Yoneda Masashi, Sato Yoichi, Nakamura Kimihide, Yokohama Shiro, Kono Toru, Watanobe Hajime, Terano Akira
Department of Gastroenterology, Dokkyo University School of Medicine, Kitakobayashi 880, Mibu, Tochigi 321-0293, Japan.
Eur J Pharmacol. 2003 Oct 8;478(2-3):173-7. doi: 10.1016/j.ejphar.2003.08.040.
The involvement of capsaicin-sensitive afferent neurons and calcitonin gene-related peptide (CGRP) in central thyrotropin-releasing hormone (TRH)-induced hepatic cytoprotection was investigated in rats. Both systemic capsaicin pretreatment and intravenous administration of CGRP receptor antagonist, human CGRP-(8-37), completely abolished the protective effect of intracisternal TRH analog (RX-77368; p-Glu-His-(3,3'-dimethyl)-Pro-NH2, 5 ng) against carbon tetrachloride (CCl4)-induced acute liver injury, assessed by serum alanin aminotransferase levels and histological changes. These data demonstrate the involvement of capsaicin-sensitive afferent neurons and CGRP in central TRH-induced hepatic cytoprotection.
在大鼠中研究了辣椒素敏感传入神经元和降钙素基因相关肽(CGRP)在中枢促甲状腺激素释放激素(TRH)诱导的肝脏细胞保护中的作用。全身性辣椒素预处理和静脉注射CGRP受体拮抗剂人CGRP-(8-37),均完全消除了脑池内TRH类似物(RX-77368;对-谷氨酸-组氨酸-(3,3'-二甲基)-脯氨酰胺,5 ng)对四氯化碳(CCl4)诱导的急性肝损伤的保护作用,该保护作用通过血清丙氨酸转氨酶水平和组织学变化来评估。这些数据表明辣椒素敏感传入神经元和CGRP参与了中枢TRH诱导的肝脏细胞保护。