Research Article
BTK Promotes Atherosclerosis by Regulating Oxidative Stress, Mitochondrial Injury, and ER Stress of Macrophages
Figure 4
BTK knockdown suppressed the ox-LDL-induced NK-κB activation and inhibited M1 polarization. (a) The phosphorylation level of p65 protein was significantly reduced by the knockdown of BTK. (b) BTK knockdown inhibited the nucleus translocation of p65 in macrophages. (c) BTK knockdown reduced the number of M1 macrophages and significantly increased the M2 anti-inflammatory macrophages. (d) iNOS was downregulated, while COX-2 was upregulated on the mRNA level caused by BTK knockdown. (e) The knockdown of BTK significantly reduced the protein expression level of phosphorylated IRF3. The threshold of statistical significance was set at .
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