPQCD. The difference between JPQCD and 5-ASA groups was not statistically significant(P > 0.05). Comparing with the DSS group, due to using JPQCD and 5-ASA, significant suppression of activation in DSSinduced NF-κB and increased phosphorylation of IκB in mice with experimental colitis occurred(P < 0.05). The difference between the JPQCD group and the 5-ASA group was not statistically significant(P > 0.05). CONCLUSION Activation of the NF-κB signaling pathway is inhibited by JPQCD, which shows the potential mechanism by which JPQCD treats UC. | Lie Zheng Ya-Li Zhang Yan-Cheng Dai Xuan Chen De-Liang Chen Yue-Ting Dai Zhi-Peng Tang | 2017 | World Journal of Gastroenterology2017，23，7： | 30 |
| 3 | Aspirin and pravastatin reduce lectin-like oxidized low density lipoprotein receptor-1 expression, adhesion molecules and oxidative stress in human coronary artery endothelial cells显示文摘背景氧化应力和发炎是在动脉粥样硬化的致病的重要的步。我们要求了特别在联合,阿司匹林和 pravastatin 的治疗学的集中可以在 endothelial 房间,和这个概念压制氧化应力和发炎,这在人的冠的动脉 endothelial 房间( HCAEC )被检验冠的动脉 endothelial 房间是的 .Methods 人与氧化低的密度 iipoprotein 有教养、对待( ox-LDL ,为 24 个小时的 60 g/ml )独自一个,或与阿司匹林( 1 , 2 或 5 mmol/L )预先对待, pravastatin ( 1 , 5 或 10 mol/L )或他们的联合( 1 mmol/在各自的处理以后, superoxide 阴离子生产, p38 mitogen 激活蛋白质 kinase 和抄写因素 NF-B 激活,象lectin一样 ox-LDL receptor-1 ( LOX-1 )的蛋白质表示和粘附分子,和单核白血球粘附是极大地得到的 measured.Results Ox-LDL 处理它的受体 LOX-1 表示, superoxide 阴离子生产和煽动性的反应,它被 aspidn ( 1 mmol/L )或 pravastatin ( 5 mol/L )的低集中最低限度地影响,但是是显著地减少的 b p38 mitogen 的激活激活蛋白质 kinase 和 NF-B,细胞间的粘附 molecule-1 和单核白血球的表示趋化性的 protein-1,被阿司匹林或 pravastatin 仅仅温和地独自影响,被他们的联合显著地稀释。作为后果,对 endothelial 房间的单核白血球粘附被二个代理人的联合显著地稀释。著名抗氧化剂 -tocopherol 和 -tocopherol 在 ox-LDL-mediated 上有类似的禁止的效果这些学习的阿司匹林和 pravastatin.Conclusions 的联合关于 endothelial 指向了在 aspidn 和 pravastatin 之间的一个积极相互作用的氧化压力和 LOX-1 表示以及单核白血球粘附生物学。抗氧化剂和随后的反煽动性的效果可以是潜在的下属机制之一。 | CHEN Jia-wei ZHOU Shi-bei TAN Zhi-ming | 2010 | Chinese Medical Journal2010，，12： | 24 |
| 4 | 不同透析膜的生物特性及临床应用显示文摘 | 谢红浪 季大玺 | 2004 | 肾脏病与透析肾移植杂志2004，13，4： | 22 |
| 5 | Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury显示文摘Macrophage inflammatory protein(MIP)-2 is one of the CXC chemokines and is also known as chemokine CXC ligand(CXCL2). MIP-2 affects neutrophil recruitment and activation through the p38 mitogen-activatedprotein-kinase-dependent signaling pathway, by binding to its specific receptors, CXCR1 and CXCR2. MIP-2 is produced by a variety of cell types, such as macrophages, monocytes, epithelial cells, and hepatocytes, in response to infection or injury. In liver injury, activated Kupffer cells are known as the major source of MIP-2. MIP-2-recruited and activated neutrophils can accelerate liver inflammation by releasing various inflammatory mediators. Here, we give a brief introduction to the basic molecular and cellular sources of MIP-2, and focus on its physiological and pathological functions in acute liver injury induced by concanavalin A, lipopolysaccharides, irradiation, ischemia/reperfusion, alcohol, and hypoxia, and hepatectomy-induced liver regeneration and tumor colorectal metastasis. Further understanding of the regulatory mechanisms of MIP-2 secretion and activation may be helpful to develop MIP-2-targeted therapeutic strategies to prevent liver inflammation. | Chao-Chao Qin Yan-Ning Liu Ying Hu Ying Yang Zhi Chen | 2017 | World Journal of Gastroenterology2017，23，17： | 21 |
