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- 1. 炎症の病因における白血球内皮細胞接着 leukocyte endothelial adhesion in the pathogenesis of inflammation
- 2. 白血球粘着不全症 leukocyte adhesion deficiency
- 3. Mechanisms of vasoocclusion in sickle cell disease
- 4. 移植免疫 transplantation immunobiology
- 5. 冠動脈疾患における血小板の役割 the role of platelets in coronary heart disease
- Chitosan oligosaccharides downregulate the expression of E-selectin and ICAM-1 induced by LPS in endothelial cells by inhibiting MAP kinase signaling.
- Li Y, Xu Q, Wei P, Cheng L, Peng Q, Li S, Yin H, Du Y.Author information Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, Liaoning, P.R. China.AbstractThe expression of adhesion molecules in endothelial cells elicited by lipopolysaccharide (LPS) is involved in the adhesive interaction between endothelial cells and monocytes in inflammation. In this study, in order to characterize the anti-inflammatory effects of chitosan oligosaccharides (COS) on LPS‑induced inflammation and to elucidate the underlying mechanisms, the mRNA levels of E-selectin and intercellular adhesion molecule-1 (ICAM-1) were measured in porcine iliac artery endothelial cells (PIECs). When these cells were treated with COS, the LPS-induced mRNA expression of E-selectin and ICAM-1 was reduced through the inhibition of the signal transduction cascade, p38 mitogen‑activated protein kinase (MAPK)/extracellular regulated protein kinase 1/2 (ERK1/2) and nuclear factor-κB (NF-κB). Moreover, through the inhibition of p38 MAPK and ERK1/2, COS suppressed the LPS-induced NF-κB p65 translocation. We found that COS suppressed the phosphorylation of p38 MAPK and the translocation of NF-κB p65 into the nucleus in a dose-dependent manner, and inhibited the adhesion of U973 cells to PIECs. Based on these results, it can be concluded that COS downregulate the expression of E-selectin and ICAM-1 by inhibiting the phosphorylation of MAPKs and the activation of NF-κB in LPS-treated PIECs. Our study demonstrates the valuable anti-inflammatory properties of COS.
- International journal of molecular medicine.Int J Mol Med.2014 Feb;33(2):392-400. doi: 10.3892/ijmm.2013.1589. Epub 2013 Dec 13.
- The expression of adhesion molecules in endothelial cells elicited by lipopolysaccharide (LPS) is involved in the adhesive interaction between endothelial cells and monocytes in inflammation. In this study, in order to characterize the anti-inflammatory effects of chitosan oligosaccharides (COS) on
- PMID 24336934
- Carnosol inhibits cell adhesion molecules and chemokine expression by tumor necrosis factor-α in human umbilical vein endothelial cells through the nuclear factor-κB and mitogen-activated protein kinase pathways.
- Yao H1, Chen Y1, Zhang L2, He X1, He X1, Lian L1, Wu X1, Lan P1.Author information 1Department of Colorectal Surgery, The Sixth Affiliated Hospital of Sun Yat-Sen University, Guangdong Gastrointestinal Hospital, Guangzhou, Guangdong 510655, P.R. China.2Laboratory of Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China.AbstractInflammatory bowel diseases (IBD) are gastrointestinal disorders associated with chronic inflammatory processes. Carnosol has been demonstrated to possess anti-inflammatory properties. This study examined the suppressive effect of carnosol on the expression of cell adhesion molecules (CAMs) and chemokines in human umbilical vein endothelial cells (HUVECs) and the possible underlying mechanism. The effect of carnosol on CAM and chemokine expression in HUVECs was identified by western blotting and ELISA, respectively. nuclear factor (NF)-κB activation of HUVECs was analyzed using the TransAM NF-κB Family kit. The effect of carnosol on the tumor necrosis factor (TNF)-α-induced activation of the NF-κB and mitogen-activated protein kinase (MAPK) pathways, and was subsequently analyzed using western blotting. Carnosol not only inhibited TNF-α-induced protein expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 and E-selectin in HUVECs, but also suppressed interleukin (IL)-8 and monocyte chemoattractant protein (MCP)-1 expression. In addition, carnosol inhibited the TNF-α-induced phosphorylation of p-65 and IκB-α, as well as the activation of NF-κB. The same result was observed in TNF-α-stimulated phosphorylation of ERK1/2 and p-38. It was demonstrated that carnosol inhibited TNF-α-induced CAM and chemokine expression in HUVECs. The underlying mechanism may be associated with the blocking of the NF-κB and MAPK pathways. These results indicate that carnosol may be a novel therapeutic agent for targeting endothelial cells in IBDs.
- Molecular medicine reports.Mol Med Rep.2014 Feb;9(2):476-80. doi: 10.3892/mmr.2013.1839. Epub 2013 Dec 3.
- Inflammatory bowel diseases (IBD) are gastrointestinal disorders associated with chronic inflammatory processes. Carnosol has been demonstrated to possess anti-inflammatory properties. This study examined the suppressive effect of carnosol on the expression of cell adhesion molecules (CAMs) and chem
- PMID 24316968
- Isoflurane on brain inflammation.
