Acute lung injury (ALI) is a severe inflammatory disorder that causes respiratory failure. Cases of ALI are reported with increasing mortality rates each year. In this study, we investigated the anti-inflammatory role of tomentosin and its fundamental mechanisms against lipopolysaccharide (LPS)-induced ALI via the suppression of Toll-like receptor (TLR4)/nuclear factor-kappa beta (NF-κB) pathway in a mouse model of sepsis. ALI was induced to BALB/c mice through the administration of 10 μg of LPS concomitantly with tomentosin (20 and 25 mg/kg) treatment. Dexamethasone was used as a standard drug. Inflammatory cells were measured using a hemocytometer; myeloperoxidase (MPO) enzyme activity and pro-inflammatory cytokines were determined using commercial kits. The lung tissues of animals were examined histologically. The expression level of TLR4/NF-κB signaling molecules were analyzed by Western blotting. Tomentosin treatment decreased lung edema and reduced the levels of macrophages, lymphocytes, and neutrophils in the bronchoalveolar lavage fluid. Tomentosin also suppressed the status of pro-inflammatory markers and reduced the activation of iNOS, MPO, COX-2, and PGE2 in the lung. Tomentosin appreciably down-regulated the NF-κB/TLR4 signaling pathway in sepsis mice. Histological study also showed the protective effects of tomentosin. These findings show that tomentosin protects the LPS-induced ALI via suppression of TLR4/NF-κB signaling pathway in sepsis mice. Tomentosin could be a promising therapeutic agent to treat sepsis.

中文翻译：

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绒毛膜素抑制脓毒症小鼠模型中脂多糖诱导的急性肺损伤和炎性反应，通过抑制NF-κB途径。

急性肺损伤（ALI）是导致呼吸衰竭的严重炎症性疾病。据报道，每年ALI病例的死亡率都在增加。在这项研究中，我们通过抑制Toll样受体（TLR4）/核因子-κB（NF-κB）途径研究了tomentosin的抗炎作用及其针对脂多糖（LPS）诱导的ALI的基本机制。败血症的小鼠模型。通过同时给予10μgLPS和tomentosin（20和25 mg / kg）处理，可以诱导BALB / c小鼠ALI。地塞米松被用作标准药物。使用血细胞计数器测量炎症细胞；使用商业试剂盒确定了髓过氧化物酶（MPO）酶的活性和促炎细胞因子。组织学检查动物的肺组织。通过Western印迹分析TLR4 /NF-κB信号分子的表达水平。绒毛膜球蛋白治疗可减少肺水肿，并降低支气管肺泡灌洗液中巨噬细胞，淋巴细胞和中性粒细胞的水平。tomentosin还抑制了炎症标记物的状态，并降低了肺中iNOS，MPO，COX-2和PGE2的活化。绒毛膜蛋白可明显降低脓毒症小鼠的NF-κB/ TLR4信号通路。组织学研究还显示了绒毛膜毒素的保护作用。这些发现表明，tomentosin通过抑制败血症小鼠中的TLR4 /NF-κB信号通路来保护LPS诱导的ALI。绒毛膜球蛋白可能是治疗脓毒症的有前途的治疗剂。支气管肺泡灌洗液中的淋巴细胞和中性粒细胞。tomentosin还抑制了炎症标记物的状态，并降低了肺中iNOS，MPO，COX-2和PGE2的活化。绒毛膜蛋白可明显降低脓毒症小鼠的NF-κB/ TLR4信号通路。组织学研究还显示了绒毛膜毒素的保护作用。这些发现表明，tomentosin通过抑制败血症小鼠中的TLR4 /NF-κB信号通路来保护LPS诱导的ALI。绒毛膜球蛋白可能是治疗脓毒症的有前途的治疗剂。支气管肺泡灌洗液中的淋巴细胞和中性粒细胞。tomentosin还抑制了炎症标记物的状态，并降低了肺中iNOS，MPO，COX-2和PGE2的活化。绒毛膜蛋白可明显降低脓毒症小鼠的NF-κB/ TLR4信号通路。组织学研究还显示了绒毛膜毒素的保护作用。这些发现表明，tomentosin通过抑制败血症小鼠中的TLR4 /NF-κB信号通路来保护LPS诱导的ALI。绒毛膜球蛋白可能是治疗脓毒症的有前途的治疗剂。组织学研究还显示了绒毛膜毒素的保护作用。这些发现表明，tomentosin通过抑制败血症小鼠中的TLR4 /NF-κB信号通路来保护LPS诱导的ALI。绒毛膜球蛋白可能是治疗脓毒症的有前途的治疗剂。组织学研究还显示了绒毛膜毒素的保护作用。这些发现表明，tomentosin通过抑制败血症小鼠中的TLR4 /NF-κB信号通路来保护LPS诱导的ALI。绒毛膜球蛋白可能是治疗脓毒症的有前途的治疗剂。