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KMID : 1120320190050000007
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Osteoporosis and Sarcopenia
2019 Volume.5 No. 0 p.7 ~ p.7
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Chondroprotective activity of Dalbergia sissoo mitigated further progression of MIA induced Osteoarthritis in rat model by increased SOX-9 and downregulated MMPs expressions
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Kothari Priyanka
Tripathi Ashish Kumar
Trivedi Ritu
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Abstract
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Introduction: Osteoarthritis (OA) is highly prevalent and debilitating disorder of the joints in which cartilage and underlying bone is most affected. Osteoarthritis is a multiple factor associated chronic degenerative disease.
Objectives: The purpose of this study was to evaluate the anti-osteoarthritic and chondro-protective effects of DSE on the MIA injected OA rats. Previously our study reported the positive effects of the DSE on cartilaginous cells to enhance the fracture healing in rats however its positive effects on OA model remains unknown.
Methodology: For Mimic OA model in animals, MIA was injected in Rats knee joint. Treatment was immediately started next day to MIA. In-vivo doses of DSE 250 and 500 mg.kg-1day-1 were given orally for 28 days daily. Samples analysed by H&E and Toluidine blue Stainings, Micro CT parameters, Serum ELISA. Potent compound from DSE that is CAFG was also studied in-vitro on primary chondrocytes. CAFG were treated with IL-1β on chondrocytes and analysed by qPCR, Western and IF.
Results: DSE has reduced swelling and inflammation in knee joints of MIA animals. Cartilage degradation and deterioated subchondral bone in MIA model was restored in DSE treatment 250 and 500 mg.kg-1day-1 both. In MIA, chondrocytes vanished in cartilage up to calcified cartilage, which affected proteoglycan synthesis. DSE prevented chondrocytes apoptosis and proteoglycan degradation which was verified in H&E and Toluidin blue staining. Micro CT data shows that Subchondral bone loss and elevated serum level of cartilage degradation CTX-II & COMP and inflammation marker IL-1β was restored in DSE. Sox-9 is a characteristic marker of chondrocytes which is the only residing cells in cartilage and produces matrix. In OA Sox-9 decreased and MMPs increased which degrades cartilage matrix. In-vitro CAFG increased Sox-9, Aggrecan and Col-II expression and decreased MMPs levels in IL-1β induced chondrocytes. Increased expression of Sox-9 was confirmed by IF.
Conclusion: Our outcomes shows that DSE has chondro protective activity which prevented joint cartilage in animals and inhibited further progression of MIA induced OA. Along this CAFG also has chondro protective activity.
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