- Altay O1, Suzuki H1, Hasegawa Y1, Ostrowski RP1, Tang J1, Zhang JH2.Author information 1Department of Physiology, Loma Linda University School of Medicine, Loma Linda, USA.2Department of Physiology, Loma Linda University School of Medicine, Loma Linda, USA; Department of Neurosurgery, Loma Linda University School of Medicine, Loma Linda, USA. Electronic address: firstname.lastname@example.org.AbstractBrain inflammation may play an important role in the pathophysiology of early brain injury after subarachnoid hemorrhage (SAH). Our aim was to demonstrate brain inflammation development and to determine whether isoflurane, a clinically available volatile anesthetic agent, prevents brain inflammation after SAH. This study used 162 8-week-old male CD-1 mice. We induced SAH with endovascular perforation in mice and randomly assigned animals to sham-operated (n=21), SAH+vehicle-air (n=35) and SAH+2% isoflurane (n=31). In addition to the evaluation of brain injury (neurological scores, brain edema and Evans blue dye extravasation), brain inflammation was evaluated by means of expression changes in markers of inflammatory cells (ionized calcium binding adaptor molecule-1, myeloperoxidase), cytokines (tumor necrosis factor [TNF]-α, interleukin-1β), adhesion molecules (intercellular adhesion molecule [ICAM]-1, P-selectin), inducers of inflammation (cyclooxygenase-2, phosphorylated c-Jun N-terminal kinase [p-JNK]) and endothelial cell activation (von Willebrand factor) at 24h post-SAH. Sphingosine kinase inhibitor (N, N-dimethylsphingosine [DMS]) and sphingosine-1-phosphate receptor-1/3 antagonist (VPC23019) were used to block isoflurane's effects (n=22, each). SAH caused early brain injury, which was associated with inflammation so that all evaluated markers of inflammation were increased. Isoflurane significantly inhibited both brain injury (P<0.001, respectively) and inflammation (myeloperoxidase, P=0.022; interleukin-1β, P=0.002; TNF-α, P=0.015; P-selectin, P=0.010; ICAM-1, P=0.016; p-JNK, P<0.001; cyclooxygenase-2, P=0.003, respectively). This beneficial effect of isoflurane was abolished with DMS and VPC23019. Isoflurane may suppress post-SAH brain inflammation possibly via the sphingosine-related pathway.
- Neurobiology of disease.Neurobiol Dis.2014 Feb;62:365-71. doi: 10.1016/j.nbd.2013.09.016. Epub 2013 Sep 29.
- Brain inflammation may play an important role in the pathophysiology of early brain injury after subarachnoid hemorrhage (SAH). Our aim was to demonstrate brain inflammation development and to determine whether isoflurane, a clinically available volatile anesthetic agent, prevents brain inflammation
- PMID 24084689
- Serum Adhesion Molecule Levels as Prognostic Markers in Patients with Early Systemic Sclerosis: A Multicentre, Prospective, Observational Study
- Hasegawa Minoru,Asano Yoshihide,Endo Hirahito,Fujimoto Manabu,Goto Daisuke,Ihn Hironobu,Inoue Katsumi,Ishikawa Osamu,Kawaguchi Yasushi,Kuwana Masataka,Ogawa Fumihide,Takahashi Hiroki,Tanaka Sumiaki,Sato Shinichi,Takehara Kazuhiko
- PLoS ONE 9(2), e88150, 2014-02-06
- … Concentrations of intercellular adhesion molecule (ICAM) -1, E-selectin, L-selectin, and P-selectin in serum samples from all patients were measured by enzyme-linked immunosorbent asssay (ELISA). … Results: At their first visit, serum levels of ICAM-1, E-selection, P-selectin were significantly elevated and serum L-selectin levels were significantly reduced in patients with SSc compared with healthy controls. …
- NAID 120005457100
- Exacerbation of Intracranial Aneurysm and Aortic Dissection in Hypertensive Rat Treated With the Prostaglandin F–Receptor Antagonist AS604872
- Fukuda Miyuki,Aoki Tomohiro,Manabe Toshiaki,Maekawa Akiko,Shirakawa Takayuki,Kataoka Hiroharu,Takagi Yasushi,Miyamoto Susumu,Narumiya Shuh
- Journal of Pharmacological Sciences, 2014
- … Notably, AS604872 induced expression of pro-inflammatory genes such as E-selectin in lesions and significantly enhanced macrophage infiltration. … Suppression of surface expression of E-selectin with cimetidine prevented macrophage infiltration and aortic dissection. …
- NAID 130004700281
- Effects of Eicosapentaenoic Acid on Platelet Function in Patients Taking Long-Term Aspirin Following Coronary Stent Implantation
- Takada Kaoru,Ishikawa Shuichi,Yokoyama Naoyuki,Hosogoe Naoyoshi,Isshiki Takaaki
- International Heart Journal 55(3), 228-233, 2014
- … Furthermore, no significant differences were observed in the expression of PAC-1 and CD62P on the platelet surface membranes or in the soluble P-selectin concentration. …
- NAID 130004449394
- Selectins (cluster of differentiation 62 or CD62) are a family of cell adhesion molecules (or CAMs). All selectins are single-chain transmembrane glycoproteins that share similar properties to C-type lectins due to a related amino terminus and ...
- 白血球（単球、好中球）は、表面に、セレクチン（穴）と結合するセレクチンリガンド（鍵） として、糖鎖（シアリルLe抗原など）を有している。白血球は、この糖鎖リガンド（鍵)により 、セレクチン（穴）を発現した血管内皮細胞と接触し、血管の表面を転がるようになる（ ...