Astilbin suppresses collagen-induced arthritis via the dysfunction of lymphocytes

Cai, Yu; Chen, Tao; Xu, Qiang

doi:10.1007/s00011-003-1179-3

Cited by 63 publications

(44 citation statements)

References 29 publications

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“…The mechanism of inhibition involved selective induction of apoptosis in liver-infiltrating T lymphocytes, activated spleen T cells, and activated Jurkat cells, without affecting hepatocytes, naive spleen T cells, nonactivated Jurkat cells, or other tissue cells (7,8 ). Astilbin also prevented concanavalin A-induced liver injury by reducing tumor necrosis factor-␣ (TNF-␣) production and T lymphocyte adhesion (9 ), and it significantly suppressed collageninduced arthritis by causing the dysfunction of lymphocytes and inhibiting lymphocyte migration (10,11 ).…”

mentioning

confidence: 99%

Identification of a New Metabolite of Astilbin, 3′-O-Methylastilbin, and Its Immunosuppressive Activity against Contact Dermatitis

Guo

Feng

et al. 2007

Clinical Chemistry

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Background: Astilbin is a flavonoid isolated from the rhizome of Smilax glabra. In a previous study, we revealed its unique immunosuppressive activity, a selective inhibition against activated T lymphocytes. This characteristic of astilbin is beneficial for the treatment of human immune diseases. Methods: We incubated astilbin with rat liver microsomal/cytosolic fractions and isolated the metabolite of astilbin, which was fully characterized by mass spectrometry (MS) and nuclear magnetic resonance (NMR) spectroscopy. We administered astilbin orally via a gastric tube to rats at 0.22 mmol/kg and collected whole blood samples after 30 min and urine samples after 0 to 12 h. We applied HPLC and liquid chromatography/MS to measure the metabolite in the samples, and we assayed cytokine expression by reverse-transcription PCR. Results: After incubation of astilbin with rat liver microsomal/cytosolic fractions, we detected a new metabolite of astilbin and isolated it from the culture solution. We characterized this metabolite by MS and NMR techniques as 3-O-methylated astilbin. We detected the metabolite in both blood and urine samples after oral administration of astilbin, and the metabolite inhibited picryl chloride-induced ear swelling in mice and suppressed the expression of tumor necrosis factor-␣ and interferon-␥, similarly to astilbin. Conclusion: This is the first identification of 3-Omethylastilbin as a new flavonoid, as well as an active metabolite of astilbin in vivo, and is helpful for study-

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confidence: 99%

Identification of a New Metabolite of Astilbin, 3′-O-Methylastilbin, and Its Immunosuppressive Activity against Contact Dermatitis

Guo

Feng

et al. 2007

Clinical Chemistry

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“…This flavanoid has been reported to show antioxidative [10], insecticidal [11], antibacterial [12], antimicrobial [13] antinociceptive and antiedematogenic [14] activities formerly. Our study has demonstrated its immunosuppressive activities including improvement of immunologic liver injury [15], collagen-induced arthritis [16] and contact hypersensitivity Figure 1 Effect of astilbin on the adhesion of Jurkat cells to fibronectin, type IV collagen, hyaluronate or ECV-304 cells. A, Jurkat cells were activated with 10 μg/ml Con A for 12, 24, 36 and 48 h, respectively.…”

Section: Introductionmentioning

confidence: 96%

Astilbin inhibits the adhesion of T lymphocytes via decreasing TNF-α and its associated MMP-9 activity and CD44 expression

Lü

Fěng

et al. 2008

International Immunopharmacology

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“…Astilbin was also found to possess obvious lipidlowering and anti-atherosclerosis effects [5,6] . Recent studies showed that astilbin can inhibit the production of nitric oxide (NO) and the activitiy of matrix metalloproteinase-2 and -9 (MMP-2, MMP-9) [11,12] . These immuno-inhibitory, T-cell-activating, anti-I/R and lipid-lowering actions of astilbin can significantly contribute to the control of chronic transplant arteriosclerosis.…”

Section: Discussionmentioning

confidence: 99%

The inhibitory effect of astilbin on the arteriosclerosis of murine thoracic aorta transplant

Zhao

Zhang

et al. 2009

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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The inhibitory effect of astilbin on transplant arteriosclerosis in murine model of thoracic aorta transplantation was examined. Model of rat thoracic aorta transplantation was established. Ninety rats were divided into three groups. In isograft group, the thoracic aorta of Brown Norway (BN) rat was anastomosed with the abdominal aorta of another BN rat. In allograft group, the thoracic aorta of BN rat was anastomosed with the abdominal aorta of Lewis rat. In astilbin group, the rats receiving allo-transplantation were given astilbin 5 mg/kg per day for a time of 28 days. The donor thoracic aorta and the recipient abdominal aorta were anastomosed by means of a polyethylene cannula (inner diameter: 1.5 mm, length: 3 mm length). The grafts were histologically examined for structural changes. The areas of arterial lumen and endatrium were calculated. Our results showed that, in the allograft group, 28 days after allografting, conspicuous proliferation of smooth muscles and infiltration with a great number of inflammatory cells were found in the tunica intima and tunica media. Astilbin significantly inhibited the proliferation of smooth muscles and ameliorated the infiltration of inflammatory cells thereby prevent against the development of transplant arteriosclerosis. It is concluded that asltilbin can effectively prevent the development of arteriosclerosis in allotransplant by inhibiting the proliferation of smooth muscles and inhibit the proliferation of smooth muscles in tunica of intima and media and reducing infiltration of the inflammatory cells.

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Astilbin suppresses collagen-induced arthritis via the dysfunction of lymphocytes

Abstract: Astilbin may act as an efficient therapeutic agent for arthritis like CsA but with less toxicity. Its mechanism includes a selective suppression on lymphocyte functions via reducing MMP and NO production.

Cited by 63 publications

References 29 publications

Identification of a New Metabolite of Astilbin, 3′-O-Methylastilbin, and Its Immunosuppressive Activity against Contact Dermatitis

Identification of a New Metabolite of Astilbin, 3′-O-Methylastilbin, and Its Immunosuppressive Activity against Contact Dermatitis

Astilbin inhibits the adhesion of T lymphocytes via decreasing TNF-α and its associated MMP-9 activity and CD44 expression

The inhibitory effect of astilbin on the arteriosclerosis of murine thoracic aorta transplant

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