Results: Mortality in sympathectomised mice was significantly
higher than that in sham operated mice following administration
of Jo-2. This result was also supported by apoptosis data in
which sympathectomised livers exhibited a significant elevation
in the number of apoptotic hepatocytes and caspase-3 activity
after Jo-2 treatment compared with sham operated livers.
Moreover, pretreatment with norepinephrine dose dependently
inhibited the hepatic sympathectomy induced increase in
mortality after Jo-2 injection. Antiapoptotic protein levels of
FLICE inhibitory protein, Bcl-xL, and Bcl-2 in the liver were
significantly lower in sympathectomised mice at one and two
hours following Jo-2 treatment than in sham operated animals.
In addition, interleukin 6 supplementation dose dependently
suppressed the hepatic sympathectomy induced increase in
mortality after Jo-2 treatment.
Conclusions: These results suggest that norepinephrine released
from the hepatic sympathetic nerve plays a critical role in
protecting the liver from Fas mediated fulminant hepatitis,
possibly via mechanisms including antiapoptotic proteins and
interleukin 6.
Chida, Y. and Sudo, N. and Takaki, A. and Kubo, C. (2005)
The hepatic sympathetic nerve plays a critical role in preventing
Fas induced liver injury in mice. Gut, 54 (7). pp. 994-1002.
ISSN 00175749