6-Shogaol inhibits monosodium urate crystal-induced inflammation--an in vivo and in vitro study.
Gout is a rheumatic disease that is manifestated by an intense inflammation secondary to monosodium urate crystal deposition in joints. In the present study, we assessed the effect of 6-shogaol (isolated active principle from ginger) on monosodium urate crystal-induced inflammation in mice; an experimental model for gouty arthritis and compared it with that of the non-steroidal anti-inflammatory drug, indomethacin. Paw volume and levels/activities of lysosomal enzymes, lipid peroxidation, anti-oxidant status and inflammatory mediator TNF-alpha were determined in control and monosodium urate crystal-induced mice. The levels of beta-glucuronidase and lactate dehydrogenase were also measured in monosodium urate crystal-incubated polymorphonuclear leucocytes (PMNL) in vitro. The levels of lysosomal enzymes, lipid peroxidation, and inflammatory mediator tumour necrosis factor-alpha and paw volume were increased significantly and the activities of anti-oxidant status were in turn decreased in monosodium urate crystal-induced mice, whereas these changes were reverted to near normal levels upon 6-shogaol administration. In vitro, 6-shogaol reduced the level of beta-glucuronidase and lactate dehydrogenase in monosodium urate crystal-incubated polymorphonuclear leucocytes in concentration dependent manner when compared to control cells. The present results clearly indicated that 6-shogaol exerted a strong anti-inflammatory effect and can be regarded as useful tool for the treatment of acute gouty arthritis.
Sabina
Evan Prince
EP
School of Bio Sciences and Technology, VIT University, Vellore 632 014, Tamil Nadu, India.
Rasool
Mahaboobkhan
M
Mathew
Lazar
L
Ezilrani
Panneerselvam
P
Indu
Haridas
H
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D000975:Antioxidants / Q000378:metabolism; D002396:Catechols / Q000494:pharmacology*; D003460:Crystallization; D004305:Dose-Response Relationship, Drug; D004487:Edema / Q000139:chemically induced / Q000517:prevention & control; D005260:Female; D020939:Zingiber officinale / Q000737:chemistry; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007249:Inflammation / Q000209:etiology* / Q000517:prevention & control*; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D008247:Lysosomes / Q000187:drug effects / Q000201:enzymology; D008297:Male; D051379:Mice; D009504:Neutrophils / Q000187:drug effects; D013154:Spleen / Q000187:drug effects / Q000201:enzymology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D014527:Uric Acid / Q000037:antagonists & inhibitors* / Q000633:toxicity*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D002396:Catechols; D014409:Tumor Necrosis Factor-alpha; D014527:Uric Acid; C040115:shogaol; D007213:Indomethacin