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Ethanol Inhibits Gastric Acid Secretion in Rats Through Increased AMP-Kinase Activity

机译:乙醇通过增加AMP激酶活性抑制大鼠胃酸的分泌

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The effects of ethanol on gastric acid secretion remain controversial. The present study examines the effect of low-dose (2%) short term (15-20min) ethanol exposure on gastric acid secretion via a potential interaction with AMP-activated protein kinase (AMPK). Real-time fluorescence digital imaging was used to provide functional evidence for the interaction of ethanol and AMPK in modulating secretagogue-induced acid secretion. Individual rat gastric glands were loaded with the pH-sensitive dye BCECF and the secretagogues carbachol (200 mu M) or histamine (200 mu M) were added to induce secretion. Rates of pH recovery were calculated as Delta pH(i)/Delta t. In one series of experiments, secretagogue-induced acid secretion was inhibited by 2% ethanol, or the AMPK activator AICAR monophosphate (AICAR) (20 mM). In a separate series, 2% ethanol was added in combination with compound C (20 mu M), an AMPK inhibitor, to prevent activation of AMPK. 2% ethanol significantly suppressed stimulated acid secretion. In order to confirm modulation of AMPK activity by ethanol, the specific AMPK inhibitor compound C was used, which reversed the inhibitory effects of ethanol on stimulated acid secretion. This study demonstrates that low dose ethanol (2%) inhibits secretagogue-dependent acid secretion by activation of the AMPK pathway in rat gastric parietal cells.
机译:乙醇对胃酸分泌的影响仍存在争议。本研究通过与AMP激活的蛋白激酶(AMPK)的潜在相互作用,研究了低剂量(2%)短期(15-20min)乙醇暴露对胃酸分泌的影响。实时荧光数字成像用于提供乙醇和AMPK在调节促分泌素诱导的酸分泌中相互作用的功能证据。在单个大鼠胃腺中加载pH敏感染料BCECF,并加入促分泌剂卡巴胆碱(200μM)或组胺(200μM)诱导分泌。 pH恢复率计算为ΔpH(i)/Δt。在一系列实验中,促分泌素诱导的酸分泌被2%乙醇或AMPK活化剂AICAR一磷酸(AICAR)(20 mM)抑制。在单独的系列中,将2%的乙醇与AMPK抑制剂化合物C(20μM)组合加入,以防止AMPK活化。 2%的乙醇显着抑制刺激的酸分泌。为了确定乙醇对AMPK活性的调节,使用了特定的AMPK抑制剂化合物C,它逆转了乙醇对刺激的酸分泌的抑制作用。这项研究表明,低剂量乙醇(2%)可通过激活大鼠胃壁细胞中的AMPK途径来抑制促分泌素依赖性酸分泌。

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