Effects of <i>Dokhwalgisaeng-tang</i> on Monosodium Iodoacetate-Induced Osteoarthritis in Rats

Objectives To evaluate whether Dokhwalgisaeng-tang (DGT) reduces progression of disease in a monosodium iodoacetate (MIA)-induced osteoarthritis animal model.Methods Osteoarthritis was induced by intra-articular injection of MIA in rats.DGT was orally administered for 14 days at low (240 mg/kg) or high (479 mg/kg) doses, with indomethacin (2 mg/kg) used as a positive control.Outcome measures included hind limb weight-bearing distribution, oxidative stress markers, inflammatory cytokines, cartilage matrix components, matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs), and histopathological changes in joint cartilage.Results DGT significantly improved hind limb weight-bearing distribution in MIA-induced osteoarthritic rats, suggesting pain relief.It dose-dependently reduced serum reactive oxygen species and significantly decreased malondialdehyde levels in serum and joint tissue.DGT also attenuated inflammatory responses by reducing serum tumor necrosis factor-and interleukin-6 levels.In joint tissues, DGT suppressed in ducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-, and inter leukin-1 expression, which was associated with inhibition of nuclear factor-B and p38 signaling pathways.In addition, DGT regulated nicotinamide adenine dinucleotide phosphate oxidase (NOX)-related proteins, including NOX2, p22 phox , and p47 phox , supporting its antioxidative and anti-inflammatory effects.High-dose DGT preserved cartilage matrix components, maintaining aggrecan and glycosaminoglycan levels relative to controls.It also inhibited cartilage-degrading MMPs, including MMP-1, MMP-2, MMP-8, and MMP-13, while modulating TIMP-3.Histopathological analysis showed reduced cartilage erosion and proteoglycan loss in DGT-treated rats.Conclusions DGT showed protective effects against MIA-induced osteoarthritis by reducing oxidative stress and inflammation and preserving cartilage integrity. (