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Gastroprotective and safety effects of WIN-34B, a novel treatment for osteoarthritis, compared to NSAIDs
- Huh, Jeong-Eun, Lee, Won-Il, Seo, Byung-Kwan, Baek, Yong-Hyeon, Lee, Jae-Dong, Choi, Do-Young, Park, Dong-Suk
- Journal of ethnopharmacology 2011 v.137 no.2 pp. 1011-1017
- Lonicera japonica, acute toxicity, blood chemistry, chronic toxicity, flowers, gastric mucosa, herbs, medicine, models, mortality, nonsteroidal anti-inflammatory agents, oral administration, osteoarthritis, prostaglandins, rats, roots
- ETHNOPHARMACOLOGICAL RELEVANCE: The dried flowers of Lonicera japonica, also known as Japanese honeysuckle, and the dried root of Anemarrhena asphodeloides, the component herbs of WIN-34B, are traditionally used in Eastern medicine to treat various inflammatory conditions including arthritis. OBJECTIVE: To study the acute and chronic toxicities of WIN-34B and to compare its effects on gastric mucosa with those of diclofenac, a widely used NSAID, and celecoxib, a selective COX-2 inhibitor. MATERIALS AND METHODS: To investigate acute toxicity, we orally administered a single dose of 5000mg/kg WIN-34B to rats. To investigate chronic toxicity, we orally administered 500, 1000 or 2000mg/kg WIN-34B to rats daily for 13 weeks. To assess its effects on gastric mucosa, rats received either a single dose or repeated doses of WIN-34B (400, 1000, or 2000mg/kg), diclofenac (10, 40, or 80mg/kg), celecoxib (100 or 1000mg/kg), or vehicle, after which samples of gastric mucosa were assessed grossly and histologically. We also measured tissue activity of myeloperoxidase and synthesis of eicosanoids, including prostaglandin E₂ (PGE₂) and leukotriene B₄ (LTB₄). To further assess its effects, we administered WIN-34B to rats either intraperitoneally or orally, measured gastric injury scores using a rat model of diclofenac-induced gastric injury, and measured eicosanoid synthesis. RESULTS: WIN-34B showed no signs of acute or chronic toxicity in terms of general behavior, gross appearance of the internal organs, blood chemistry, or mortality. WIN-34B did not cause significant gastric mucosal damage after single or repeated doses. In contrast, diclofenac and celecoxib both caused gastric damage. In terms of eicosanoid synthesis, WIN-34B significantly suppressed LTB₄ synthesis while both diclofenac and celecoxib increased LTB₄ synthesis. WIN-34B slightly reduced PGE₂ production, while both diclofenac and celecoxib significantly reduced PGE₂ production. In a rat model of diclofenac-induced gastric injury, WIN-34B significantly suppressed LTB₄ synthesis and restored PGE₂ release. CONCLUSIONS: These results demonstrate that WIN-34B did not cause acute or chronic toxicity in male or female rats. In addition, WIN-34B did not cause significant gastric mucosal damage, instead appearing to protect the mucosa from diclofenac-induced gastric damage through the regulation of PGE₂ and LTB₄.