| 6 | Cellular and molecular regulation of innate inflammatory responses显示文摘由模式识别受体(PRR ) 的病原体的天生的察觉到在在自我和非自我部件之间的天生的辨别起必要作用,导致天生的有免疫力的防卫和煽动性的回答的产生。天生的煽动性的反应的开始,激活和分辨率被相互作用的一个复杂网络在有免疫力、非有免疫力的系统的众多的细胞、分子的部件之中调停。当时一控制并且有益的天生的煽动性的反应是批评的因为病原体的消除和织物动态平衡, dysregulated 或持续发炎的维护导致象长期的感染那样的病理学的条件,煽动性的自体免疫的疾病。在这评论,我们为天生的免疫和煽动性的回答的建立和规定在我们细胞、分子的机制的理解讨论一些最近的进展。 | Juan Liu Xuetao Cao | 2016 | Cellular & Molecular Immunology2016，13，6： | 20 |
| 7 | “上火”“发炎”与自由基的关系显示文摘在广泛文献检索基础上,对'上火'和'自由基'的关系进行了审视,为深入理解中医药现代化、中西医结合提供资料。 | 葛娜 巩江 倪士峰 骆蓉芳 赵婷 路锋 吴洋博 曹梦晔 | 2011 | 辽宁中医药大学学报2011，13，2： | 14 |
| 8 | Effects of matrix metalloproteinase 9 inhibition on the blood brain barrier and inflammation in rats following cardiopulmonary resuscitation显示文摘跟随心肺的复活(CPR ) 的背景 Neuroprotective 策略是在紧急情况和批评照顾药的一个重要焦点。矩阵 metalloproteinases (MMP ) ,因为它的功能,特别 MMP9 在焦点的大脑 ischemia/reperfusion 损害吸引了许多注意。在在老鼠的焦点的服的局部缺血模型, SB-3CT 能压制 MMP9 的表示,减轻大脑浮肿,并且在 120 只老鼠随机被分到假冒操作( n=40 )的 CPR.Methods 以后的全球服的 ischemia-reperfusion 损害上没有研究,复活处理(n= 40 ),并且复活控制(n= 40 )组。假冒操作组老鼠仅仅是 anesthetized 并且气管地把管子插进,当复活处理和复活控制组也由窒息受到了心脏的拘捕时。在复活处理组, SB-3CT 在恢复自发的循环(ROSC ) 以后 intraperitoneally 被注射,定义为 supraventricular 节奏和吝啬的动脉的压力(地图) 的恢复为超过 5 分钟的 60 公里 Hg。没有 SB-3CT 的注射,复活控制组也实现了 ROSC。老鼠被执行,样品在死亡以后立即被拿,然后在 3, 9, 24,和 48 个小时(n=8 ) 。 MMP9 蛋白质的大脑织物表示, MMP9 mRNA ,水内容, Evans 蓝内容, TNF --一, IL-1 ,和 IL-6 被测量,并且大脑织物 ultramicrostructure 在复活控制组,与电子 microscopy.Results 学习了 MMP9 蛋白质和 mRNA 的大脑织物表示,水内容, Evans 蓝内容, TNF --一, IL-1 ,和 IL-6 显著地在 3 个小时被提高,并且在复活以后在 24 个小时达到顶点,什么时候与假冒操作组相比( P < 0.05 )。织物 ultramicrostructure 也在复活控制组变化了。由对比,尽管所有这些索引与假冒操作相比在复活处理组被增加,组织(P < 0.05 ) ,他们比在复活控制组低(P < 0.05 ) 。MMP9 蛋白质和 mRNA 的结论表示,水内容, Evans 蓝内容, TNF -- 一, IL-1,和 IL-6 在 CPR 以后在老鼠大脑织物增加了,显示血大脑障碍和过量的混乱煽动性的反应。MMP9 表示与 SB-3CT 被减少,导致减少的大脑损害。 | HE Zhi-jie HUANG Zi-tong CHEN Xiao-tong ZOU Zi-jun | 2009 | Chinese Medical Journal2009，，19： | 11 |
| 9 | Panax notoginseng Saponins Protect Kidney from Diabetes by Up-regulating Silent Information Regulator 1 and Activating Antioxidant Proteins in Rats显示文摘Objective: To explore the mechanism of the protective effects of Panax notoginseng saponins(PNS) on kidney in diabetic rats. Methods: Diabetic rat model was obtained by intravenous injection of alloxan, and the rats were divided into model, PNS-100 mg/(kg·day) and PNS-200 mg/(kg·day) groups, 10 each. Another 10 rats injected with saline were served as control. Periodic acid-Schiff staining and immunological histological chemistry were used to observe histomorphology and tissue expression of bone morphogenetic protein-7(BMP-7). Silent information regulator 1(SIRT1) was silenced in rat mesangial cells by RNA interference. The mR NA expressions of SIRT-1, monocyte chemoattractant protein-1(MCP-1), transforming growth factor β1(TGF-β1) and plasminogen activator inhibitor-1(PAI-1) were analyzed by reverse transcription polymerase chain reaction. The protein expressions of SIRT1 and the acetylation of nuclear factor κB(NF-κB) P65 were determined by western blotting. The concentration of MCP-1, TGF-β1 and malondialdehyde(MDA) in culture supernatant were detected by enzyme-linked immuno sorbent assay. The activity of superoxide dismutase(SOD) was detected by the classical method of nitrogen and blue four. Results: In diabetic model rats, PNS could not only reduce blood glucose and lipid(P<0.01), but also increase protein level of BMP-7 and inhibit PAI-1 expression for suppressing fibrosis of the kidney. In rat mesangial cells, PNS could up-regulate the expression of SIRT1(P<0.01) and in turn suppress the transcription of TGF-β1(P<0.05) and MCP-1(P<0.05). PNS could also reverse the increased acetylation of NF-κB p65 by high glucose. In addition, redox regulation factor MDA was down-regulated(P<0.05) and SOD was up-regulated(P<0.01), which were both induced by SIRT1 up-regulation. Conclusions: PNS could protect kidney from diabetes with the possible mechanism of up-regulating SIRT1, therefore inhibiting inflammation through decreasing the induction of inflammatory cytokines and TGF-β1, as well as activating antioxidant proteins. | 杜月光 汪丽佩 钱俊文 章科娜 柴可夫 | 2016 | Chinese Journal of Integrative Medicine2016，22，12： | 11 |
