Anti-inflammatory mechanism of Kaempferia parviflora in murine macrophage cells (RAW 264.7) and in experimental animals.
BACKGROUND
The rhizomes of Kaempferia parviflora Wall. ex Baker have been used in Thailand for treatment of gout, apthous ulcer, peptic ulcer and abscesses.


OBJECTIVE
In our previous study, the crude ethanol extract of Kaempferia parviflora and its compound (5, 5-hydroxy-3,7,3',4'-tetramethoxyflavone), was reported to show nitric oxide (NO) inhibition in RAW 264.7 cells. The present study is thus investigated the anti-inflammatory mechanism of Kaempferia parviflora extract and compound 5 against inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) mRNA expressions.


METHODS
The extract of Kaempferia parviflora and its compound were tested against NO and prostaglandin E(2) (PGE(2)) releases using RAW264.7 cells as well as studied on anti-inflammatory activity in carrageenan-induced rat paw edema and acute toxicity in mice.


RESULTS
The results revealed that the ethanol extract of Kaempferia parviflora markedly inhibited PGE(2) release with an IC(50) value of 9.2 microg/ml. This plant extract and compound 5 also suppressed mRNA expression of iNOS in dose-dependent manners, whereas COX-2 mRNA expression was partly affected. According to the in vivo study, chloroform and hexane fractions greater decreased rat paw edema than ethanol, ethyl acetate and water fractions.


CONCLUSIONS
The mechanisms for anti-inflammatory activity of Kaempferia parviflora and compound 5 are mainly due to the inhibition of iNOS mRNA expression but partly through that of COX-2 mRNA.
Department of Pharmacognosy and Pharmaceutical Botany, Faculty of Pharmaceutical Sciences, Prince of Songkla University, Kanchanawanit Street, Hat-Yai, Songkhla 90112, Thailand.
Chutha
C
Sae-wong
Pimpimon
P
Tansakul
Supinya
S
Tewtrakul
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D002351:Carrageenan; D002460:Cell Line; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000378:metabolism; D004487:Edema / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control; D005528:Foot / Q000473:pathology; D006586:Hexanes; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors / Q000633:toxicity; D008264:Macrophages / Q000187:drug effects*; D008297:Male; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors; D018517:Plant Roots / Q000737:chemistry; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D012997:Solvents; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D030521:Zingiberaceae / Q000737:chemistry*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D006586:Hexanes; D008070:Lipopolysaccharides; D012997:Solvents; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D012313:RNA; D002351:Carrageenan; D052247:Nitric Oxide Synthase Type II; D015232:Dinoprostone