4.7 Article

Callerya atropurpurea suppresses inflammation in vitro and ameliorates gastric injury as well as septic shock in vivo via TLR4/MyD88-dependent cascade

期刊

PHYTOMEDICINE
卷 105, 期 -, 页码 -

出版社

ELSEVIER GMBH
DOI: 10.1016/j.phymed.2022.154338

关键词

Callerya atropurpurea; Anti-inflammation; TLR4; Macrophage; Gastritis; Septic shock

资金

  1. National Institute of Biological Resources (NIBR) - Ministry of Environment (MOE) of the Republic of Korea
  2. Korea Basic Science Institute (National research Facilities and Equipment Center) - Ministry of Education [NIBR202006202]
  3. [2020R1A6C101A191]
  4. Korea Environmental Industry & Technology Institute (KEITI) [NIBR202006202] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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This study investigated the anti-inflammatory mechanisms of Callerya atropurpurea ethanol extract (Ca-EE) both in vitro and in vivo. The results showed that Ca-EE significantly reduced the production of inflammatory cytokines, protected cells from damage, and inhibited multiple signaling pathways. Gastritis and septic shock were also alleviated by Ca-EE. These findings suggest that Ca-EE has the potential to be used as a treatment for inflammatory diseases.
Background: Callerya atropurpurea is a traditional plant in a tropical zone discovered to have anti-inflammatory functions. Purpose: we want to investigate the mechanism related to anti-inflammation of C. atropurpurea ethanol extract (Ca-EE) both in vitro and in vivo. Study design: Murine macrophage cells and mouse models for gastritis and septic shock were conducted to evaluate the abilities of Ca-EE in anti-inflammation. Methods: Ca-EE was tested by HPLC and LC-MS/MS. NO outcome was checked by Griess reagent test. Cell viabilities were evaluated using MTT assay. Inflammatory cytokines were determined via RT-PCR and ELISA. The mechanism of Ca-EE in anti-inflammation was investigated by luciferase reporter gene assay and immunoblot in transcription level and protein level respectively. Gastric injury and septic shock administrated with Ca-EE were studied by H&E, PCR, and immunoblot. Results: Ca-EE significantly decreased LPS-induced NO production, but hardly stimulated the expression of NO itself. It not only showed no cytotoxicity, but also protected cells from LPS damage. Moreover, Ca-EE decreased TLR4 expression, altered MyD88 recruitment and TRAF6, and suppressed the phospho-Src/PI3K/AKT. Ca-EE inhibited downstream signaling P38, JNK and NF-kappa B. Finally, Ca-EE alleviated HCl/EtOH-induced gastritis and LPS/poly (I:C)-induced septic shock through the previously mentioned signaling cascades. Conclusion: Ca-EE exhibited an integrated and promising mechanism against TLR4-related inflammation, which shows potential for treating gastritis, septic shock, and other inflammatory diseases.

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