| 10 | Fluoxetine inhibited extracellular matrix of pulmonary artery and inflammation of lungs in monocrotaline-treated rats显示文摘 | Xue-qin LI Han-ming WANG Chun-guang YANG Xin-hua ZHANG Dan-dan HAN Huai-liang WANG | 2011 | Acta Pharmacologica Sinica2011，32，2： | 11 |
| 11 | Therapeutic potential of flavonoids in inflammatory bowel disease: A comprehensive review显示文摘The inflammatory process plays a central role in the development and progression of numerous pathological situations,such as inflammatory bowel disease(IBD),autoimmune and neurodegenerative diseases,metabolic syndrome,and cardiovascular disorders. IBDs involve inflammation of the gastrointestinal area and mainly comprise Crohn's disease(CD) and ulcerative colitis(UC). Both pathological situations usually involve recurring or bloody diarrhea,pain,fatigue and weight loss. There is at present no pharmacological cure for CD or UC. However,surgery may be curative for UC patients. The prescribed treatment aims to ameliorate the symptoms and prevent and/or delay new painful episodes. Flavonoid compounds are a large family of hydroxylated polyphenolic molecules abundant in plants,including vegetables and fruits which are the major dietary sources of these compounds for humans,together with wine and tea. Flavonoids are becoming very popular because they have many health-promoting and disease-preventive effects. Most interest has been directed towards the antioxidant activity of flavonoids,evidencing a remarkable free-radical scavenging capacity. However,accumulating evidence suggests that flavonoids have many other biological properties,including anti-inflammatory,antiviral,anticancer,and neuroprotective activities through different mechanisms of action. The present review analyzes the available data about the different types of flavonoids and their potential effectiveness as adjuvant therapy of IBDs. | Ali Salaritabar Behrad Darvishi Farzaneh Hadjiakhoondi Azadeh Manayi Antoni Sureda Seyed Fazel Nabavi Leo R Fitzpatrick Seyed Mohammad Nabavi Anupam Bishayee | 2017 | World Journal of Gastroenterology2017，23，28： | 10 |
| 12 | Homocysteine mediates transcriptional changes of the inflammatory pathway signature genes in human retinal pigment epithelial cells显示文摘AIM:To test whether homocysteine(Hcy) can influence the transcriptional profile, we hypothesized that Hcy can lead to the induction of proinflammatory molecules in the retinal cells of aging people.METHODS:An unbiased in vitro inflammatory pathway focused study was designed employing retinal pigment epithelial(RPE) cell line, ARPE-19. Cells were cultured in the presence or absence of Hcy to capture target genes' expression profile. Three different concentrations of Hcy were added in the culture medium of confluent monolayers. c RNAs were made from the isolated total RNAs and the labeled c RNA probes were hybridized to microarrays specific for human disease pathway inflammatory cytokines, chemokines and their receptor gene