Jeon Chan-Mi, Shin In-Sik, Shin Na-Rae, Hong Ju-Mi, Kwon Ok-Kyoung, Kim Jung-Hee, Oh Sei-Ryang, Bach Tran-The, Hai Do-Van, Quang Bui-Hong, Choi Sang-Ho, Lee Joongku, Myung Pyung-Keun, Ahn Kyung-Seop
Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongwon‑gu, Cheongju‑si, Chungcheongbuk‑do 28116, Republic of Korea.
IEBR, Vietnam Academy of Science and Technology (VAST), Cay Giay, Ha Noi, Vietnam.
Int J Mol Med. 2016 Apr;37(4):1091-8. doi: 10.3892/ijmm.2016.2515. Epub 2016 Mar 3.
Clausena anisata (Willd.) Hook.f. ex Benth. (CA), which is widely used in traditional medicine, reportedly exerts antitumor, anti-inflammatory and other important therapeutic effects. The aim of the present study was to investigate the potential therapeutic effects of CA in a mouse model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) and in LPS-stimulated RAW 264.7 cells. Male C57BL/6 mice were administered treatments for 3 days by oral gavage. On day 3, the mice were instilled intranasally with LPS or PBS followed 3 h later by oral CA (30 mg/kg) or vehicle administration. In vitro, CA decreased nitric oxide (NO) production and pro-inflammatory cytokines, such as interleukin (IL)-6 and prostaglandin E2 (PGE2), in LPS-stimulated RAW 264.7 cells. CA also reduced the expression of pro-inflammatory mediators, such as cyclooxygenase-2. In vivo, CA administration significantly reduced inflammatory cell numbers in the bronchoalveolar lavage fluid (BALF) and suppressed pro-inflammatory cytokine levels, including tumor necrosis factor-α (TNF-α), IL-6, and IL-1β, as well as reactive oxygen species production in the BALF. CA also effectively reduced airway inflammation in mouse lung tissue of an LPS-induced ALI mouse model, in addition to decreasing inhibitor κB (IκB) and nuclear factor-κB (NF-κB) p65 phosphorylation. Taken together, the findings demonstrated that CA inhibited inflammatory responses in a mouse model of LPS-induced ALI and in LPS-stimulated RAW 264.7 cells. Thus, CA is a potential candidate for development as an adjunctive treatment for inflammatory disorders, such as ALI.
臭节草（Clausena anisata (Willd.) Hook.f. ex Benth.，简称CA）在传统医学中广泛应用，据报道具有抗肿瘤、抗炎等重要治疗作用。本研究旨在探讨CA对脂多糖（LPS）诱导的急性肺损伤（ALI）小鼠模型以及LPS刺激的RAW 264.7细胞的潜在治疗作用。雄性C57BL/6小鼠通过灌胃给药3天。在第3天，经鼻向小鼠滴注LPS或PBS，3小时后口服CA（30 mg/kg）或给予赋形剂。在体外，CA可降低LPS刺激的RAW 264.7细胞中一氧化氮（NO）的产生以及白细胞介素（IL）-6和前列腺素E2（PGE2）等促炎细胞因子的水平。CA还降低了环氧合酶-2等促炎介质的表达。在体内，给予CA可显著减少支气管肺泡灌洗液（BALF）中的炎性细胞数量，并抑制促炎细胞因子水平，包括肿瘤坏死因子-α（TNF-α）、IL-6和IL-1β，以及BALF中活性氧的产生。此外，CA还能有效减轻LPS诱导的ALI小鼠模型肺组织中的气道炎症，同时降低抑制因子κB（IκB）和核因子-κB（NF-κB）p65的磷酸化水平。综上所述，这些研究结果表明，CA可抑制LPS诱导AL小鼠模型和LPS刺激的RAW 264.7细胞中的炎症反应。因此，CA有潜力作为ALI等炎症性疾病辅助治疗药物进行开发。
