Ethanol extracts of Sanguisorba officinalis L. suppress TNF-α/IFN-γ-induced pro-inflammatory chemokine production in HaCaT cells

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• 作者：Ju-Hye Yang ; Youn-Hwan Hwang ; Min-Jung Gu ; Won-Kyung Cho ; ^{wkcho@kiom.re.kr" class="auth_mail" title="E-mail the corresponding author} ; Jin Yeul Ma ; ^{jyma@kiom.re.kr" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Sanguisorba officinalis L. ; HaCaT ; Keratinocytes ; Anti-inflammation ; Chemokine ; NF-κB/p65
• 刊名：Phytomedicine
• 出版年：2015
• 出版时间：15 December 2015
• 年：2015
• 卷：22
• 期：14
• 页码：1262-1268
• 全文大小：1670 K

文摘

Sanguisorba officinalis L. (SOL) is a perennial plant widely distributed in Asia, its roots are well-known as a traditional herbal medicine to treat burns, chronic intestinal infections, scalds, and inflammation in Korea. Also, the roots of SOL are used for treatment of many types of allergic skin diseases, including urticarial, eczema, and allergic dermatitis.

Purpose

In this study we investigated the underlying mechanism of anti-inflammatory effect of an ethanol extract of SOL roots (ESOL).

Study design

The ability of ESOL to inhibit inflammatory skin disorder was tested in human keratinocyte HaCaT cells.

Methods

Viability test using MTT assay were used to determine non-cytotoxic concentrations of ESOL on HaCaT cells. ESOL-mediated inhibition of the tumor necrosis factor (TNF)-α/interferon (IFN)-γ-induced production of pro-inflammatory chemokines—such as macrophage-derived chemokine (MDC), regulated on activation, normal T-cell expressed and secreted (RANTES), interleukin (IL)-8, and thymus and activation regulated chemokine (TARC)—at the mRNA level was determined by real-time reverse transcription-polymerase chain reaction (RT-PCR). The ability of ESOL to reduce the expression of pro-inflammatory marker proteins was evaluated by Western blot analysis and immunocytochemistry.

Results

ESOL reduced the production of MDC, RANTES, IL-8, and TARC in HaCaT cells stimulated with TNF-α/IFN-γ at both protein and mRNA levels. ESOL also suppressed the phosphorylation of signal transducer and activator of transcription (STAT)-1, extracellular signal-regulated kinase (ERK), and inhibited both nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha (IκB-α) degradation and the nuclear translocation of NF-κB/p65. ESOL exerts anti-inflammatory effects by suppressing the expression of TNF-α/IFN-γ-stimulated chemokines and pro-inflammatory molecules via a blockade NF-κB, STAT-1, and ERK activation.

Conclusion

Our results suggest the preventive potential of ESOL as a herbal medicine for the treatment of inflammatory skin diseases.