The Journal of surgical research · 2003
High expression of the CD14 gene and interleukin-1beta gene in the liver and lungs of cirrhotic rats after partial hepatectomy.
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Takeda Yoshihisa, Arii Shigeki, Mori Akira, Imamura Masayuki
Аннотация
BACKGROUND: A hepatic resection is invasive for cirrhotic patients because postoperative complications, such as hepatic disturbance sometimes resulting in hepatic failure and pulmonary disturbances, are frequent and serious. We investigated here the alteration of the CD14 and inflammatory cytokine genes expressed in the liver and lungs after partial hepatectomy (PH) of a cirrhotic rat model to help elucidate the pathophysiological change occurring during the postoperative course of hepatectomized cirrhotic patients.
MATERIALS AND METHODS: Wistar rats were orally administrated carbon tetrachloride once a week for 14 weeks to induce liver cirrhosis. In comparison with cirrhotic and normal rats, we analyzed the expression of the CD14, tumor necrosis factor-alpha, and interleukin (IL)-1beta genes in remnant liver and whole lung tissue during 48 h after 30% partial hepatectomy with Northern blottings and measured asparatate aminotransferase (AST) in serum for evaluation of postoperative hepatic injury. Gadolinium chloride (GdCl3; 7 mg/kg body weight) was intravenously injected 24 h before partial hepatectomy to suppress Kupffer cells (KC) activation.
RESULTS: The expression of the CD14 and IL-1beta genes moderately increased at 6 h and peaked at 12 h in parallel with the time course of AST values after PH only in cirrhotic rats. GdCl(3) significantly inhibited the elevation of AST similar to the inhibition of the expression of the CD14 and IL-1beta genes after PH. In addition, the expression of these genes showed marked enhancement in the lungs of the cirrhotic hepatectomy model.
CONCLUSIONS: KC activation was responsible for hepatic injury after PH, and the CD14 system appeared to be an early trigger for KC activation followed by induction of inflammatory cytokine IL-1beta synthesis leading to hepatic injury. Furthermore, the CD14 system was suggested to participate in respiratory disturbances after hepatectomy in cirrhosis.
MATERIALS AND METHODS: Wistar rats were orally administrated carbon tetrachloride once a week for 14 weeks to induce liver cirrhosis. In comparison with cirrhotic and normal rats, we analyzed the expression of the CD14, tumor necrosis factor-alpha, and interleukin (IL)-1beta genes in remnant liver and whole lung tissue during 48 h after 30% partial hepatectomy with Northern blottings and measured asparatate aminotransferase (AST) in serum for evaluation of postoperative hepatic injury. Gadolinium chloride (GdCl3; 7 mg/kg body weight) was intravenously injected 24 h before partial hepatectomy to suppress Kupffer cells (KC) activation.
RESULTS: The expression of the CD14 and IL-1beta genes moderately increased at 6 h and peaked at 12 h in parallel with the time course of AST values after PH only in cirrhotic rats. GdCl(3) significantly inhibited the elevation of AST similar to the inhibition of the expression of the CD14 and IL-1beta genes after PH. In addition, the expression of these genes showed marked enhancement in the lungs of the cirrhotic hepatectomy model.
CONCLUSIONS: KC activation was responsible for hepatic injury after PH, and the CD14 system appeared to be an early trigger for KC activation followed by induction of inflammatory cytokine IL-1beta synthesis leading to hepatic injury. Furthermore, the CD14 system was suggested to participate in respiratory disturbances after hepatectomy in cirrhosis.