The ginsenoside metabolite compound K exerts its anti-inflammatory activity by downregulating memory B cell in adjuvant-induced arthritis

Jingyu Chen, Qingtong Wang, Huaxun Wu, Kangkang Liu, Yujing Wu, Yan Chang, Wei Wei

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Context: Compound K (CK, 20-O-d-glucopyranosyl-20(S)-protopanaxadiol), a novel ginsenoside metabolite, is structurally a member of the dammarane-type triterpene saponins. Several studies have identified the anti-inflammatory activity of CK. Our previous study demonstrated that CK exerted its anti-inflammatory effect via inhibition of abnormal activation and differentiation of T cells. However, its mechanism of action on B cells remains unclear. Objective: The objective of this study is to investigate the effect and underlying mechanisms of CK’s effects on memory B cells in the setting of adjuvant-arthritis (AA). Materials and methods: Complete Freund’s adjuvant was used to induce AA in rats. Rats were administered, either CK (10, 40, and 160 mg/kg), once daily for 15 d, or methotrexate (MTX; 0.5 mg/kg) once every 3 d, for a total of six times. To evaluate the anti-inflammatory effect of CK, a global assessment and a swollen joint count of AA rats were performed every 3 d. Spleen index and histopathology were examined. Subsets of B cells including CD45R+IgM+ (total B cells) and CD45R+CD27+ (memory B cells) and expression of CD40 and CD40L were assayed by flow cytometry. Results: Compared with the AA rats, global assessment scores and swollen joint counts were significantly lower in the treated groups received CK (40 and 160 mg/kg; p < 0.05 and p < 0.01, respectively). CK (40 and 160 mg/kg) decreased the spleen index (p < 0.01), and alleviated hyperplasia of lymph nodes (p < 0.05 and p < 0.01, respectively) and marginal zone (p < 0.05) in the spleen. In addition, CK (40 and 160 mg/kg) suppressed memory B cell subsets (p < 0.05), and suppressed CD40L expression on T cells and CD40 expression on B cells (p < 0.05 and p < 0.01, respectively). Discussion and conclusion: This study demonstrated that CK downregulated memory B cells in AA rats, and this down-regulation may be T-cell dependent.

Original languageEnglish (US)
Pages (from-to)1280-1288
Number of pages9
JournalPharmaceutical Biology
Volume54
Issue number7
DOIs
StatePublished - Jul 2 2016
Externally publishedYes

Fingerprint

Experimental Arthritis
B-Lymphocytes
Anti-Inflammatory Agents
Down-Regulation
B-Lymphocyte Subsets
CD40 Ligand
Spleen
T-Lymphocytes
Joints
Ginsenosides
Triterpenes
Freund's Adjuvant
Saponins
Methotrexate
Hyperplasia
Immunoglobulin M
ginsenoside M1
Flow Cytometry
Lymph Nodes

Keywords

  • Autoimmune
  • inflammation
  • triterpene saponins

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology
  • Pharmaceutical Science
  • Drug Discovery
  • Complementary and alternative medicine

Cite this

The ginsenoside metabolite compound K exerts its anti-inflammatory activity by downregulating memory B cell in adjuvant-induced arthritis. / Chen, Jingyu; Wang, Qingtong; Wu, Huaxun; Liu, Kangkang; Wu, Yujing; Chang, Yan; Wei, Wei.

In: Pharmaceutical Biology, Vol. 54, No. 7, 02.07.2016, p. 1280-1288.

Research output: Contribution to journalArticle

Chen, Jingyu ; Wang, Qingtong ; Wu, Huaxun ; Liu, Kangkang ; Wu, Yujing ; Chang, Yan ; Wei, Wei. / The ginsenoside metabolite compound K exerts its anti-inflammatory activity by downregulating memory B cell in adjuvant-induced arthritis. In: Pharmaceutical Biology. 2016 ; Vol. 54, No. 7. pp. 1280-1288.
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AU - Liu, Kangkang

AU - Wu, Yujing

AU - Chang, Yan

AU - Wei, Wei

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N2 - Context: Compound K (CK, 20-O-d-glucopyranosyl-20(S)-protopanaxadiol), a novel ginsenoside metabolite, is structurally a member of the dammarane-type triterpene saponins. Several studies have identified the anti-inflammatory activity of CK. Our previous study demonstrated that CK exerted its anti-inflammatory effect via inhibition of abnormal activation and differentiation of T cells. However, its mechanism of action on B cells remains unclear. Objective: The objective of this study is to investigate the effect and underlying mechanisms of CK’s effects on memory B cells in the setting of adjuvant-arthritis (AA). Materials and methods: Complete Freund’s adjuvant was used to induce AA in rats. Rats were administered, either CK (10, 40, and 160 mg/kg), once daily for 15 d, or methotrexate (MTX; 0.5 mg/kg) once every 3 d, for a total of six times. To evaluate the anti-inflammatory effect of CK, a global assessment and a swollen joint count of AA rats were performed every 3 d. Spleen index and histopathology were examined. Subsets of B cells including CD45R+IgM+ (total B cells) and CD45R+CD27+ (memory B cells) and expression of CD40 and CD40L were assayed by flow cytometry. Results: Compared with the AA rats, global assessment scores and swollen joint counts were significantly lower in the treated groups received CK (40 and 160 mg/kg; p < 0.05 and p < 0.01, respectively). CK (40 and 160 mg/kg) decreased the spleen index (p < 0.01), and alleviated hyperplasia of lymph nodes (p < 0.05 and p < 0.01, respectively) and marginal zone (p < 0.05) in the spleen. In addition, CK (40 and 160 mg/kg) suppressed memory B cell subsets (p < 0.05), and suppressed CD40L expression on T cells and CD40 expression on B cells (p < 0.05 and p < 0.01, respectively). Discussion and conclusion: This study demonstrated that CK downregulated memory B cells in AA rats, and this down-regulation may be T-cell dependent.

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