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首页> 外文期刊>American Journal of Physiology >Involvement of endogenous CRF in carbon tetrachloride-induced acute liver injury in rats.
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Involvement of endogenous CRF in carbon tetrachloride-induced acute liver injury in rats.

机译：内源性CRF参与四氯化碳诱导的大鼠急性肝损伤。

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摘要

Central neuropeptides play important roles in many physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Central injection of corticotropin-releasing factor (CRF) aggravates carbon tetrachloride (CCl4)-induced acute liver injury through the sympathetic nervous pathway in rats. However, still nothing is known about a role of endogenous neuropeptides in the brain in hepatic pathophysiological regulations. Involvement of endogenous CRF in the brain in CCl4-induced acute liver injury was investigated by centrally injecting a CRF receptor antagonist in rats. Male fasted Wistar rats were injected with CRF receptor antagonist alpha-helical CRF-(9-41) (0.125-5 microg) intracisternally just before and 6 h after CCl4 (2 ml/kg) administration, and blood samples were obtained before and 24 h after CCl4 injection for measurement of hepatic enzymes. The liver sample was removed 24 h after CCl4 injection, and histological changes were examined. Intracisternal alpha-helical CRF-(9-41) dose dependently (0.25-2 microg) reduced the elevation of alanine aminotransferase and aspartate aminotransferase levels induced by CCl4. Intracisternal alpha-helical CRF-(9-41) reduced CCl4-induced liver histological changes, such as centrilobular necrosis. The effect of central CRF receptor antagonist on CCl4-induced liver injury was abolished by sympathectomy and 6-hydroxydopamine pretreatment but not by hepatic branch vagotomy or atropine pretreatment. These findings suggest the regulatory role of endogenous CRF in the brain in experimental liver injury in rats.
机译：中枢神经肽在通过自主神经系统介导的许多生理和病理生理调节中起重要作用。关于肝胆系统，几种神经肽在大脑中起作用以调节胆汁分泌，肝血流量和肝增殖。集中注射促肾上腺皮质激素释放因子（CRF）可通过大鼠交感神经通路加重四氯化碳（CCl4）诱导的急性肝损伤。但是，关于内源性神经肽在大脑中在肝病理生理调节中的作用，仍然一无所知。通过在大鼠中央注射CRF受体拮抗剂，研究了内源性CRF在CCl4诱导的急性肝损伤中对大脑的参与。在雄性禁食的Wistar大鼠中，在CCl4（2 ml / kg）施用之前和之后6 h内，脑池内CRF受体拮抗剂α-螺旋CRF-（9-41）（0.125-5 microg）进行了注射，并于24和24之前获得了血液样本注射CCl4后h进行肝酶测定。注射CCl4 24小时后取出肝脏样品，并检查组织学变化。颅内注射α-螺旋CRF-（9-41）剂量依赖性（0.25-2微克）降低了CCl4诱导的丙氨酸转氨酶和天冬氨酸转氨酶水平的升高。颅内腔α-螺旋CRF-（9-41）减少了CCl4诱导的肝组织学改变，例如小叶中心坏死。交感神经切除术和6-羟基多巴胺预处理消除了中央CRF受体拮抗剂对CCl4诱导的肝损伤的作用，而肝分支迷走神经切断术或阿托品预处理则没有。这些发现表明内源性CRF在大鼠实验性肝损伤中的调节作用。

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