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Polychlorinated Biphenyl Quinone Promotes Atherosclerosis through Lipid Accumulation and Endoplasmic Reticulum Stress via CD36.

Polychlorinated biphenyls (PCBs) are persistent organic environmental pollutants. According to previous epidemiological reports, PCBs exposure is highly related to atherosclerosis. However, few studies of PCBs metabolites and atherosclerosis and corresponding mechanism studies are scarce. In this study, we evaluated a quinone-type PCB metabolite, namely 2,3,5-trichloro-6-phenyl- [1,4] -benzoquinone (PCB29-pQ), on the promoting of atherosclerosis. Aortic plaques were increased in PCB29-pQ-treated ApoE-/- mice [5 mg/kg body weight, intraperitoneally (i.p.) injection once a week for twelve continuously weeks, high-fat feeding]. We observed lipids accumulation and the release of pro-inflammatory factors, interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in ApoE-/- mice. In addition, we found that PCB29-pQ promoted the levels of total cholesterol (TC), free cholesterol (FC), triglyceride (TG), and cholesteryl ester (CE). Mechanism investigation indicated that PCB29-pQ induces the activation of three branches of endoplasmic reticulum (ER) stress response, i.e., phosphorylated protein kinase R-like ER kinase (p-PERK), eukaryotic translation initiation factor 2α (eIF2α) and transcription factor 6 (ATF6), which is responsible for downstream necrosis. More importantly, we found the silence of CD36 is able to reverse PCB29-pQ-induced adverse effects completely. Overall, our results suggested that PCB29-pQ achieves lipid accumulation, ER stress response, apoptosis and the release of pro-inflammatory cytokines via CD36, ultimately leading to atherosclerosis.