Anti-Inflammatory and Chondro-Protective Effects of Acidic Polysaccharide from Enteromorpha Prolifera in Experimental Models of Osteoarthritis In-Vitro and In-Vivo. (December 2022)

• Record Type: Journal Article
• Authors: Wang, Chih-Chien; Lu, Jeng-Wei; Chiang, Kuang-Hsing; Cheng, Yu-Shuan; Chu, You-Hsiang; Peng, Yi-Jen; Cheng, Chia-Hui; Chang, Chia-Yu; Chuu, Jiunn-Jye
• Is Part Of: Cartilage. Volume 13:Number 4(2022)
• Page Start: 157
• Page End: 170
• Publication Date: 2022-12
• Subjects: osteoarthritis -- enteromorpha prolifera -- oxidative stress -- chondrocyte -- interleukin-1β; Cartilage -- Periodicals; 616.7
• DOI: 10.1177/19476035221129573
• Languages: English
• ISSNs: 1947-6035

Abstract

Objective: Osteoarthritis (OA) progression has been shown to increase the expression of inflammatory cytokines in joints, leading to the destruction of cartilage matrix. Interleukin (IL)-1β is a potent inflammatory cytokine associated with osteoarthritic synovial fluid. The protective effects of polysaccharides from Enteromorpha prolifera against acute hepatic injury was reported. Design: In this study, we examined the effects of Enteromorpha polysaccharide extracts (EPEs) in the treatment of OA. The effects of the EPEs were assessed using an IL-1β-stimulated SW1353 and SW982 cells. The expression levels of specific mRNA and proteins were evaluated using semi-quantitative reverse transcription polymerase chain reaction (sqRT-PCR) and western immunoblotting. An OA animal study involving C57BL/6J mice was also conducted to assess the effects on tactile sensitivity and anterior cruciate ligament transection (ACLT). Results: Acidic polysaccharide extract (APE) was shown to significantly reduce cytokine and chemokine mRNA levels in IL-1β-stimulated SW1353 and SW982 cells and attenuate the expression of proinflammatory cytokines and p38/AP-1 in SW1353 cells. APE was also shown to minimize the effect of osteolytic lesions in the knee joints of ACLT-induced osteoarthritic mice. Conclusions: APE is a potent inhibitor of joint degeneration associated with OA.