micro-array panels as per manufacture's recommendations. Two Hcy up-regulated molecules:IL6 and CEBPB were further validated via Western blot analysis. Hcy's effect on ARPE-19 cellular morphology and genomic DNA integrity were also evaluated.RESULTS:Gene microarray analyses of RPE cells in response to Hcy treatment revealed alterations in the expressions of several inflammatory gene transcripts such as CCL5, CEBPB, IL13RA2, IL15 RA, IL6, IL8 and CXCL3 that were up-regulated. The transcripts for C3, CCL2, IL11 RA and IL18 genes exhibited down-regulation. The IL6 and CEBPB expressions were subsequently validated at the protein levels. Treatment of the retinal cells with increasing Hcy concentration influenced their density in culture however their morphology and DNA integrity remained unaffected. CONCLUSION:These findings suggest that Hcy can potentially mediate the expression of chemokines,cytokines and interleukins receptors in the retinal cells without having any debilitating effects on their morphology and the genomic DNA integrity. | Mahavir Singh Suresh C Tyagi | 2017 | International Journal of Ophthalmology(English edition)2017，10，5： | 10 |
| 13 | 类风湿性关节炎动物模型应用研究进展显示文摘类风湿性关节炎是一种慢性疾病 ,症状为关节僵硬及发炎、脆弱、丧失可动性、畸形。研究此类疾病的有效方法是建立、研究并应用动物模型。因此 ,用动物模型研究人类疾病的有效性是动物模型选择的最重要的标准。但不同的动物模型具有不同的特点 ,应根据实验的要求选择适当的模型。 | 陆声 梁崇礼 林月秋 | 2001 | 中国实验动物学杂志2001，11，2： | 10 |
| 14 | Th17 involvement in nonalcoholic fatty liver disease progression to non-alcoholic steatohepatitis显示文摘The nonalcoholic fatty liver disease(NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD encompasses a wide histological spectrum ranging from benign simple steatosis to non-alcoholic steatohepatitis(NASH). Sustained inflammation in the liver is critical in this process. Hepatic macrophages, including liver resident macropaghes(Kupffer cells), monocytes infiltrating the injured liver, as well as specific lymphocytes subsets play a pivotal role in the initiation and perpetuation of the inflammatory response, with a major deleterious impact on the progression of fatty liver to fibrosis. During the last years, Th17 cells have been involved in the development of inflammation not only in liver but also in other organs, such as adipose tissue or lung. Differentiation of a na?ve T cell into a Th17 cell leads to pro-inflammatory cytokine and chemokine production with subsequent myeloid cell recruitment to the inflamed tissue. Th17 response can be mitigated by T regulatory cells that secrete anti-inflammatory cytokines. Both T cell subsets need TGF-β for their differentiation and a characteristic plasticity in their phenotype may render them new therapeutic targets. In this review, we discuss the role of the Th17 pathway in NAFLD progression to NASH and to liver fibrosis analyzing different animal models of liver injury and human studies. | Carla Melisa Chackelevicius Sabrina Eliana Gambaro Claudio Tiribelli Natalia Rosso | 2016 | World Journal of Gastroenterology2016，22，41： | 10 |
