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- 주제어 : Acute inflammatory lung injury (검색결과 5 건)
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Effects of Omega-3 Fatty Acid on Endotoxin-induced Acute Lung Injury in Rabbits
Eun-A Jang,Sung-Kuk Son,Jeong-Hyeon Kang,Seongheon Lee,Sang-Hyun Kwak 대한의생명과학회 2021 Biomedical Science Letters Vol.27 No.1
This study was undertaken to clarify the effects of omega-3 fatty acid on endotoxin-induced acute lung injury. Rabbits were randomly assigned to one of four groups. Each group received intravenous infusion of saline only, saline and Escherichia coli endotoxin, omegaven infuison (0.5 mL/kg/hr) and endotoxin, lipoven (0.5 mL/kg/hr) and endotoxin respectively. Infusion of saline was started 0.5 hr before the infusion of saline or endotoxin, and omegaven and lipoven were started 2 hours after endotoxin infusion for 4 hours. The lungs of rabbits were ventilated with 40% oxygen. Mean blood pressure, heart rate, arterial oxygen tension (PaO₂), and peripheral blood leukocyte were recorded. The wet/dry (W/D) weight ratio of lung and lung injury score were measured, and analysis of bronchoalveolar lavage fluid (BALF) was done. Endotoxin decreased PaO₂, and peripheral blood leukocyte and platelet count. And it increased W/D ratio of lung, lung injury score and leukocyte count, percentage of PMN cells, concentration of IL-8 in BALF. Omegaven attenuated all these changes except for peripheral blood leukocyte counts. Omegaven attenuated endotoxin-induced acute lung injury in rabbits mainly by inhibiting neutrophil and IL-8 responses, which may play a central role in endotoxin-related lung injury.
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Jihee Lee 대한생리학회-대한약리학회 1998 The Korean Journal of Physiology & Pharmacology Vol.2 No.2
<P> Stimulated alveolar macrophages and neutrophils produce nitric oxide, a free radical by an inducible nitric oxide synthase(iNOS), which reacts with superoxide anion to form peroxynitrite, a more highly reactive toxic species. The objectives of the present study were to evaluate acute inflammatory lung injury and to determine iNOS mRNA induction and nitric oxide production by rat broncho-alveolar lavage cells following intratracheal treatment of silica. After 4 h exposure to silica, differential counts of broncho- alveolar lavage cells and lactate dehydrogenase(LDH) activity as well as total protein in the broncho-alveolar lavage fluid were determined. Broncho-alveolar lavage cells were also assayed for iNOS mRNA and the productions of nitrite and nitrate measured in the cells cultured. Differential analysis of broncho-alveolar lavage cells showed that the number of alveolar macrophages slightly decreased following silica treatment; however, red blood cells, lymphocytes, and neutrophils significantly were increased by 9-, 14-, and 119-fold following silica treatment, respectively, compared with the saline control. It was also found significant increases in the LDH activity and total protein in the lavage fluid obtained from silica-treated rats, indicating silica-induced acute lung injury. Northern blot analysis demonstrated that the steady state levels of iNOS mRNA in broncho-alveolar lavage cells were increased following silica treatment. The productions of nitrite and nitrate in the cultured cells were significantly increased by 2-fold following silica treatment, respectively, which were attenuated by the NOS inhibitor Nω-nitro-L-arginine-methyl ester(L-NAME) and partially reversed by<SUB> </SUB>L-arginine. These findings suggest that nitric oxide production in alveolar macrophages and recruited neutrophils is increased in response to silica. Nitric oxide may contribute in part to acute inflammatory lung injury.
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Hong-bo Zhang,Li-chao Sun,Li-da Zhi,Qian-kuan Wen,Zhi-wei Qi,Sheng-tao Yan,Wen Li,Guo-qiang Zhang 대한약학회 2017 Archives of Pharmacal Research Vol.40 No.10
Sepsis is a systemic inflammatory responsesyndrome caused by severe infections. Astilbin is a dihydroflavonolderivative found in many medicinal and foodplants with multiple pharmacological functions. To investigatethe effects of astilbin on sepsis-induced acute lunginjury (ALI), cecal ligation and puncture was performed onrats to establish a sepsis-induced ALI model; these ratswere then treated with astilbin at different concentrations. Lung injury scores, including lung wet/dry ratio, proteinleakage, myeloperoxidase activity, and inflammatory cellinfiltration were determined to evaluate the effects ofastilbin on sepsis-induced ALI. We found that astilbintreatment significantly attenuates sepsis-induced lunginjury and improves survival rate, lung injury scores, lungwet/dry ratio, protein leakage, myeloperoxidase activity,and inflammatory cell infiltration. Astilbin treatment alsodramatically decreased the production of inflammatorycytokines and chemokines in bronchoalveolar lavage fluid. Further, astilbin treatment inhibited the expression andproduction of macrophage inhibitory factor (MIF), whichinhibits the inflammatory response. Collectively, these datasuggest that astilbin has a protective effect against sepsisinducedALI by inhibiting MIF-mediated inflammatoryresponses. This study provides a molecular basis for astilbinas a new medical treatment for sepsis-induced ALI.
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박지원,류형원,안혜인,민재홍,김승만,김민구,권옥경,황다슬,김수용,최상호,Zamora Nelson,Rosales Kattia,오세량,이재원,안경섭 한국미생물·생명공학회 2020 Journal of microbiology and biotechnology Vol.30 No.11
A number of species of the genus Trichilia (Meliaceae) exhibit anti-inflammatory effects. However, the effect of Trichilia martiana C. DC. (TM) on lipopolysaccharide (LPS)-induced inflammation has not, to the best of our knowledge, yet been determined. Therefore, in the present study, the antiinflammatory effect of TM on LPS-stimulated RAW264.7 macrophages was evaluated. The ethanol extract of TM (TMEE) significantly inhibited LPS-induced nitric oxide (NO), prostaglandin 2 (PGE2), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). TMEE also reduced the levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β and IL- 6. The upregulation of mitogen-activated protein kinases (MAPKs) and NF-κB activation was revealed to be downregulated following TMEE pretreatment. Furthermore, TMEE was indicated to lead to the nucleus translocation of nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and the expression of heme oxygenase-1 (HO-1). In H292 airway epithelial cells, the pretreatment of TMEE significantly downregulated the production of LPS-stimulated IL-1β, and TMEE was indicated to increase the expression of HO-1. In animal models exhibiting LPS-induced acute lung injury (ALI), treatment with TMEE reduced the levels of macrophages influx and TNF-α production in the bronchoalveolar lavage fluid (BALF) of ALI mice. Additionally, TMEE significantly downregulated the activation of ERK, JNK and IκB, and upregulated the expression of HO-1 in the lungs of ALI mice. In conclusion, the results of the current study demonstrated that TMEE could exert a regulatory role in the prevention or treatment of the endotoxin-mediated inflammatory response.
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