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半夏凝集素通过诱导促炎细胞因子的释放、核因子-κB信号通路的激活以及活性氧的过量产生,对巨噬细胞发挥促炎作用。

Pinellia ternata lectin exerts a pro-inflammatory effect on macrophages by inducing the release of pro-inflammatory cytokines, the activation of the nuclear factor-κB signaling pathway and the overproduction of reactive oxygen species.

作者信息

Yu Hong-Li, Zhao Teng-Fei, Wu Hao, Pan Yao-Zong, Zhang Qian, Wang Kui-Long, Zhang Chen-Chao, Jin Yang-Ping

机构信息

School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China.

出版信息

Int J Mol Med. 2015 Oct;36(4):1127-35. doi: 10.3892/ijmm.2015.2315. Epub 2015 Aug 19.

DOI:10.3892/ijmm.2015.2315
PMID:26310942
Abstract

Pinellia ternata (PT) is a widely used traditional Chinese medicine. The raw material has a throat-irritating toxicity that is associated with the PT lectin (PTL). PTL is a monocot lectin isolated from the tubers of PT, which exhibits mouse peritoneal acute inflammatory effects in vivo. The present study aimed to investigate the pro-inflammatory effect of PTL on macrophages. PTL (50 µg/ml)‑stimulated macrophages enhanced the chemotactic activity of neutrophils. PTL (50, 100, 200 and 400 µg/ml) significantly elevated the production of cytokines [tumor necrosis factor‑α (TNF-α) , interleukin (IL)‑1β and IL‑6]. PTL (25, 50 and 100 µg/ml) induced intracellular reactive oxygen species (ROS) overproduction. PTL also caused transfer of p65 from the macrophage cytoplasm to the nucleus and activated the nuclear factor‑κB (NF‑κB) signaling pathway. Scanning electron microscope images revealed severe cell swelling and membrane integrity defection of macrophages following PTL (100 µg/ml) stimulation, which was also associated with inflammation. PTL had pro‑inflammatory activity, involving induced neutrophil migration, cytokine release, ROS overproduction and the activation of the NF-κB signaling pathway, which was associated with the activation of macrophages.

摘要

半夏是一种广泛应用的传统中药。其原材料具有咽喉刺激性毒性,这与半夏凝集素(PTL)有关。PTL是一种从半夏块茎中分离出的单子叶植物凝集素,在体内表现出对小鼠腹膜的急性炎症作用。本研究旨在探讨PTL对巨噬细胞的促炎作用。PTL(50µg/ml)刺激的巨噬细胞增强了中性粒细胞的趋化活性。PTL(50、100、200和400µg/ml)显著提高了细胞因子[肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-1β和IL-6]的产生。PTL(25、50和100µg/ml)诱导细胞内活性氧(ROS)过量产生。PTL还导致p65从巨噬细胞胞质转移至细胞核,并激活核因子-κB(NF-κB)信号通路。扫描电子显微镜图像显示,PTL(100µg/ml)刺激后巨噬细胞出现严重的细胞肿胀和膜完整性缺陷,这也与炎症相关。PTL具有促炎活性,包括诱导中性粒细胞迁移、细胞因子释放、ROS过量产生以及NF-κB信号通路的激活,这与巨噬细胞的活化有关。

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