实验性牙周炎诱导雄性大鼠腮腺中 cAMP 依赖性的淀粉酶活性增加。

Experimental periodontitis induces a cAMP-dependent increase in amylase activity in parotid glands from male rats.

机构信息

Cátedra de Farmacología, Facultad de Odontología, Universidad de Buenos Aires, Marcelo T de Alvear 2142 (1122AAH), Buenos Aires, Argentina.

出版信息

Inflammation. 2009 Dec;32(6):357-63. doi: 10.1007/s10753-009-9142-2.

DOI:10.1007/s10753-009-9142-2

PMID:19669869

Abstract

It is known that subjects with periodontitis show enhanced amylase concentration in saliva. Our purpose was to analyze the release of amylase in parotid glands from rats with experimental periodontitis and controls. We present evidence that periodontitis induces an increase in resting amylase activity and release without changes in isoproterenol-induced amylase secretion. Changes in amylase were reverted by the inhibition of the adenylyl cyclase by SQ 22536, the cyclooxygenase type 1 by FR 122047 and by blocking the vasoactive intestinal peptide (VIP) receptor with VIP 6-28. Parotid glands from rats with periodontitis showed an increase in cAMP levels that was also reverted in the presence of SQ 22536, FR 122047 and VIP 6-28. We concluded that both PGE(2) and VIP are produced in parotid glands from rats with periodontitis and, by activating their own receptors in acinar cells, induce cAMP accumulation leading to an increase in amylase basal secretion.

摘要

已知牙周炎患者唾液中的淀粉酶浓度升高。我们的目的是分析实验性牙周炎大鼠和对照组大鼠腮腺中淀粉酶的释放。我们有证据表明，牙周炎诱导基础状态下淀粉酶活性和释放增加，而异丙肾上腺素诱导的淀粉酶分泌没有变化。通过抑制腺苷酸环化酶 SQ 22536、环氧化酶 1 型 FR 122047 和血管活性肠肽（VIP）受体 VIP 6-28，可使淀粉酶发生的变化得到逆转。牙周炎大鼠的腮腺中 cAMP 水平升高，在 SQ 22536、FR 122047 和 VIP 6-28 存在的情况下，这种升高也得到了逆转。我们得出结论，PGE2 和 VIP 都在牙周炎大鼠的腮腺中产生，并通过激活其在腺泡细胞中的自身受体，诱导 cAMP 积累，导致淀粉酶基础分泌增加。