Zhao Q, Lu X
Department of Pathology, Medical College, People's Armed Police Force of China, Tianjin.
Zhonghua Bing Li Xue Za Zhi. 1997 Apr;26(2):96-9.
To study the effects of dexamethasone on cAMP production induced by prostaglandin E2 (PGE2) in cultured rabbit aortic smooth muscle cells.
cAMP concentration was determined by protein-competition-contact assay.
Dexamethasone significantly inhibited cAMP accumulation induced by PGE2 in a dose dependent manner in the range between 10 pmol/L and 10 nmol/L. The inhibitory effect grew stronger as the time of pretreatment extended. Adenylate cyclase activity induced by PGE2 was significantly reduced in the cells pretreated with dexamethasone.
The results strongly suggest that dexamethasone inhibits cAMP production induced by PGE2 in cultured aortic smooth muscle cells and the inhibitory effect is exerted at the level of adenylate cyclase. In addition, the inhibitory effect of PGE2 on cultured smooth muscle cell proliferation was resisted by dexamethasone, anyhow no direct enhancing effect on cell proliferation by dexamethasone was detected.
研究地塞米松对培养的兔主动脉平滑肌细胞中前列腺素E2(PGE2)诱导的环磷酸腺苷(cAMP)生成的影响。
采用蛋白质竞争结合分析法测定cAMP浓度。
地塞米松在10 pmol/L至10 nmol/L范围内以剂量依赖方式显著抑制PGE2诱导的cAMP积累。随着预处理时间延长,抑制作用增强。用地塞米松预处理的细胞中,PGE2诱导的腺苷酸环化酶活性显著降低。
结果有力表明,地塞米松抑制培养的主动脉平滑肌细胞中PGE2诱导的cAMP生成,且抑制作用在腺苷酸环化酶水平发挥。此外,地塞米松对抗了PGE2对培养的平滑肌细胞增殖的抑制作用,但未检测到地塞米松对细胞增殖有直接增强作用。