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. 2019 Dec 8;25:9346–9356. doi: 10.12659/MSM.917287

Figure 3.

Figure 3

Knockdown of SYK reduced peritoneal mesothelial cell (PMC) fibrosis and inflammation in conditions of high glucose. (A, B) After knockdown of SYK and pretreating the rat PMCs with the SYK inhibitor, SYK expression was significantly reduced. ** P<0.01 vs. shNC. * P<0.05 vs. control. (C) High glucose treatment promoted upregulation of SYK, but the effect was significantly reversed after knockdown of SYK or pretreatment with SYK inhibitor. (D) High glucose treatment induced the transformation of peritoneal mesothelial cells to fibroblast-like cells, which was blocked by knockdown of SYK or pretreatment with the SYK inhibitor. Scale bar, 500 μm. (E) High glucose treatment induced the release of inflammatory cytokines, and the release of these factors was significantly reduced after knockdown of SYK or pretreating PMCs with its inhibitor. ** P<0.01 and *** P<0.001 vs. control. ** P<0.01 and *** P<0.001 vs. HG. * P<0.05 and ** P<0.01 vs. HG+shNC. (F) High glucose treatment promoted the upregulated expression of α-SMA, collagen I, vimentin, and VEGF-A, while the expression of E-cadherin was significantly inhibited. However, this effect was reversed after knockdown of SYK or pretreatment with its inhibitor. All experiments were independently conducted in triplicate. HG – high glucose.