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. 2020 Mar 26;16(11):1798–1810. doi: 10.7150/ijbs.39947

Figure 6.

Figure 6

COX-2 deletion abolished the effect of HMGA1 overexpression and STAT3 agonist reversed the role of HMGA1 silence. (A-C): H9c2 cardiomyocytes were transfected with AAV9-HMGA1 then stimulated with LPS and treated with celecoxib (COX-2 inhibitor). (A)RT-PCR analyses for transcriptional level of inflammatory cytokines (TNF-α, IL-1, IL-6) in each group (n = 6). (B)TUNEL staining results for the detection of the apoptosis-positive cells in each group (n =6). (C) The protein expression level of pro-apoptotic cytochrome C was examined by western blotting and was normalized to GAPDH (n=6). *P<0.05 vs. the LPS group; #P<0.05 vs. the AAV9-HMGA1+LPS group. The data were shown as the mean±SD and were compared by one-way ANOVA with Tukey post hoc analysis. (D-F): H9c2 cardiomyocytes were processed with siHMGA1 then stimulated with LPS and treated with colivelin (a STAT3 agonist, 1uM). (D) RT-PCR analyses for transcriptional level of inflammatory cytokines (TNF-α, IL-1, IL-6) in each group (n = 6). (E)The apoptotic cells in each group were detected by TUNEL staining (n =6). (F) Western blotting result for the detection of cytochrome C and the expression level was normalized to GAPDH in each group (n=6). *P<0.05 vs. the LPS group; #P<0.05 vs. the si-HMGA1+LPS group. The data were shown as the mean±SD and were compared by one-way ANOVA with Tukey post hoc analysis.