Reactive oxygen species are messengers in maintenance of human and guinea pig gallbladder tonic contraction.
Reactive oxygen species are messengers in maintenance of human and guinea pig gallbladder tonic contraction.
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DOI：
10.1152/ajpgi.00206.2007
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发表时间：
2007-09
期刊：
影响因子：
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通讯作者：
Ping Cong;Zuoliang Xiao;P. Biancani;J. Behar
中科院分区：
文献类型：
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作者：
Ping Cong;Zuoliang Xiao;P. Biancani;J. Behar
人和豚鼠胆囊（GB）的紧张性收缩依赖于PGE（2）和血栓素A（2）（TxA（2））的基础水平。参与这些野牡丹素的发生的途径尚未阐明。我们的目的是研究活性氧（ROS）的来源，以及它们是否有助于通过产生基础前列腺素水平的GB紧张性收缩的发生。在用ROS清除剂（Tiron和过氧化氢酶）、夹竹桃麻素（NADPH氧化酶的抑制剂）和NOX-1小干扰RNA（siRNA）处理的人和豚鼠GB肌条中研究紧张性收缩。用特异性抗体测定了GB肌细胞NADPH氧化酶的亚基及其功能。ROS清除剂降低GB紧张性收缩和H（2）O（2）和PGE（2）水平。夹竹桃素也抑制紧张性收缩。针对GB肌细胞中NADPH氧化酶亚基的抗体降低了H（2）O（2）和PGE（2）水平。NOX-1 siRNA转染降低了强直性收缩、NOX-1表达以及H（2）O（2）和PGE（2）水平。Tiron和夹竹桃苷抑制预期的张力增加和H（2）O（2）水平引起的肌肉条拉伸。H2 O2通过依次增加磷酸化p38和cPLA 2的血小板活化因子样脂质来增加PGE 2和TxA 2的水平。NADPH氧化酶产生的H（2）O（2）参与信号转导途径，通过激活PAF、p38和cPLA（2）产生胰头素维持GB紧张性收缩。
The tonic contraction of human and guinea pig gallbladder (GB) is dependent on basal levels of PGE(2) and thromboxane A(2) (TxA(2)). The pathway involved in the genesis of these prostaglandins has not been elucidated. We aimed to examine the source of reactive oxygen species (ROS) and whether they contribute to the genesis of GB tonic contraction by generating basal prostaglandin levels. Tonic contraction was studied in human and guinea pig GB muscle strips treated with ROS scavengers (Tiron and catalase), apocynin (an inhibitor of NADPH oxidase), and NOX-1 small interference RNA (siRNA). The subunits of NADPH oxidase and their functional roles were determined with specific antibodies in GB muscle cells. ROS scavengers reduced the GB tonic contraction and H(2)O(2) and PGE(2) levels. Apocynin also inhibited the tonic contraction. Antibodies against subunits of NADPH oxidase present in GB muscle cells lowered H(2)O(2) and PGE(2) levels. NOX-1 siRNA transfection reduced the tonic contraction, NOX-1 expression, and levels of H(2)O(2) and PGE(2). Tiron and apocynin inhibited the expected increase in tension and H(2)O(2) levels induced by stretching of muscle strips. H(2)O(2) increased the levels of PGE(2) and TxA(2) by increasing platelet-activating factor-like lipids that phosphorylate p38 and cPLA(2) sequentially. H(2)O(2) generated by NADPH oxidase participates in a signal transduction pathway that maintains the GB tonic contraction by activating PAF, p38, and cPLA(2) to generate prostaglandins.