RESUMEN
To clarify the recovery patterns of spontaneous activity and liver damage after different stressors, female Fischer 344 rats were treated with <I>Propionibacterium aches</I> (<I>P, aches</I>) or water immersion stress before lipopolysaccharide (LPS) injection. They were then examined for wheel running activity, serum corticosterone concentration, serum alanine aminotransferase (ALT) activity, histological appearance of liver and plasma tumor necrosis factor alpha (TNF-a) concentration.<BR>The recovery in physical activity of <I>P. aches</I>-treated rats was faster than that of water immersion rats. One day after the stressors, serum corticosterone cancentration and ALT activity of <I>P. acnes</I>-treated rats were higher than that of water immersion rats. In addition, increases in serum ALT activity and plasma TNF- a, as well as massive necrosis of the liver in <I>P. acnes</I>-treated rats were observed seven days after stress treatment. The <I>P. acnes</I>-LPS rats also showed a reduction in survival rate after 24 hours. These results suggest that <I>P. acnes</I> stress causes serious inflammation when stimulated by LPS. Although rapid recovery in physical activity was not inhibited by <I>P. acnes</I> stress, it differed from the response of water immersion stress.
RESUMEN
To clarify the recovery patterns of spontaneous activity and liver damage after different stressors, female Fischer 344 rats were treated with <I>Propionibacterium aches</I> (<I>P, aches</I>) or water immersion stress before lipopolysaccharide (LPS) injection. They were then examined for wheel running activity, serum corticosterone concentration, serum alanine aminotransferase (ALT) activity, histological appearance of liver and plasma tumor necrosis factor alpha (TNF-a) concentration.<BR>The recovery in physical activity of <I>P. aches</I>-treated rats was faster than that of water immersion rats. One day after the stressors, serum corticosterone cancentration and ALT activity of <I>P. acnes</I>-treated rats were higher than that of water immersion rats. In addition, increases in serum ALT activity and plasma TNF- a, as well as massive necrosis of the liver in <I>P. acnes</I>-treated rats were observed seven days after stress treatment. The <I>P. acnes</I>-LPS rats also showed a reduction in survival rate after 24 hours. These results suggest that <I>P. acnes</I> stress causes serious inflammation when stimulated by LPS. Although rapid recovery in physical activity was not inhibited by <I>P. acnes</I> stress, it differed from the response of water immersion stress.
RESUMEN
In previous studies, acute exercise might induce inflammatory cytokines from immunological cells, but it was not clear that tumor necrosis factor (TNF) -α in the liver was induced by acute exercise. In this study, we first measured the changes from acute exercise in plasma TNF-α, lipopolysaccharide (LPS), interferon (IFN) -γ and prostaglandin (PG) E2 ; from and investigated the effect of acute exercise on TNF-α expression in the liver. Then we examined the response of TNF-α to PGE2 in isolated Kupffer cells. Female Fischer 344 rats were run on a treadmill at 21 m/min for 60 min on a 15% grade. Although the portal venous plasma endotoxin concentration in the exercised group was higher than that in the resting group, plasma TNF-α was not detected in either group. In addition, plasma IFN-γ, which accelerates TNF-α production, was not detected. TNF-α mRNA expression in the liver didn't change significantly. On the other hand, plasma PGE2, which is an inhibitor of TNF-α production, markedly increased immediately after the exercise. In addition, PGE2 inhibited TNF-α production by LPS-stimulated Kupffer cells in in vitro. These results sug gest that LPS-induced TNF-α expression in rat liver is inhibited by an increase of PGE2 during acute exercise.