Laboratory animal research · 2026
Ameliorative effect of Gastrodia elata Blume extract on inflammation in a rat model of osteoarthritis.
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Lee Yeon Su, Jung Da Eun, Seo Ji Won, Na Hyeon Jeong, Park Jeong Su, Hong Jin Woo, Lee Hyeon Ju, Shin Jae-Ho
Аннотация
BACKGROUND: Osteoarthritis (OA) is characterized by progressive articular cartilage degeneration, in which inflammatory mediators drive MMP-mediated matrix breakdown and chondrocyte apoptosis, ultimately leading to pain and functional impairment. Although often described as a "wear-and-tear" disease, increasing evidence highlights immune/inflammatory signaling as a key contributor to OA progression. Gastrodia elata Blume (GEB) has reported anti-inflammatory and immunomodulatory activities, but its preventive potential in OA remains unclear. This study evaluated GEB extract in a widely used monosodium iodoacetate (MIA)-induced OA rat model. Male Sprague-Dawley rats (5 weeks old) were assigned to CON, OA, OA + L-GEB, and OA + H-GEB groups; GEB was administered orally once daily for 5 weeks, and OA was induced by intra-articular MIA (3 mg/50 µL) at day 21.
RESULTS: GEB improved gross cartilage surface appearance and histopathological outcomes (HE, Safranin O, Alcian blue; Mankin and OARSI scores), showing reduced cartilage damage and better preservation of proteoglycan staining compared with the OA group. Consistently, GEB decreased IL-6, MMP-13, and cleaved caspase-3 in cartilage (IHC) and reduced TUNEL-positive cells, indicating suppression of inflammatory signaling and chondrocyte apoptosis. RT-qPCR further showed downregulation of NF-κB, IL-6, MMP-9, MMP-13, and TIMP-1 mRNA levels in GEB-treated groups versus OA.
CONCLUSIONS: GEB extract attenuated inflammatory and catabolic responses and inhibited chondrocyte apoptosis in MIA-induced OA, supporting its potential as a prophylactic strategy for localized inflammatory pathology such as osteoarthritis.
RESULTS: GEB improved gross cartilage surface appearance and histopathological outcomes (HE, Safranin O, Alcian blue; Mankin and OARSI scores), showing reduced cartilage damage and better preservation of proteoglycan staining compared with the OA group. Consistently, GEB decreased IL-6, MMP-13, and cleaved caspase-3 in cartilage (IHC) and reduced TUNEL-positive cells, indicating suppression of inflammatory signaling and chondrocyte apoptosis. RT-qPCR further showed downregulation of NF-κB, IL-6, MMP-9, MMP-13, and TIMP-1 mRNA levels in GEB-treated groups versus OA.
CONCLUSIONS: GEB extract attenuated inflammatory and catabolic responses and inhibited chondrocyte apoptosis in MIA-induced OA, supporting its potential as a prophylactic strategy for localized inflammatory pathology such as osteoarthritis.