Wang Changzhi, Huandike Meiyier, Yang Yingxia, Zhang Huijie, Feng Guiyu, Meng Xiaoying, Zhang Pingxin, Liu Juan, Li Jinyu, Chai Limin
Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.
Nephropathy Department, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.
Phytother Res. 2021 May;35(5):2807-2823. doi: 10.1002/ptr.7026. Epub 2021 Jan 23.
Caulis Lonicerae, the dried stem of Lonicera japonica, has been confirmed to have antiinflammatory and antioxidant therapeutic effects. In the present study, we aimed to evaluate the functional mechanism of glycosides extracted from Caulis Lonicerae on the inflammatory proliferation of interleukin-1 beta (IL-1β)-mediated fibroblast-like synoviocytes (FLSs) from rats. Rat FLSs (RSC-364) co-cultured with lymphocytes induced by IL-1β were used as a cell model. Glycosides in a freeze-dried powder of aqueous extract from Caulis Lonicerae were identified using high-performance liquid chromatography-electrospray ionization/mass spectrometry. After treatment with glycosides, the inflammatory proliferation of FLS, induced by IL-1β, decreased significantly. Flow cytometry analysis showed that treatment with glycosides restored the abnormal balance of T cells by intervening in the proliferation and differentiation of helper T (Th) cells. Glycosides also inhibited the activation of Janus kinase signal transducer and activator of transcription (JAK-STAT) and nuclear factor (NF)-κB signaling pathways by suppressing the protein expression of key molecules in these pathways. Therefore, we concluded that the glycosides of Caulis Lonicerae can intervene in the differentiation of Th cells, suppressing the activation of JAK-STAT and NF-κB signaling pathways, contributing to the inhibitory effect on inflammatory proliferation of FLS co-cultured with lymphocytes induced by pro-inflammatory cytokines.
忍冬藤，即忍冬的干燥茎枝，已被证实具有抗炎和抗氧化治疗作用。在本研究中，我们旨在评估从忍冬藤中提取的糖苷对白细胞介素-1β（IL-1β）介导的大鼠成纤维样滑膜细胞（FLS）炎症增殖的作用机制。将与IL-1β诱导的淋巴细胞共培养的大鼠FLS（RSC-364）用作细胞模型。采用高效液相色谱-电喷雾电离/质谱法鉴定忍冬藤水提取物冻干粉中的糖苷。用糖苷处理后，IL-1β诱导的FLS炎症增殖显著降低。流式细胞术分析表明，糖苷处理通过干预辅助性T（Th）细胞的增殖和分化恢复了T细胞的异常平衡。糖苷还通过抑制这些信号通路中关键分子的蛋白表达来抑制Janus激酶信号转导子和转录激活子（JAK-STAT）以及核因子（NF）-κB信号通路的激活。因此，我们得出结论，忍冬藤糖苷可干预Th细胞的分化，抑制JAK-STAT和NF-κB信号通路的激活，从而对与促炎细胞因子诱导的淋巴细胞共培养的FLS的炎症增殖产生抑制作用。
