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. 2021 Aug 25;24(5):744. doi: 10.3892/mmr.2021.12384

Figure 6.

Figure 6.

Protein O-GlcNAc levels interfere with the phosphorylation of p38 MAPK, ERK1/2 and CaMKII. (A) Protein levels of O-GlcNAc, OGA, OGT, p-p38 MAPK, p-ERK1/2 and p-CaMKII in cultured aortas that received either AON or AIH treatment in the presence of DMSO, PugNAc or ST045849. (B) Protein levels of O-GlcNAc, OGA, OGT, p-p38 MAPK, p-ERK1/2 and p-CaMKII in cultured aortas from the CON or CIH rats in the presence of DMSO, PugNAc or ST045849. Experimental groups were as follows: i) AON, 3-h normoxia treatment; ii) AIH, 3-h intermittent hypxia treatment; iii) CON, normoxic (21% O2) condition; and iv) CIH, intermittent hypoxia cycles (6–8% O2 for 2 min and 21% O2 for 2 min). Data are presented as the mean ± SD (n=3). *P<0.05. O-GlcNAc, O-linked-β-N-acetylglucosamine; CaMKII, Ca2+/calmodulin-dependent kinase II; OGA, O-GlcNAcase; OGT, O-GlcNAc transferase; AIH, acute intermittent hypoxia; CON, control; CIH, chronic intermittent hypoxia; p-, phosphorylated; t-, total protein.