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. 2021 May 18;29:30–41. doi: 10.1016/j.jot.2021.03.005

Fig. 5.

Fig. 5

Losartan diminishes expression of OA-related genes through PPARγ-mediated TGF-β1/Smad2/3 signaling pathway inactivation in chondrocytes. Normal chondrocytes were used as controls, and OA chondrocytes were treated with or without losartan ​+ ​PBS or losartan ​+ ​TGF-β1. A, Expression of PPARγ, TGF-β1, Smad2, and Smad3, along with the extent of Smad2 and Smad3 phosphorylation in chondrocytes evaluated by Western blot analysis normalized to GAPDH. B, Expression of MMP-13, ADAMTS-4, ADAMTS-5, HtrA1, iNOS, and Collagen II in chondrocytes evaluated by Western blot analysis normalized to GAPDH. C, The levels of IL-6, IL-1β, TNF-α, and COX-2 in chondrocytes evaluated by ELISA. OA chondrocytes were treated with losartan ​+ ​PPARγ siRNA ​+ ​PBS or losartan ​+ ​PPARγ siRNA ​+ ​TGF-β1. D, Expression of PPARγ, TGF-β1, Smad2, and Smad3, along with the extent of Smad2 and Smad3 phosphorylation in chondrocytes evaluated by Western blot analysis normalized to GAPDH. E, Expression of MMP-13, ADAMTS-4, ADAMTS-5, HtrA1, iNOS, and Collagen II in chondrocytes evaluated by Western blot analysis normalized to GAPDH. F, The levels of IL-6, IL-1β, TNF-α, and COX-2 in chondrocytes evaluated by ELISA. The experiment was repeated three times. ∗p ​< ​0.05 vs. control chondrocytes or OA chondrocytes treated with losartan ​+ ​PPARγ siRNA ​+ ​PBS; #p ​< ​0.05 vs. OA chondrocytes treated with losartan ​+ ​PBS.