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L-Menthol alleviates cigarette smoke extract induced lung injury in rats by inhibiting oxidative stress and inflammation via nuclear factor kappa B, p38 MAPK and Nrf2 signalling pathways

机译:L-MENTOL通过核因子Kappa B,P38 MAPK和NRF2信号传导途径抑制氧化应激和炎症,减轻香烟烟雾诱导大鼠肺损伤

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摘要

L-Menthol is the main ingredient of peppermint which affects various pharmacological effects such as anti-inflammation and anti-oxidative activity. In this study, we aimed to evaluate the potential effects of L-menthol on cigarette smoke extract (CSE) induced lung injury in rats. Morphology assessment results revealed that administration with L-menthol (5, 10 or 20 mg kg(-1) d(-1)) significantly alleviated CSE-induced lung injury. Besides, L-menthol significantly reduced the inflammatory response by suppressing the production of tumor necrosis factor-alpha (TNE-alpha), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) via downregulating nuclear factor kappa B (NF-kappa B) and p38 MAPK pathways. Meanwhile, L-menthol decreased the levels of oxidative stress markers including malondialdehyde (MDA) and myeloperoxidase (MPO) whereas it increased the amount of glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) through activation of the Nrf2 pathway. Furthermore, the expression of MMP-9 and TIMP-1 in lungs was reduced after treatment with L-menthol, and this indicated that L-menthol might have a potential effect on airway remodeling. Moreover, immunohistochemistry analyses indicated that L-menthol could suppress the infiltration of CD4(+) and CD8(+ )T cells in lung tissues and this was probably due to the immune regulation activity of L-menthol. Taken together, our findings support that L-menthol might be a potential candidate for the treatment of CSE-induced lung injury in rats.
机译:L-Menthol是薄荷的主要成分,影响各种药理作用,如抗炎和抗氧化活性。在这项研究中,我们旨在评估L-Menthol对卷烟烟雾提取物(CSE)诱导的大鼠肺损伤的潜在影响。形态学评估结果表明,用L-薄荷醇(5,10或20mg kg(-1)d(-1))给药显着缓解CSE诱导的肺损伤。此外,L-MENTHOL通过下调核因子Kappa抑制肿瘤坏死因子-α(TNE-α),白细胞介素-1β(IL-6)和白细胞介素-1-6(IL-6)显着降低炎症反应B(NF-KAPPA B)和P38 MAPK途径。同时,L-薄荷醇降低了氧化醛(MDA)和髓氧化酶(MPO)的氧化应激标记物的水平,而它增加了谷胱甘肽(GSH),谷胱甘肽过氧化物酶(GSH-PX),超氧化物歧化酶(SOD)和总抗氧化能力的量(T-AOC)通过激活NRF2途径。此外,用L-Menthol处理后,减少了MMP-9和肺部中的TIMP-1的表达,这表明L-薄荷醇对气道重塑具有潜在影响。此外,免疫组织化学分析表明,L-薄荷醇可以抑制肺组织中CD4(+)和CD8(+)T细胞的渗透,这可能是由于L-薄荷醇的免疫调节活性。我们的研究结果支持,L-Menthol可能是治疗大鼠CSE肺肺损伤的潜在候选者。

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  • 来源
    《RSC Advances》 |2018年第17期|共11页
  • 作者单位

    Shandong Univ Sch Pharmaceut Sci 44 West Wenhua Rd Jinan 250012 Shandong Peoples R China;

    Shandong Univ Sch Pharmaceut Sci 44 West Wenhua Rd Jinan 250012 Shandong Peoples R China;

    Shandong Univ Sch Pharmaceut Sci 44 West Wenhua Rd Jinan 250012 Shandong Peoples R China;

    Shandong Univ Qilu Hosp Dept Clin Pharm 107 West Wenhua Rd Jinan 250012 Shandong Peoples R China;

    Shandong Univ Sch Pharmaceut Sci 44 West Wenhua Rd Jinan 250012 Shandong Peoples R China;

    Shandong Univ Sch Pharmaceut Sci 44 West Wenhua Rd Jinan 250012 Shandong Peoples R China;

    Shandong Univ Sch Pharmaceut Sci 44 West Wenhua Rd Jinan 250012 Shandong Peoples R China;

    Shandong Univ Sch Pharmaceut Sci 44 West Wenhua Rd Jinan 250012 Shandong Peoples R China;

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  • 中图分类 化学;
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