Ginsenoside metabolite compound K attenuates inflammatory responses of adjuvant-induced arthritis rats

Huaxun Wu, Jingyu Chen, Qingtong Wang, Xiaoyi Jia, Shasha Song, Pingfan Yuan, Kangkang Liu, Lihua Liu, Yunfang Zhang, Aiwu Zhou, Wei Wei

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Objective: To investigate the effects of ginsenoside metabolite compound K (CK) on adjuvant-induced arthritis (AA) rats and the partial mechanisms focused on the function of immunocyte (B cell and macrophage) and effectors' cell (fibroblast-like synoviocyte, FLS). Methods: Animals were divided randomly into nine groups including control, AA, CK (5, 10, 20, 40, 80, and 160 mg/kg, i.g.), and MTX (0.5 mg/kg, i.g.). The effects of CK on AA rats are evaluated by swelling of the paw, histopathology of joint, and inflammatory cytokine production in serum. To further investigate the effects of CK on the function of B cell, peritoneal macrophage, and FLS from AA rats, we examined the proliferation of B cell and FLS by [3H] thymidine incorporation, and the phagocytic function of peritoneal macrophage was measured by neutral red uptake. Cytokines and antibodies in serum and the supernatant from peritoneal macrophage and FLS were measured by ELISA kit. Results: CK suppressed the severity of AA rats by attenuating the paw swelling and histopathology of joint. CK can inhibit the proliferation of B cell and autoantibody levels, and suppressed the phagocytic function of peritoneal macrophage and secreted pro-inflammatory cytokines TNF-α, IFN-γ, and IL-17 and up-regulated the level of protective cytokines IL-10. CK attenuated the proliferation of FLS, and balanced the ratio of RANKL to OPG in AA rats. Conclusion: Our results suggest that CK may attenuate the severity of AA rats, partially by influencing the function of immunocyte (B cell and macrophage) and effectors' cells (FLS) in AA.

Original languageEnglish (US)
Pages (from-to)124-129
Number of pages6
JournalImmunopharmacology and Immunotoxicology
Volume36
Issue number2
DOIs
StatePublished - Apr 1 2014
Externally publishedYes

Fingerprint

Ginsenosides
Experimental Arthritis
Metabolites
Rats
Macrophages
Fibroblasts
Peritoneal Macrophages
Cells
Cytokines
B-Lymphocyte Subsets
B-Lymphocytes
Swelling
Joints
Neutral Red
Interleukin-17
ginsenoside M1
Serum
Interleukin-10
Autoantibodies
Thymidine

Keywords

  • Adjuvant-induced arthritis
  • B cell
  • Fibroblast-like synoviocytes
  • Ginsenoside metabolite compound K
  • Peritoneal macrophage

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Toxicology
  • Pharmacology

Cite this

Ginsenoside metabolite compound K attenuates inflammatory responses of adjuvant-induced arthritis rats. / Wu, Huaxun; Chen, Jingyu; Wang, Qingtong; Jia, Xiaoyi; Song, Shasha; Yuan, Pingfan; Liu, Kangkang; Liu, Lihua; Zhang, Yunfang; Zhou, Aiwu; Wei, Wei.

In: Immunopharmacology and Immunotoxicology, Vol. 36, No. 2, 01.04.2014, p. 124-129.

Research output: Contribution to journalArticle

Wu, H, Chen, J, Wang, Q, Jia, X, Song, S, Yuan, P, Liu, K, Liu, L, Zhang, Y, Zhou, A & Wei, W 2014, 'Ginsenoside metabolite compound K attenuates inflammatory responses of adjuvant-induced arthritis rats', Immunopharmacology and Immunotoxicology, vol. 36, no. 2, pp. 124-129. https://doi.org/10.3109/08923973.2014.880717
Wu, Huaxun ; Chen, Jingyu ; Wang, Qingtong ; Jia, Xiaoyi ; Song, Shasha ; Yuan, Pingfan ; Liu, Kangkang ; Liu, Lihua ; Zhang, Yunfang ; Zhou, Aiwu ; Wei, Wei. / Ginsenoside metabolite compound K attenuates inflammatory responses of adjuvant-induced arthritis rats. In: Immunopharmacology and Immunotoxicology. 2014 ; Vol. 36, No. 2. pp. 124-129.
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abstract = "Objective: To investigate the effects of ginsenoside metabolite compound K (CK) on adjuvant-induced arthritis (AA) rats and the partial mechanisms focused on the function of immunocyte (B cell and macrophage) and effectors' cell (fibroblast-like synoviocyte, FLS). Methods: Animals were divided randomly into nine groups including control, AA, CK (5, 10, 20, 40, 80, and 160 mg/kg, i.g.), and MTX (0.5 mg/kg, i.g.). The effects of CK on AA rats are evaluated by swelling of the paw, histopathology of joint, and inflammatory cytokine production in serum. To further investigate the effects of CK on the function of B cell, peritoneal macrophage, and FLS from AA rats, we examined the proliferation of B cell and FLS by [3H] thymidine incorporation, and the phagocytic function of peritoneal macrophage was measured by neutral red uptake. Cytokines and antibodies in serum and the supernatant from peritoneal macrophage and FLS were measured by ELISA kit. Results: CK suppressed the severity of AA rats by attenuating the paw swelling and histopathology of joint. CK can inhibit the proliferation of B cell and autoantibody levels, and suppressed the phagocytic function of peritoneal macrophage and secreted pro-inflammatory cytokines TNF-α, IFN-γ, and IL-17 and up-regulated the level of protective cytokines IL-10. CK attenuated the proliferation of FLS, and balanced the ratio of RANKL to OPG in AA rats. Conclusion: Our results suggest that CK may attenuate the severity of AA rats, partially by influencing the function of immunocyte (B cell and macrophage) and effectors' cells (FLS) in AA.",
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AU - Wu, Huaxun

