BNTA, a potent extracellular matrix (ECM) modulator, facilitates cartilage structural molecule synthesis on chondrocytes by activating superoxide dismutase 3 (SOD3). BNTA promotes cartilage extracellular matrix generation and inhibits osteoarthritis development. BNTA has the potential for the research of osteoarthritis[1].
BNTA (0.01-10 μM; 1-7 d) does not decrease cell viability of human osteoarthritis chondrocytes and rat primary chondrocytes[1].BNTA (0.1 μM; 2 d) increases SOX9 protein markedly[1].BNTA (0.1 μM; 2 d) remarkably increases the COL2A1 and SOX9 protein levels in IL1β-induced rat OA chondrocytes[1].BNTA (10 μM; 5 d) increases proteoglycan staining in ATDC5 cells[1].BNTA (0.01-10 μM; 6 h) upregulates the expression levels of ECM-related genes COL2A1, ACAN, proteoglycan 4 (PRG4), and SRY-box 9 (SOX9) in human OA chondrocytes[1].BNTA (0.01-10 μM; 6 h) increases Col2a1, Acan, Prg4, and Sox9 mRNA levels, with maximum effects around 0.1 μM in IL1β-induced rat OA chondrocytes[1].BNTA (0.01-1 μM; 2 or 3 w) enhances anabolism and inhibited inflammatory response in osteoarthritis cartilage explants[1]. Cell Viability Assay[1] Cell Line: Human OA chondrocytes
BNTA (0.015-1.5 mg/kg; intra-articular injection; twice a week for 4 and 8 weeks) could attenuate OA progression developed after anterior cruciate ligament transection (ACLT) in rats[1]. Animal Model: Male SD rats weighing 80 g are induced by ACLT[1]
[1]. Shi Y, et, al. A small molecule promotes cartilage extracellular matrix generation and inhibits osteoarthritis development. Nat Commun. 2019 Apr 23; 10(1): 1914.