| 15 | Sweroside ameliorates a-naphthylisothiocyanate- induced cholestatic liver injury in mice by regulating bile acids and suppressing pro-inflammatory responses显示文摘瞄准:Sweroside 是有多样的生物活动的 iridoid glycoside。在现在的学习,我们在 α 上调查了 sweroside 的效果; -naphthylisothiocyanate (ANIT ) 在 mice.Methods 导致了 cholestatic 肝损害:老鼠收到了 sweroside (120 mg· kg −1·d−1, ig ) 或积极控制 INT-747 (12 mg· kg −1·d−1, ig ) 为 5 d,和 ANIT (75 mg/kg, ig ) 在 d 上被管理 3。老鼠是 d 上的 euthanized 5,并且浆液生物化学的标记,肝的胆汁酸和组织学的变化被分析。与支持 inflammatory 调停人和胆汁酸新陈代谢有关的基因的肝的表示也被估计。主要鼠标 hepatocytes 暴露于肝的胆汁酸的重新组成的混合物,它显著地在对待 ANIT 的鼠标,和房间生存能力被提高,与支持 inflammatory 调停人有关的基因的表示是 examined.Results:sweroside 或 INT-747 的管理有效地改善了在老鼠的导致 ANIT 的 cholestatic 肝损害由显著地减少的浆液证实了在肝纸巾的生物化学的标记和稀释病理学的变化。而且, sweroside 或 INT-747 的管理显著地减少了单个肝的胆汁酸的导致 ANIT 的举起,例如 β -MCA, CA,和 TCA,它象支持 inflammatory 回答一样与它为胆汁酸合成和运输负责的基因的表示上的效果有关。没有影响房间 viability.Conclusion,有重新组成的胆汁酸混合的老鼠 hepatocytes 的处理导致了重要支持 inflammatory 回答:Sweroside 由恢复胆汁酸合成和运输到他们的正常层次,以及压制支持 inflammatory 回答在老鼠稀释导致 ANIT 的 cholestatic 肝损害。 | Qiao-ling YANG Fan YANG Jun-ting GONG Xiao-wen TANG Guang-yun WANG Zheng-tao WANG Li YANG | 2016 | Acta Pharmacologica Sinica2016，37，9： | 9 |
| 16 | Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases显示文摘Colonic inflammation is required to heal infections, wounds, and maintain tissue homeostasis. As the seventh hallmark of cancer, however, it may affect all phases of tumor development, including tumor initiation, promotion, invasion and metastatic dissemination, and also evasion immune surveillance. Inflammation acts as a cellular stressor and may trigger DNA damage or genetic instability, and, further, chronic inflammation can provoke genetic mutations and epigenetic mechanisms that promote malignant cell transformation. Both sporadical and colitis-associated colorectal carcinogenesis are multi-step, complex processes arising from the uncontrolled proliferation and spreading of malignantly transformed cell clones with the obvious ability to evade the host's protective immunity. In cells upon DNA damage several protooncogenes, including c-MYC are activated in parelell with the inactivation of tumor suppressor genes. The target genes of the c-MYC protein participate in different cellular functions, including cell cycle, survival, protein synthesis, cell adhesion, and microRNA expression. The transcriptional program regulated by c-MYC is context dependent, therefore the final cellular response to elevated c-MYC levels may range from increased proliferation to augmented apoptosis. Considering physiological intestinal homeostasis, c-MYC displays a fundamental role in the regulation of cell proliferation and crypt cell number. However, c-MYC gene is frequently deregulated in inflammation, and overexpressed in both sporadic and colitis-associated colon adenocarcinomas. Recent results demonstrated that endogenous c-MYC is essential for efficient induction of p53-dependent apoptosis following DNA damage, but c-MYC function is also involved in and regulated by autophagy-related mechanisms, while its expression is affected by DNA-methylation, or histone acetylation. Molecules directly targeting c-MYC, or agents acting on other genes involved in the c-MYC pathway could be selected for combined regiments. However, due to its context-dependent cellular function, it is clinically essential to consider which cytotoxic drugs are used in combination with c-MYC targeted agents in various tissues. Increasing our knowledge about MYCdependent pathways might provide direction to novel anti-inflammatory and colorectal cancer therapies. | Ferenc Sipos Gábor Firneisz Györgyi Mũzes | 2016 | World Journal of Gastroenterology2016，22，35： | 9 |
