AIM: To study the anti-inflammatory mechanisms of sodium glycyrrhetina
te (SG). METHODS: Rat chemical peritonitis was used. The protein conte
nt and prostaglandin E-2 (PGE(2)) content in exudate were measured by
Folin-phenol assay and RIA, respectively. SOD activity in neutrophils
(Neu) was determined by pyrogallol-NBT colorimetry. cAMP content in Ne
u was detected by competitive protein binding assay. RESULTS: In perit
onitis caused by histamine, SG 10 - 20 mg.kg(-1) im reduced exudate vo
lume and Neu counts, and 5 - 20 mg.kg(-1) im lowered the protein conte
nt in exudate. In peritonitis induced by carrageenan, SG 20 mg.kg(-1)
im reduced exudate volume, Neu counts, protein content and PGE(2) cont
ent in exudate, increased SOD activity in Neu, but did not affect beta
-glucuronidase release from Neu. In peritonitis induced by arachidonic
acid, SG 20 mg.kg(-1) im reduced Neu counts, protein content, and PGE
(2) content in exudate, and attenuated the reduction of cAMP level in
Neu. CONCLUSION: SG exerts its anti-inflammatory action by lowering pe
rmeability of capillaries in inflammatory site, inhibiting Neu emigrat
ion and PGE(2) biosynthesis, and scavenging oxygen free radicals.