BMSC-Derived Exosomes Ameliorate Osteoarthritis by Inhibiting Pyroptosis of Cartilage via Delivering miR-326 Targeting HDAC3 and STAT1//NF-κB p65 to Chondrocytes

Figure 5

MiR-326 inhibited chondrocyte pyroptosis by targeting HDAC3 and activating the STAT1/NF-κB p65 signaling pathway. (a) Overexpression of HDAC3 could counteract the accelerated proliferation of OA chondrocytes induced by miR-326 mimics; (b) overexpression of HDAC3 could counteract the enhanced migration of OA chondrocytes induced by miR-326 mimics; (c) overexpression of HDAC3 could counteract the increased mRNA levels of chondrogenic genes (COL2A1, SOX9, Agg, and Prg4) induced by miR-326 mimics in OA chondrocytes; (d) the dual luciferase gene report confirmed the targeting relationship between miR-326 and HDAC3; (e) overexpression of HDAC3 could reverse the reduction of proinflammatory factors (IL-1β, IL-18, IL-6, and TNF-α) in OA chondrocyte culture medium induced by miR-326 mimics; (f) Overexpression of HDAC3 could reverse the decrease of DNA-binding activity of NF-κB p65 in OA chondrocytes induced by miR-326 mimics; (g) overexpression of HDAC3 could reverse the decrease of Caspase-1 activity in OA chondrocytes induced by miR-326 mimics; (h) immunofluorescence results showed that overexpression of HDAC3 could reverse the decrease level of GSDMD and cleaved Caspase-1 in OA chondrocytes induced by miR-326 mimics; (i) Western blot results showed that overexpression of HDAC3 could counteract the activation of STAT1/NF-κB p65 signaling pathway in OA chondrocytes induced by miR-326 mimics; (j) Western blot results showed that overexpression of HDAC3 could reverse the decrease level of pyroptosis-related proteins (NLRP3, ASC, GSDMD, Caspase-1, IL-1β, and IL-18) in OA chondrocytes induced by miR-326 mimics; , .

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