AU - Chen, Jingyu

AU - Wang, Qingtong

AU - Jia, Xiaoyi

AU - Song, Shasha

AU - Yuan, Pingfan

AU - Liu, Kangkang

AU - Liu, Lihua

AU - Zhang, Yunfang

AU - Zhou, Aiwu

AU - Wei, Wei

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N2 - Objective: To investigate the effects of ginsenoside metabolite compound K (CK) on adjuvant-induced arthritis (AA) rats and the partial mechanisms focused on the function of immunocyte (B cell and macrophage) and effectors' cell (fibroblast-like synoviocyte, FLS). Methods: Animals were divided randomly into nine groups including control, AA, CK (5, 10, 20, 40, 80, and 160 mg/kg, i.g.), and MTX (0.5 mg/kg, i.g.). The effects of CK on AA rats are evaluated by swelling of the paw, histopathology of joint, and inflammatory cytokine production in serum. To further investigate the effects of CK on the function of B cell, peritoneal macrophage, and FLS from AA rats, we examined the proliferation of B cell and FLS by [3H] thymidine incorporation, and the phagocytic function of peritoneal macrophage was measured by neutral red uptake. Cytokines and antibodies in serum and the supernatant from peritoneal macrophage and FLS were measured by ELISA kit. Results: CK suppressed the severity of AA rats by attenuating the paw swelling and histopathology of joint. CK can inhibit the proliferation of B cell and autoantibody levels, and suppressed the phagocytic function of peritoneal macrophage and secreted pro-inflammatory cytokines TNF-α, IFN-γ, and IL-17 and up-regulated the level of protective cytokines IL-10. CK attenuated the proliferation of FLS, and balanced the ratio of RANKL to OPG in AA rats. Conclusion: Our results suggest that CK may attenuate the severity of AA rats, partially by influencing the function of immunocyte (B cell and macrophage) and effectors' cells (FLS) in AA.

AB - Objective: To investigate the effects of ginsenoside metabolite compound K (CK) on adjuvant-induced arthritis (AA) rats and the partial mechanisms focused on the function of immunocyte (B cell and macrophage) and effectors' cell (fibroblast-like synoviocyte, FLS). Methods: Animals were divided randomly into nine groups including control, AA, CK (5, 10, 20, 40, 80, and 160 mg/kg, i.g.), and MTX (0.5 mg/kg, i.g.). The effects of CK on AA rats are evaluated by swelling of the paw, histopathology of joint, and inflammatory cytokine production in serum. To further investigate the effects of CK on the function of B cell, peritoneal macrophage, and FLS from AA rats, we examined the proliferation of B cell and FLS by [3H] thymidine incorporation, and the phagocytic function of peritoneal macrophage was measured by neutral red uptake. Cytokines and antibodies in serum and the supernatant from peritoneal macrophage and FLS were measured by ELISA kit. Results: CK suppressed the severity of AA rats by attenuating the paw swelling and histopathology of joint. CK can inhibit the proliferation of B cell and autoantibody levels, and suppressed the phagocytic function of peritoneal macrophage and secreted pro-inflammatory cytokines TNF-α, IFN-γ, and IL-17 and up-regulated the level of protective cytokines IL-10. CK attenuated the proliferation of FLS, and balanced the ratio of RANKL to OPG in AA rats. Conclusion: Our results suggest that CK may attenuate the severity of AA rats, partially by influencing the function of immunocyte (B cell and macrophage) and effectors' cells (FLS) in AA.

KW - Adjuvant-induced arthritis

KW - B cell

KW - Fibroblast-like synoviocytes

KW - Ginsenoside metabolite compound K

KW - Peritoneal macrophage

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