イソプロテレノール刺激によってラット耳下腺において転写調節される炎症性サイトカイン遺伝子

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It is well known that hypertrophy and hyperplasia of rat parotid glands are significantly induced after repeated treatment with a β-adrenergic agonist, isoproterenol (IPR). However, the mechanisms of enlargement of the parotid glands caused by IPR treatment are largely unknown. Recently, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) have been reported to be involved in enlargement of various tissues. To elucidate the mechanisms of IPR-induced enlargement in the parotid glands, both cytokines as well as several transcription factors in the parotid glands were examined. The TNF-α and IL-1β protein production in the parotid gland increased from the 2nd day to the 7th day by daily administration of IPR. Expressions of TNF-α and IL-1β genes also increased transiently at 15 h and 18 h after a single administration of IPR, respectively. Both expression levels returned to the same level as the control after 21 h. Caspase-3/7 activity in the soluble fraction of the parotid glands increased from the 3rd day and became 2.5 times that observed in the control on the 7th day after daily IPR treatment. The amounts of nuclear factor κB (NF-κB) and activator protein 1 (AP-1) transcription factors increased after a single treatment with IPR, whereas the activity of c-Jun N-terminal kinase (JNK) in the parotid glands significantly decreased from the 2nd day after daily treatment with IPR. The results suggested that stimulation of the β-adrenergic receptor enhances the expressions of TNF-α and IL-1β, and that both proteins may contribute to the process causing enlargement of rat parotid glands treated with IPR.
福岡歯科大学学会の論文
2006-06-30

イソプロテレノール刺激によってラット耳下腺において転写調節される炎症性サイトカイン遺伝子

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