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Water extract of medicinal ink (WEMI) attenuates lipopolysaccharide-induced NO production of Raw264.7 cells via downregulating JAK2/STAT3-mediated iNOS expression.

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机构： [a]Institute of Traditional Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan [b]Ruijin Hospital Affiliated to Medical College of Shanghai Jiaotong University, Shanghai, China [c]Sichuan Provincial Orthopedics Hospital, Chengdu, Sichuan, China [d]National Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei, Taiwan [e]LO-Sheng Hospital Ministry of Health and Welfare, Taipei, Taiwan [f]College of Oral Medicine, Taipei Medical University, Taipei, Taiwan [g]Program in Molecular Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan [h]Biomedical Industry Ph.D. Program, National Yang Ming Chiao Tung University, Taipei, Taiwan

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Medicinal ink is used as a traditional topical medicine for treating inflammatory diseases via detoxification, relieving pain, hemostasis, and reducing swelling. However, the effect of medicinal ink on the inhibition of inflammatory responses and the underlying molecular mechanism remain unclear.The present study aimed to investigate the anti-inflammatory function of water extract of medical ink (WEMI) and elucidate its active mechanisms.Cell viability was assessed using crystal violet staining assay. Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected by ELISA. Nitric oxide (NO) production was measured by Griess assay. The activation of inflammatory signaling molecules stimulated by lipopolysaccharide (LPS) was evaluated by assessing levels of inducible nitric oxide synthase (iNOS), phosphorylated Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) using Western blot assay.Water extract of medical ink (WEMI) did not present cytotoxic effect on murine macrophage Raw264.7 cells. High dosage of WEMI slightly rescued LPS-suppressed cell viability of Raw264.7 cells. WEMI did not induce NO production or IL-6 secretion, though WEMI significantly induced secretion of TNF-α on Raw264.7 cells not stimulated with LPS. On the other hand, LPS effectively stimulated inflammation on Raw264.7 cells; however, WEMI dramatically reduced LPS-induced NO production. WEMI alleviated LPS-stimulated IL-6 secretion but did not affect the content of TNF-α. In addition, WEMI effectively reduced expression of iNOS by abolishing LPS-mediated phosphorylation of JAK2 and STAT3 but not TLR4-mediated NF-κB and MAPK molecules.Our findings suggest that WEMI targets of the JAK2/STAT3-mediated iNOS expression play a key role in alleviating LPS-induced inflammatory responses in RAW264.7 macrophages. Therefore, medicinal ink may be a potential topical agent for treating fasciitis or synovitis via regulating the immune system.Copyright © 2021 Elsevier B.V. All rights reserved.

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出版当年[2021]版：

大类 | 2 区

医学

小类 | 1 区全科医学与补充医学 2 区植物科学 2 区药物化学 2 区药学

最新[2023]版：

大类 | 2 区

医学

小类 | 1 区药物化学 1 区全科医学与补充医学 1 区药学 1 区植物科学

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第一作者机构： [a]Institute of Traditional Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan

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通讯机构： [a]Institute of Traditional Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan [g]Program in Molecular Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan [h]Biomedical Industry Ph.D. Program, National Yang Ming Chiao Tung University, Taipei, Taiwan [*1]Institute of Traditional Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.,

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