Study on anti-inflammatory mechanism of dendrocandin U from Dendrobium huoshanense

Journal Information

J. Hefei Univ. Tech. (Nat. Sci.), Feb.2026, Vol.49 No.2: 214-219

DOI: 10.3969/j.issn.1003-5060.2026.02.011

Authors

ZHANG Yangqiaoqiao $ ^{1} $, JIANG Hui $ ^{1} $, ZHANG Fengyun $ ^{2} $, LI Qiangming $ ^{1} $, LUO Jianping $ ^{1} $

(1. School of Food and Biological Engineering, Hefei University of Technology, Hefei 230601, China; 2. School of Basic Medical Sciences, Anhui Medical University, Hefei 230032, China)

Abstract and Keywords

Abstract: To study the anti-inflammatory mechanism of dendrocandin U from $ Dendrobium\ huoshanense $, a model of LPS-induced inflammation in RAW264.7 cells was established. The release of NO was detected by Griess method, the mRNA expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor $ \alpha $ (TNF- $ \alpha $) and interleukin-1 $ \beta $ (IL-1 $ \beta $) were detected by quantitative real-time polymerase chain reaction (RT-qPCR), and the expressions of proteins related to nuclear factor $ \kappa\beta $-B (NF- $ \kappa\beta $), mitogen-activated protein kinases (MAPKs) and Akt signaling pathways were detected by Western blot. The results showed that dendrocandin U significantly inhibited LPS-induced NO release and mRNA expressions of iNOS, TNF- $ \alpha $ and IL-1 $ \beta $ in RAW264.7 cells (P<0.01). Meanwhile, dendrocandin U significantly inhibited LPS-induced phosphorylation of I $ \kappa $B, p65, ERK1/2, JNK1/2, p38 and Akt (P<0.05). Dendrocandin U could inhibit LPS-induced inflammatory responses in RAW264.7 cells by inhibiting the activation of NF- $ \kappa $B, MAPKs and Akt signaling pathways.

Keywords: Dendrobium huoshanense; dendrocandin U; inflammation; nuclear factor kappa-B(NF- $ \kappa $B) signaling pathway; mitogen-activated protein kinases(MAPKs) signaling pathway; Akt signaling pathway

作者信息

张杨巧巧 $ ^{1} $，江慧 $ ^{1} $，张凤云 $ ^{2} $，李强明 $ ^{1} $，罗建平 $ ^{1} $

(1. 合肥工业大学食品与生物工程学院, 安徽合肥 230601; 2. 安徽医科大学基础医学院, 安徽合肥 230032)

摘要和关键词

摘要: 为了研究霍山石斛中联苄类化合物 dendrocandin U 的抗炎作用机制,文章建立脂多糖(LPS)诱导的 RAW264.7 细胞炎症模型,运用 Griess 法检测 NO 的释放量,运用实时定量聚合酶链式反应(polymerase chain reaction, PCR)检测诱导型一氧化氮合酶(inducible nitric oxide synthase, iNOS)、肿瘤坏死因子- $ \alpha $ (tumor necrosis factor $ \alpha $, TNF- $ \alpha $)和白细胞介素-1 $ \beta $ (interleukin-1 $ \beta $, IL-1 $ \beta $) mRNA 的表达,运用 Western Blot 检测核因子 $ \kappa $B (nuclear factor $ \kappa $B, NF- $ \kappa $B)、丝裂原活化蛋白激酶 (mitogen-activated protein kinases, MAPKs) 和 Akt 信号通路相关蛋白的表达。研究发现,dendrocandin U 可显著抑制 LPS 诱导的 RAW264.7 细胞 NO 释放,iNOS、TNF- $ \alpha $, IL-1 $ \beta $ 的 mRNA 表达 (P<0.01) 以及 I $ \kappa $B, p65、ERK1/2、JNK1/2、p38、Akt 磷酸化 (P<0.05)。结果表明,dendrocandin U 可能是通过抑制 NF- $ \kappa $B, MAPKs 和 Akt 信号通路的激活来抑制 LPS 诱导的 RAW264.7 细胞炎症反应。

关键词: 霍山石斛；dendrocandin U；炎症；NF- $ \kappa $B 信号通路；MAPKs 信号通路；Akt 信号通路

Funding

安徽省科技重大专项资助项目（18030801112）

合肥工业大学学报(自然科学版)

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