| 17 | High fat diet dysregulates microRNA-17-5p and triggers retinal inflammation:Role of endoplasmic-reticulum-stress显示文摘AIM To elucidate how high diet-induced endoplasmic reticulum-stress upregulates thioredoxin interacting protein expression in Müller cells leading to retinal inflammation. METHODS Male C57Bl/J mice were fed either normal diet or 60% high fat diet for 4-8 wk. During the 4 wk study, mice received phenyl-butyric acid(PBA); endoplasmic reticulum-stress inhibitor; for 2 wk. Insulin resistance was assessed by oral glucose tolerance. Effects of palmitate-bovine serum albumin(BSA)(400 μmol/L) were examined in retinal Müller glial cell line and primary Müller cells isolated from wild type and thioredoxin interacting protein knock-out mice. Expression of thioredoxin interacting protein, endoplasmic reticulum-stress markers, mi R-17-5p m RNA, as well as nucleotide-binding oligomerization domain-like receptor protein(NLRP3) and IL1β protein was determined.RESULTS High fat diet for 8 wk induced obesity and insulin resistance evident by increases in body weight and impaired glucose tolerance. By performing quantitative real-time polymerase chain reaction, we found that high fat diet triggered the expression of retinal endoplasmic reticulum-stress markers(P < 0.05). These effects were associated with increased thioredoxin interacting protein and decreased mi R-17-5p expression, whichwere restored by inhibiting endoplasmic reticulumstress with PBA(P < 0.05). In vitro, palmitate-BSA triggered endoplasmic reticulum-stress markers, which was accompanied with reduced mi R-17-5p and induced thioredoxin interacting protein m RNA in retinal Müller glial cell line(P < 0.05). Palmitate upregulated NLRP3 and IL1β expression in primary Müller cells isolated from wild type. However, using primary Müller cells isolated from thioredoxin interacting protein knock-out mice abolished palmitate-mediated increase in NLRP3 and IL1β.CONCLUSION Our work suggests that targeting endoplasmic reticulumstress or thioredoxin interacting protein are potential therapeutic strategies for early intervention of obesityinduced retinal inflammation. | Maha Coucha Islam N Mohamed Sally L Elshaer Osinakachuk Mbata Megan L Bartasis Azza B El-Remessy | 2017 | World Journal of Diabetes2017，8，2： | 8 |
| 18 | Divergent expression of bacterial wall sensing toll-like receptors 2 and 4 in colorectal cancer显示文摘AIM To characterize the expression of toll-like receptors(TLR) 2 and 4 in colorectal cancer(CRC) and in normal colorectal mucosa.METHODS We analysed tissue samples from a prospective series of 118 unselected surgically treated patients with CRC. Sections from formalin fixed, paraffin embedded specimens were analysed for TLR2 and TLR4 expression by immunohistochemistry. Two independent assessors evaluated separately expression at the normal mucosa, at the invasive front and the bulk of the carcinoma, and in the lymph node metastases when present. Expression levels in different locations were compared and their associations with clinicopathological features including TNM-stage and the grade of the tumour and 5-year follow-up observations were analysed.RESULTS Normal colorectal epithelium showed a gradient of expression of both TLR2 and TLR4 with low levels in the crypt bases and high levels in the surface. In CRC, expression of both TLRs was present in all cases and in the major proportion of tumour cells. Compared to normal epithelium, TLR4 expression was significantly weaker but TLR2 expression stronger in carcinoma cells. Weak TLR4 expression in the invasive front was associated with distant metastases and worse cancerspecific survival at 5 years. In tumours of the proximal colon the cancer-specific survival at 5 years was 36.9% better with strong TLR4 expression as compared with those with weak