Prevention of the destruction of acinar structure in patients with Sjögren's syndrome

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  • AOTA Keiko
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • YAMAMURA Yoshiko
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • KANI Koichi
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • TAKANO Hideyuki
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • MOTEGI Katsumi
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • MOMOTA Yukihiro
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • ISHIMARU Naozumi
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry Department of Oral Molecular Pathology, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • AZUMA Masayuki
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry

Bibliographic Information

Other Title
  • Sjögren症候群患者の唾液腺腺房構造破壊阻止
  • Sjogren症候群患者の唾液腺腺房構造破壊阻止 : セファランチンの有効性に関する臨床病理学的研究
  • Sjogren ショウコウグン カンジャ ノ ダエキセンセン ボウ コウゾウ ハカイ ソシ : セファランチン ノ ユウコウセイ ニ カンスル リンショウ ビョウリガクテキ ケンキュウ
  • —Clinicopathological study on the effectiveness of cepharanthin—
  • ―セファランチンの有効性に関する臨床病理学的研究―

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Abstract

Sjögren's syndrome (SS) is characterized by the eventual total replacement of the acinar structure by marked infiltration of lymphocytes into the salivary and lacrimal glands. We previously demonstrated that tumor necrosis factor-α (TNF-α) induced matrix metalloproteinase-9 (MMP-9) production by the stimulating transcription factor, nuclear factor-κB (NF-κB), in human salivary gland acinar cells and that cepharanthin, a biscoclaurine alkaloid, prevented the activation of TNF-α-induced NF-κB activity. In addition, we have shown that cepharanthin prevented the destruction of acinar tissues in murine SS. Thus, in this study, we investigated the clinicopathological effect of cepharanthin on the patients with SS. <br>Ten patients with a diagnosis of primary SS were enrolled in this study. They were treated with cepharanthin for three months, followed by the evaluation of salivary production, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), anti-SS-A antibody, anti-SS-B antibody, pathological examination of labial salivary gland biopsy specimens, and the symptom of drymouth. <br>Average salivary production was 4.25ml/10minutes before the study. This average production increased to 6.46ml/10minutes after the study. There were no remarkable changes in CRP, ESR, anti-SS-A antibody and anti-SS-B antibody. In pathological findings, although the decreases in infiltration of lymphocytes were observed in 5 out of 5 cases, the reduction of destruction of acinar structures was clearly detected in 5 cases. Improvement of symptom of drymouth was detected in 7 out of 10 cases. <br>These observations suggest that cepharanthin treatment might provide an efficient and useful therapeutic approach for countering the destruction of acinar tissue in salivary glands of patients with SS.

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