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Antiarthritic mechanisms of lupeol triterpenes
Author(s) -
KweifioOkai George,
De Munk Fred,
Macrides Theodore A.,
Smith Phil,
Rumble Baden A.
Publication year - 1995
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430360104
Subject(s) - lupeol , chemistry , terpene , pharmacology , biochemistry , medicine
The triterpenes lupeol (L), lupeol‐3‐palmitate (LP), and lupeol‐3‐linoleate (LL) have previously been shown to reduce joint destruction in adjuvant arthritic rats. In order to explain the relative antiarthritic effectiveness (LL>LP>L), the triterpenes were tested on the release of collagenase by rat osteosarcoma (bone tumor) cells, on the release of 5 lipoxygenase inflammatory products by human neutrophils, and on CCl 4 ‐induced hepatotoxicity in rats. The rat osteosarcoma cells released collagenase which digested type I (bone) native collagen. The collagenase release, unaffected by 50 μM lupeol, decreased in the presence of lupeol linoleate and lupeol palmitate by 97% and 78%, respectively. The 30% inhibitory concentrations (IC 30 ) of lupeol linoleate, lupeol palmitate, and lupeol on LTB 4 release by the neutrophils were 27 μM, 94 μM, and μ100 μM, respectively. All the triterpenes equally reduced hepatic fatty degeneration in CCl 4 rats, but only the triterpene esters significantly reduced LDH release (34% LL; 25% LP) and accelerated hepatic cell regeneration (LL>LP). The effectiveness of the triterpenes in the models of inflammatory and arthritic processes employed here corresponded with their relative antiarthritic effectiveness in adjuvant arthritic rats. © 1995 Wiley‐Liss, Inc.