expression(P = 0.044). In contrast, TLR2 expression levels were not associated with prognosis. Tumour cells in the lymph node metastases showed higher TLR4 expression and lower TLR2 expression than cells in primary tumours.CONCLUSION Tumour cells in CRC show downregulation of TLR4 and upregulation of TLR2. Low expression of TLR4 in the invasive front predicts poor prognosis and metastatic disease. | Karoliina Paarnio Sara Vayrynen Kai Klintrup Pasi Ohtonen Markus J Makinen Jyrki Makela Tuomo J Karttunen | 2017 | World Journal of Gastroenterology2017，23，26： | 8 |
| 19 | Perioperative'remote'acute lung injury:recent update显示文摘Perioperative acute lung injury(ALI) is a syndrome characterised by hypoxia and chest radiograph changes.It is a serious post-operative complication,associated with considerable mortality and morbidity.In addition to mechanical ventilation,remote organ insult could also trigger systemic responses which induce ALI.Currently,there are limited treatment options available beyond conservative respiratory support.However,increasing understanding of the pathophysiology of ALI and the biochemical pathways involved will aid the development of novel treatments and help to improve patient outcome as well as to reduce cost to the health service.In this review we will discuss the epidemiology of peri-operative ALI;the cellular and molecular mechanisms involved on the pathological process;the clinical considerations in preventing and managing perioperative ALI and the potential future treatment options. | Zhaosheng Jin Ka Chun Suen Daqing Ma | 2017 | The Journal of Biomedical Research2017，31，3： | 7 |
| 20 | C-reactive protein and diabetic retinopathy in Chinese patients with type 2 diabetes mellitus显示文摘AIM:To investigate the relationship between Creactive protein(CRP)and diabetic retinopathy(DR)in a cohort of Chinese patients with type 2 diabetes mellitus(T2DM).·METHODS:Community-based observational cohort study.There were 1131 participants recruited from November 2009 to September 2011 in Desheng community in urban Beijing.Patients diagnosed T2DM were recruited and underwent a standardized evaluation consisting of a questionnaire,ocular and anthropometric examinations and laboratory investigation.The presence and severity of DR were assessed by seven fields 30°color fundus photographs.Subjects were then classified into groups with no DR,any DR,or vision-threatening DR.CRP was analyzed from serum of study subjects.·RESULTS:A total of 1007 patients with T2DM were included for analysis,including 408(40.5%)men and 599(59.5%)women.The median CRP level was 1.5 mg/L for women and 1.1 mg/L for men(P=0.004,OR 0.37,95%CI0.18-0.74).After adjusting for possible covariates,higher levels of CRP were associated with lower prevalence of any DR(P=0.02,OR 0.55,95%CI 0.35-0.89),but not associated with vision-threatening DR(P=0.62,OR 0.78,95%CI 0.28-2.14).After stratification by sex,the inverseassociation between CRP and DR was found to be statistically significant in men(P=0.006,OR 0.35,95%CI0.16-0.73),but not in women(P=0.58,OR 0.88,95%CI0.29-1.16).·CONCLUSION:The data drawn from a Chinese population with T2DM suggest that increasing CRP levels may be inversely associated with development of DR. | Xiu-Fen Yang Yu Deng Hong Gu Apiradee Lim Torkel Snellingen Xi-Pu Liu Ning-Li Wang Amitha Domalpally Ronald Danis Ning-Pu Liu | 2016 | International Journal of Ophthalmology(English edition)2016，9，1： | 6 |
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