Triamcinolone acetonide

Triamcinolone acetonide inhibits basic fibroblast growth factor (bFGF) induced proliferation of retinal endothelial cells. Triamcinolone acetonide reduces chondrocyte viability and leads to cartilage destruction. Triamcinolone acetonide activates macrophage with anti-inflammatory characteristics. Triamcinolone acetonide can be used in the study of diseases such as atopic dermatitis^[1][2][3][4]. In Vitro:Triamcinolone acetonide (0.05-3 mg/mL, 48-60 h) decreases the proliferation of BRECs with increasing concentration^[1].
Triamcinolone acetonide (0.04-5 mg/mL, 24 h) reduces chondrocyte viability in both normal and osteoarthritic (OA) chondrocytes in a concentration-dependent manner^[2].
Triamcinolone acetonide (0.04-5 mg/mL, 24 h) increases the severity of cartilage structural damage, chondrocyte loss and cluster formation, and proteoglycan loss in OA cartilage^[2].
Triamcinolone acetonide (100 nM, 7 days) strongly induces monocyte differentiation towards an M2 and anti-inflammatory macrophage phenotype^[3]. In Vivo:Triamcinolone acetonide (1.43 mg/mL, Intraperitoneal injection, once a week for 6-12 weeks) enhances folate receptor beta (FRβ)-related macrophage activation and fully prevents osteophyte development in an in vivo rat model of Osteoarthritis^[3].