ISSN: 0973-7510

E-ISSN: 2581-690X

Research Article | Open Access
Nuchsupha Sunthamala , Chutimun Suebsamran, Niramon Khruaphet, Neeranuch Sankla, Janchai Janpirom, Surasak Khankhum , Rungruedee Thiwthong and Sununta Chuncher
Department of Biology, Faculty of Science, Mahasarakham University, Mahasarakham, 44150, Thailand.
J Pure Appl Microbiol. 2020;14(4):2351-2361 | Article Number: 6420 | © The Author(s). 2020
Received: 23/05/2020 | Accepted: 21/10/2020 | Published: 04/11/2020

Natural compounds represent the great capability to stimulate several cell types. Macrophage plays an important role for an effective immune response for infection and inflammation. Isoquinoline alkaloid, sanguinarine, and chelidonine are active compounds that exhibit activity on various tumor cells and immune cells. However, the effect of these compounds on the endosomal toll-like receptor (enTLR) and type I interferon (IFN) are still unclear. The monocyte-derived macrophages (MDMs) were cultured and were determined their cell viability and phagocytic activity to Staphylococcus aureus DMST8840. The nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression were also examined. The expression of enTLRs, type I IFN, and cytokines were determined by real-time PCR. Result shows that the compounds did not affect on MDM cell viability. Sanguinarine and chelidonine enhance phagocytic activity of MDM against Staphylococcus aureus DMST8840 by revealing a higher number of bacterial survival than the MDM treated by polyI:C, and the cell control after co-culture for 3 h. The production of NO has no difference amount but iNOS mRNA production was down-regulated in sanguinarine, chelidonine and their mixed treated MDM. The expressions of enTLRs and IFN-β1 mRNA were up-regulated in both compounds and their combination. Additionally, these compounds also enhance M1-liked cytokine by up-regulated IL-6 and down-regulated IL-10 and TGF-β1, respectively. Therefore, sanguinarine and chelidonine enhance enTLR and IFN-β1 expression and trend to stimulate the cell into M1-liked MDM.


Monocyte-derived macrophage, sanguinarine, chelidonine, endosomal toll-like receptor, macrophage polarization

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