Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Chungju‑si, Chungbuk 363‑883, Republic of Korea.
Ethnobotanical Society of Nepal (ESON), Central Department of Botany, Tribhuvan University, Kathmandu 44618, Nepal.
Int J Mol Med. 2017 Dec;40(6):1932-1940. doi: 10.3892/ijmm.2017.3178. Epub 2017 Oct 10.
Neem (Azadirachta indica A. Juss.) leaf has been reported to exert anti-inflammatory, antibacterial and antioxidant effects. The purpose of this study was to investigate the protective effects of neem leaf extract (NLE) against cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced pulmonary inflammation. Treatment with NLE significantly attenuated the infiltration of inflammatory cells, such as neutrophils and macrophages in bronchoalveolar lavage fluid (BALF). NLE also reduced the production of reactive oxygen species and the activity of neutrophil elastase in BALF. Moreover, NLE attenuated the release of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 in BALF. NLE inhibited the recruitment of inflammatory cells and the expression of monocyte chemoattractant protein-1 (MCP-1) in the lungs of mice with CS- and LPS-induced pulmonary inflammation. NLE also decreased the expression of inducible nitric oxide synthase (iNOS) in the lungs of the mice CS- and LPS-induced pulmonary inflammation. Furthermore, treatment with NLE significantly attenuated the activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) in the lungs mice exposed to CS and LPS. NLE also inhibited the phosphorylation of nuclear factor (NF)-κB and inhibitor of NF-κB (IκB) in the lungs of mice expose to CS and LPS. These findings thus suggest that NLE has potential for use in the treatment of chronic obstructive pulmonary disease.
印楝(Azadirachta indica A. Juss.)叶已被报道具有抗炎、抗菌和抗氧化作用。本研究旨在探讨印楝叶提取物(NLE)对香烟烟雾(CS)和脂多糖(LPS)诱导的肺部炎症的保护作用。NLE 治疗显著减轻了支气管肺泡灌洗液(BALF)中炎症细胞如中性粒细胞和巨噬细胞的浸润。NLE 还降低了 BALF 中活性氧和中性粒细胞弹性蛋白酶的产生。此外,NLE 减弱了 BALF 中促炎细胞因子如肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的释放。NLE 抑制了 CS 和 LPS 诱导的肺部炎症小鼠肺部炎症细胞的募集和单核细胞趋化蛋白-1(MCP-1)的表达。NLE 还降低了 CS 和 LPS 诱导的肺部炎症小鼠诱导型一氧化氮合酶(iNOS)的表达。此外,NLE 治疗显著减弱了 CS 和 LPS 暴露的小鼠肺部细胞外信号调节激酶(ERK)和 c-Jun N-末端激酶(JNK)的激活。NLE 还抑制了 CS 和 LPS 暴露的小鼠肺部核因子-κB(NF-κB)和 NF-κB 抑制剂(IκB)的磷酸化。这些发现表明 NLE 具有治疗慢性阻塞性肺疾病的潜力。