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ORIGINAL ARTICLE
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Adaptive immunoregulation of luteolin and chlorogenic acid in lipopolysaccharide-induced interleukin-10 expression


1 Department of Chinese Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chia-Yi, Taiwan
2 Department of Chinese Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chia-Yi; School of Post-Baccalaureate Chinese Medicine, Tzu Chi University, Hualien, Taiwan

Correspondence Address:
Chia-Chou Yeh,
Department of Chinese Medicine, Buddhist Dalin Tzu Chi General Hospital, 2, Min-Sheng Road, Dalin, Chiayi
Taiwan
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/tcmj.tcmj_23_19

Objective: To investigate the mechanism of the adaptive effect of two compounds in Lonicerae japonica flos (LJF), luteolin (LUT) and chlorogenic acid (CGA), on the expression of interleukin (IL) IL-10 and IL-6. Materials and Methods: RAW264.7 cells receiving lipopolysaccharide (LPS) were pretreated with CGA and LJF. The expression of pro-inflammatory cytokines and IL-10 was evaluated by reverse transcription-polymerase chain reaction. Moreover, the concentrations of IL-10 and IL-6 were measured by enzyme-linked immunosorbent assay in the culture medium obtained 24 h after LPS treatment. Nuclear extracts of RAW264.7 cells, pretreated with CGA or LUT and LPS, were prepared after 6 h, and C/EBPβ and C/EBPδ were measured by Western blotting. Nuclear factor-κB (NF-κB) activity was measured by electrophoretic mobility shift assay. The phosphorylated form of IκB, ERK1/2, p38, JNK, and IκB, ERK2, p38, or JNK were also measured by Western blotting. Results: CGA enhanced the LPS-induced expression of IL-10 and IL-6, and increased NF-κB, Sp1, C/EBPβ and δ. The effect of CGA is interfered with Lut by suppressing the phosphorylation of IκB and p38, and NF-κB activity. In the event, IL-6 was suppressed and IL-10 was not influenced. Conclusion: LUT and CGA, which are abundant in LJF that is one of the ingredients in Gingyo-san, have adaptive immunoregulative effect on the expression of IL-10.


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