BNTA, a potent modulator of the extracellular matrix (ECM), enhances the synthesis of cartilage structural molecules in chondrocytes by activating superoxide dismutase 3 (SOD3). BNTA exhibits promising potential for alleviating osteoarthritis by regulating cartilage formation[1].
体内研究
BNTA (0.015-1.5 mg/kg; intra-articular injection; twice a week for 4 and 8 weeks) effectively mitigated the progression of osteoarthritis induced by anterior cruciate ligament transection (ACLT) in rats[1].
体外研究
BNTA (0.01-10 μM; 1-7 days) does not reduce the viability of human osteoarthritis chondrocytes and rat primary chondrocytes[1].
NTA (0.1 μM; 2 days) significantly enhances SOX9 protein expression[1].
NTA (0.1 μM; 2 days) markedly elevates the levels of COL2A1 and SOX9 proteins in IL1β-induced rat OA chondrocytes[1].
NTA (10 μM; 5 days) enhances proteoglycan staining in ATDC5 cells[1].
NTA (0.01-10 μM; 6 hours) increases the expression levels of ECM-related genes COL2A1, ACAN, proteoglycan 4 (PRG4), and SRY-box 9 (SOX9) in human OA chondrocytes[1].
NTA (0.01-10 μM; 6 hours) enhances the mRNA levels of Col2a1, Acan, Prg4, and Sox9, with peak effects observed around 0.1 μM in IL1β-induced rat OA chondrocytes[1].
NTA (0.01-1 μM; 2 or 3 weeks) promotes anabolism and suppresses inflammatory response in osteoarthritis cartilage explants[1].
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