Table 1.
Effects of BaP on AS.
| Models | Treatment | Effects | Reference | |
|---|---|---|---|---|
| Cell model | HUVECs | 1 μmol/L BaP for 2 h | pro-inflammation and enhance COX2, CYP1A1 and cPLA2 activity; ↑ CYP1A1, ICAM1, VCAM1, ↓PTGS2, PLA2G4A, NOS3 gene expression | (51) |
| 10–25 μmol/L for 24 h | ↑ monocyte adhesion and ICAM-1 depend on AhR activation, ↑ MEK, p38-MAPK, c-Jun phosphorylation; ↑ AP-1 DNA binding | (52) | ||
| 0.5–1.5 μmol/L BPDE for 96 h | ↑ apoptosis, necrosis, ↓ ERCC1, ERCC4 and ligase I, ↑ BPDE-DNA adducts | (17) | ||
| 0–10 μmol/L for 4 or 24 h | ↑ MCP1, CYPIA1, ↓ cell viability | (48) | ||
| 10 μmol/L for 1–5 d | ↑ VEGF, and can be reversed by ERK inhibitor | (53) | ||
| 10 μM for 24h | ↑ CCL1, CYP1A1 in an AhR- and calcium-dependent manner | (32) | ||
| Human endothelial progenitor cells | 10-50 μmol/L for 24 h | ↓ proliferation, migration, adhesion, and angiogenesis, ↑ IL1β, TNFα, ROS, ↑ NF-κB activation | (54) | |
| 0.1–10 μmol/L for 5–7 d | ↓ adherent and proliferation, ↑ CYP1A1, and reversed by AhR antagonist, ↑ PAH-related adducts | (55) | ||
| Human fetoplacental ECs | 0.01–1 μmol/L for 6–24 h | ↓ angiogenesis, ↑ COX2, PTGS2 mediated by AhR activation | (33) | |
| Human coronary artery ECs | 30 μmol/L for 0–140 min | ↑ 3H-arachidonate release and apoptosis, ↑ phospholipase A2 activation | (56) | |
| Mouse aortic endothelial cells | 1 μmol/L | ↑Cu/Zn- SOD and catalase, ↑AhR, CYP1A1/1B1 protein level; ↑ GST activity and BaP detoxification; | (31) | |
| Rat VSMCs | 10 μmol/L for 24 h | ↓ NO-induced apoptosis, ↑ NF-κB and MAPK, ↑ IL6 production | (57) | |
| 0.1–2 μmol/L for 24 h | ↑ cell migration and invasion, ↑ MMPs, and inhibited by MMPs inhibitor or AhR antagonist | (58) | ||
| 0–10 μmol/L for 0–30 h | ↓ T-cadherin, and reversed by AhR antagonist a-naphthoflavone | (59) | ||
| 0.1–5μmol/L for 24 h | ↑ COX2, prostaglandin, ERK phosphorylation, and NF-κB activation; reversed by MAPK or NF-κB inhibitor | (60) | ||
| 3 μmol/L for 24 h | ↑ C/EBP-α/β, ARE/EpRE repressed, whereas AhR enhanced, GST-Ya gene expression | (61) | ||
| Mouse VSMCs | 3 μmol/L for 24 h | ↑ DNA adducts, ↑ aryl hydrocarbon hydroxylase and CYP1B1 activity | (38) | |
| 3 μmol/L for 1–5 h | ↑ CYP1A1, CYP1B1 and reversed by AhR knockout | (36) | ||
| 0.03–3 μmol/L for 24 h | ↑ ROS, ARE/EpRE, ↓ c-Ha-ras transcription | (62) | ||
| 0.3–2μmol/L for 1–5 h | ↑ c-Ha-ras and oxidative stress; inhibited by P450 or AhR inhibitor ellipticine | (63) | ||
| 10 μM for 24 h | TGFβ2 and IGF1 are potential candidates signaling pathways of AhR | (64) | ||
| HAECs, HCSMCs | 3μmol/L for 24 h | ↓ prolyl-4-hydroxylase, ↓ cellular collagen levels, atherosclerotic cap thickness | (65) | |
| Animal models | ApoE−/− mice | 5 mg/kg/bw daily for 4 d | ↑ aorta BPDE-DNA adduct, epsilon A, and HDL level | (47) |
| 5 mg/kg/bw, weekly for 2 w | ↑ aortic tissue MCP1 gene expression | (48) | ||
| 5 mg/kg/bw, weekly for 12–24 w | ↑ plaques and lipid core size; ↑ T cells and macrophages infiltration; | (49) | ||
| 5 mg/kg/bw, weekly for 24 w | ↑ PAH-DNA adducts in lung, ↑ TGFβ and TNFα release, ↑ atherosclerotic plaque size | (50) | ||
| 8.5 mg/kg/bw daily for 24 w | ↑ inflammatory response, ↑ atherosclerosis lesion size | (13) | ||
| ApoE−/− mice; CYP1A1−/− mice | 12.5 mg/kg/day | ↑ atherosclerotic lesions, ↑ ROS level, ↑ inflammatory markers; ↑ VEGF gene expression, ↑ DNA adduct formation | (39) | |
| ApoE−/−;AhRb1/b1 and ApoE−/−;AhRd/d | 10 mg/kg/bw, 5 days/week for 10–23 w | ↑(↓) plaque size and initial time, ↑(↓) AhR affinity, ↑(↓) immune response genes | (40) | |
| ApoE−/−;hSod1−/− mice | 2.5 mg/kg/bw weekly for 24 w | ↑ oxidized lipids, ↑ atherosclerotic lesions; and ↓ cell adhesion molecules, monocyte adhesion, ↓ oxidized lipids, ↓atherosclerotic lesions | (66) |
“↑” means up-regulation and “↓” means down-regulation; human aortic endothelial cells (HAECs); human coronary artery smooth muscle cells (HCSMCs); unless noted the treatment agent is BaP in all Tables.