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B. Glucosamine−Chondroitin Combination:
Glucosamine is an amino monosaccharide unit of glycosaminoglycan, which is the building block of the cartilage matrix seen within joints. Its mechanism of action may involve inhibition of inflammatory enzyme activity and stimulation of glycosaminoglycans (GAG) synthesis. Chondroitin sulfate is a long-chain polymer of repeating disaccharide units containing galactosamine sulfate and glucuronic acid and constitutes the majority of glycosaminoglycans in cartilage found on the moving surfaces of joints, or articular cartilage. Its bioavailability is well documented with up to 70% absorption after oral administration in animals and humans. Its mechanism
of action including contributing to a pool of substrate available for cartilage matrix deposition, inhibition
of proteases, stimulation of glycosaminoglycan, and collagen synthesis. When given in combination, glucosamine and chondroitin sulfate reportedly support cartilage production and protect existing cartilage by inhibiting enzymes in the joints that break down cartilage. In one study treated canine OA with a combination of glucosamine and chondroitin sulfate showed a significant anti-inflammatory effect against chemically induced inflammatory synovitis in dogs. [canapp]
CANAPP SO, MCLAUGHLIN RM, HOSKINSON JJ, ET AL: SCINTIGRAPHIC EVALUATION OF DOGS WITH ACUTE SYNOVITIS AFTER TREATMENT WITH GLUCOSAMINE HYDROCHOLORIDE AND CHONDROITIN SULFATE. J VET RES. 60:1552-1557, 1999.
C. Avocado Soybean Unsaponifiables (ASU)
The mechanism of action of ASU include suppressing TNF-α, IL-1β, COX-2, iNOS gene expression, and prostaglandin E2 and nitric oxide production in articular chondrocytes and monocyte/macrophages.3 In a canine study, ASU caused an increase in both TGF-ß isoforms as compared with the control group. TGF-ß is stimulator of extracellular matrix production (type II collagen, proteoglycan) in chondrocytes.4 In another canine
study, ASU supplemented group showed reduced development of early OA cartilage and subchondral bone lesions (macroscopic and microscopic lesion severity, subchondral bone loss) as compared to placebo treated controls.5
A recent study evaluated the effect ASU, CS and ASU + CS combination upon proinflammatory cytokine (IL-1ß, TNF-α) expression and PGE2production from synovial lining surrogate cells.7 The ASU + CS combination inhibited IL-1ß and TNF-α expression and PGE2 production better than either agent alone.7
A similar effect was noted in activated feline chondrocytes when ASU+CS+Glu pre-treated cells were compared to positive (untreated activated cells) and negative (non-activated cells) controls.9
3. AU RY, AL-TALIB TK, AU AY, ET AL. AVOCADO SOYBEAN UNSUPONIFIABLES (ASU) SUPPRESS
TNF-Α, IL-1SS, COX-2, INOS GENE EXPRESSION, AND PROSTAGLANDIN E2 AND NITRIC OXIDE PRODUCTION IN ARTICULAR CHONDROCYTES AND MONOCYTE/ MACROPHAGES. OSTEARTHRITIS & CARTILAGE. 2007,15:1249-1255
4. ALTINEL L, SARITAS ZK, KOSE KC, ET AL. TREATMENT WITH UNSAPONIFIABLE EXTRACTS OF AVOCADO AND SOYBEAN INCREASES TGF-SS1 AND TGF-SS2 LEVELS IN CANINE JOINT FLUID. TOHOKU J EXP MED. 2007,211:181-18
5. BOILEAU, C, PELLETIER JM, CARON J, ET AL. PROTECTIVE EFFECTS OF TOTAL FRACTION OF AVOCADO/SOYBEAN UNSSAPONIFIABLES ON THE STRUCTUREAL CHANGES IN EXPERIMENTAL DOG OSTEOARTHRITIS: INHIBITION OF NITRIC OXIDE SYNTHASE AND MATRIX METALLOPROTEINASE-13. ARTHRITIS RES THER. 2009,11(2):R41.
7. GRZANNA MW, OWNBY SL, HEINECKE LF, ET
AL. INHIBITION OF CYTOKINE EXPRESSION AND PROSTAGLANDIN E2 PRODUCTION IN MONOCYTE/ MACROPHAGE-LIKE CELLS BY AVOCADO/SOYBEAN UNSAPONIFIABLES AND CHONDROITIN SULFATE.
J COMPLEMENT INTEGR MED. 2010,7(1):ART10. (DOI:10.2202/1553-3840.1338).
9. PUNKE JP, AU RY, AU AY, ET AL. MODULATION
OF PROSTAGLANDIN E2 PRODUCTION IN FELINE ARTICULAR CHONDROCYTES PROPAGATED ON MONOLAYER AND DYNAMIC MICROCARRIER CULTURE. PROC AM COLL VET SURG CONF, 2007, POSTER SESSION.
Epigallocatechin Gallate
Recently, a study was conducted to evaluate the anti- inflammatory effect of ASU+epigallocatechin gallate (EGCG) on activated equine chondrocyte cell culture.10 EGCG is a major antioxidant component of green tea and has been reported to inhibit the onset and severity of induced arthritis in mice. Chondrocyte activation caused upregulated gene expression of COX-2 and increased PGE2 production and NF-kB nuclear translocation. Individually, ASU and EGCG marginally inhibited
COX-2 expression and PGE2 production in activated chondrocytes. In contrast, ASU+EGCG combination reduced COX-2 expression close to that of non-activated control levels, significantly inhibited PGE2 production and NF-ĸB translocation. NF-ĸB is an essential transcription factor for COX-2 induction. Inhibition of the NF-ĸB pathway is known to attenuate COX-2 expression. This study demonstrates that the anti-inflammatory activity of ASU and EGCG is potentiated when used in combination.10 Collectively, a large body of evidence supports the conclusion that ASU+CS+Glu inhibits the expression and production of proinflammatory mediators
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