K. Tjandra et al., ENDOGENOUS GLUCOCORTICOIDS INHIBIT NEUTROPHIL RECRUITMENT TO INFLAMMATORY SITES IN CHOLESTATIC RATS, American journal of physiology: Gastrointestinal and liver physiology, 33(5), 1996, pp. 821-825
Since glucocorticoids have been shown to inhibit leukocyte accumulatio
n to inflammatory sites (6, 9) and endogenous glucocorticoid levels ar
e elevated in our cholestatic rat model, we investigated their role du
ring acute inflammation. Sprague-Dawley rats (150-200 g) were either b
ile duct resected (BDR) or sham resected (sham). Five days later, a 2%
carrageenan solution in saline was injected subcutaneously into prefo
rmed air pouches on their backs. Animals were killed 5 h later, and in
flammatory response was quantitated by measuring the exudate volume, c
ell count, and myeloperoxidase (mainly in neutrophils) activity. We al
so pretreated BDR/sham rats with RU-486 (2 mg/kg ip), a glucocorticoid
,receptor antagonist, Ih before carrageenan injection. BDR rats exhibi
ted an impaired inflammatory response reflected by 20, 52, and 42% dec
reases in exudate volume, cell count, and myeloperoxidase activity, re
spectively (all P < 0.05). RU-486 treatment significantly increased th
e inflammatory response in BDR rats (to sham levels), but not in sham
rats. These results suggest that endogenous glucocorticoid suppresses
the inflammatory response in BDR rats.