首页> 外文期刊>Journal of Agricultural and Food Chemistry >Methanol Extract of Antrodia camphorata Protects against Lipopolysaccharide-lnduced Acute Lung Injury by Suppressing NF-kB and MARK Pathways in Mice
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Methanol Extract of Antrodia camphorata Protects against Lipopolysaccharide-lnduced Acute Lung Injury by Suppressing NF-kB and MARK Pathways in Mice

机译:樟芝的甲醇提取物通过抑制小鼠中的NF-kB和MARK途径来保护脂多糖诱导的急性肺损伤

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Antrodia camphorata (AC) has been used as a herbal medicine for drug intoxication for the treatment of inflammation syndromes and liver-related diseases in Taiwan. This study demonstrates the protective effect of the methanol extract of AC (MAC) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Mice were treated with MAC 1 h before the intratracheal (I.T.) instillation of LPS challenge model. Lung injury was evaluated 6 h after LPS induction. Pretreatment with MAC markedly improved LPS-induced histological alterations and edema in lung tissues. Moreover, MAC also inhibited the release of pro-inflammatory mediators such as nitric oxide (NO), tumor necrosis factor alpha (TNF-a), interleukin-1 beta (IL-1β), and IL-6 at 6 h in the bronchoalveolar lavage fluid (BALF) during LPS-induced lung injury. Furthermore, MAC reduced total cell number and protein concentrations in the BALF the pulmonary wet/dry weight (W/D) ratio, and myeloperoxidase activity and enhanced superoxide dismutase (SOD) activity in lung tissues. MAC also efficiently blocked protein expression of inducible nitric oxide synthase (1NOS), cyclooxygenase-2 (COX-2), and phosphorylation of mitogen-activated protein kinases (MAPKs) and inhibited the degradation of nuclear factor-kappa B (NF-kB) and MBa. This is the first investigation in which MAC inhibited acute lung edema effectively, which may provide a potential target for treating ALI. MAC may utilize the NF-kB and MAPKs pathways and the regulation of SOD activity to attenuate LPS-induced nonspecific pulmonary inflammation.
机译:樟脑牛樟芝(AC)在台湾已被用作药物中毒的草药,用于治疗炎症综合症和肝脏相关疾病。这项研究证明了AC(MAC)的甲醇提取物对脂多糖(LPS)诱导的小鼠急性肺损伤(ALI)的保护作用。在气管内(I.T.)注入LPS攻击模型前1小时,用MAC处理小鼠。 LPS诱导后6小时评估肺损伤。 MAC预处理显着改善LPS诱导的肺组织组织学改变和水肿。此外,MAC还抑制支气管肺泡中的促炎性介质(例如一氧化氮(NO),肿瘤坏死因子α(TNF-a),白细胞介素-1β(IL-1β)和IL-6)的释放。 LPS诱导的肺损伤期间灌洗液(BALF)。此外,MAC降低了BALF中的总细胞数和蛋白质浓度,降低了肺湿重/干重(W / D)比,并降低了肺组织中的髓过氧化物酶活性和超氧化物歧化酶(SOD)活性。 MAC还可以有效地阻断诱导型一氧化氮合酶(1NOS),环氧合酶2(COX-2)的蛋白表达以及丝裂原激活的蛋白激酶(MAPK)的磷酸化,并抑制核因子-κB(NF-kB)的降解。和MBa。这是MAC有效抑制急性肺水肿的首次研究,这可能为治疗ALI提供潜在的靶标。 MAC可利用NF-kB和MAPKs途径以及对SOD活性的调节来减轻LPS诱导的非特异性肺部炎症。

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