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首页> 外文期刊>Cytokine >Endogenous hydrogen sulfide reduces airway inflammation and remodeling in a rat model of asthma.
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Endogenous hydrogen sulfide reduces airway inflammation and remodeling in a rat model of asthma.

机译:内源性硫化氢可减轻哮喘大鼠模型的气道炎症和重塑。

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Endogenous hydrogen sulfide (H(2)S) is hypothesized to have an important role in systemic inflammation. We investigated if endogenous H(2)S may be a crucial mediator in airway inflammation and airway remodeling in a rat model of asthma and if endogenous H(2)S may exert its anti-inflammatory effect by inhibiting inducible nitric oxide synthase (iNOS)/NO pathway. Cystathionine-gamma-lyase (CSE; a H(2)S-synthesizing enzyme) was mainly expressed in airway and vascular smooth muscle cells in rat lung tissue. Levels of endogenous H(2)S was decreased in pulmonary tissue in ovalbumin (OVA)-treated rats. Exogenous administration of NaHS alleviated airway inflammation and airway remodeling: peak expiratory flow (PEF) increased, goblet cell hyperplasia and collagen deposition score decreased, with decreased total cells recovered from bronchoalveolar fluid (BALF) and influx of eosinophils and neutrophils. The H(2)S levels of serum and lung tissue were positively correlated with PEF and negatively correlated with the level of eosinophils and neutrophils in BALF, score of lung pathology. NaHS treatment significantly attenuated pulmonary iNOS activation in OVA-treated rats. These results suggest that the CSE/H(2)S pathway plays an anti-inflammatory and anti-remodeling part in asthma pathogenesis and could be a novel target in prevention and treatment of asthma.
机译:内源性硫化氢(H(2)S)被认为在全身性炎症中具有重要作用。我们调查了内源性H(2)S是否可能是哮喘大鼠模型中气道炎症和气道重塑的关键介质,以及内源性H(2)S是否可能通过抑制诱导型一氧化氮合酶(iNOS)发挥其抗炎作用。 / NO途径。胱硫醚-γ-裂解酶(CSE;一种H(2)S合成酶)主要在大鼠肺组织的气道和血管平滑肌细胞中表达。卵清蛋白(OVA)治疗的大鼠肺组织中内源性H(2)S的水平降低。外用NaHS缓解气道炎症和气道重塑:呼气峰值流量(PEF)增加,杯状细胞增生和胶原蛋白沉积评分降低,从支气管肺泡液(BALF)中回收的总细胞减少,嗜酸性粒细胞和嗜中性粒细胞大量涌入。血清和肺组织的H(2)S水平与PEF正相关,而与BALF(肺病理评分)中的嗜酸性粒细胞和中性粒细胞水平呈负相关。 NaHS处理可显着减弱OVA处理的大鼠的肺iNOS激活。这些结果表明,CSE / H(2)S途径在哮喘发病机理中起抗炎和抗重塑作用,并且可能成为预防和治疗哮喘的新靶标。

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