Yokohama S, Yoneda M, Watanobe H, Kono T, Nakamura K, Makino I, Terano A
Second Department of Medicine and Surgery, Asahikawa Medical College, Asahikawa, Japan.
Neurosci Lett. 2001 Nov 9;313(3):149-52. doi: 10.1016/s0304-3940(01)02268-6.
The effect of intracisternal injection of urocortin, an endogenous ligand for corticotropin-releasing factor (CRF) 2 receptor, on carbon tetrachloride (CCl4)-induced acute liver injury was investigated in rats. Intracisternal injection of urocortin dose-dependently enhanced elevation of serum alanine aminotransferase and aspartate aminotransferase levels induced by CCl4. Intracisternal urocortin also aggravated CCl4-induced histological changes of the liver. The aggravating effect of central urocortin on CCl4-induced acute liver injury was abolished by chemical sympathectomy, but not by vagotomy. These data demonstrate that urocortin acts in the brain to exacerbate acute liver injury through the sympathetic nervous system and suggest a possible involvement of the CRF2 receptor in the central CRF-induced exacerbation of acute liver injury in rats.
研究了向大鼠脑池内注射促肾上腺皮质激素释放因子（CRF）2受体的内源性配体尿皮质素对四氯化碳（CCl4）诱导的急性肝损伤的影响。向大鼠脑池内注射尿皮质素可剂量依赖性地增强CCl4诱导的血清丙氨酸氨基转移酶和天冬氨酸氨基转移酶水平的升高。脑池内注射尿皮质素还会加重CCl4诱导的肝脏组织学变化。化学去交感神经可消除中枢尿皮质素对CCl4诱导的急性肝损伤的加重作用，但迷走神经切断术则不能。这些数据表明，尿皮质素在脑内通过交感神经系统加重急性肝损伤，并提示CRF2受体可能参与中枢CRF诱导的大鼠急性肝损伤加重过程。
