Infusion of angiotensin II (AngII) to hyperlipidemic mice augments atherosclerosis and causes formation of abdominal aortic aneurysms (AAAs). Each of these AngII-induced vascular pathologies exhibit pronounced inflammation. Previous studies demonstrated that coplanar polychlorinated biphenyls (PCBs) promote inflammation in endothelial cells and adipocytes, two cell types implicated in AngII-induced vascular pathologies. The purpose of this study was to test the hypothesis that administration of PCB77 to male apolipoprotein E (ApoE) -/- mice promotes AngII-induced atherosclerosis and AAA formation. Male ApoE-/- mice were administered vehicle or PCB77 (49 mg/kg, i.p.) during week 1 and 4 (2 divided doses/week) of AngII infusion. Body weights and total serum cholesterol concentrations were not influenced by administration of PCB77. Systolic blood pressure was increased in AngII-infused mice administered PCB77 compared to vehicle (156 ± 6 vs 137 ± 5 mmHg, respectively). The percentage of aortic arch covered by atherosclerotic lesions was increased in AngII-infused mice administered PCB77 compared to vehicle (2.0 ± 0.4 vs 0.9 ± 0.1 %, respectively). Lumen diameters of abdominal aortas determined by in vivo ultrasound and external diameters of excised suprarenal aortas were increased in AngII-infused mice administered PCB77 compared to vehicle. In addition, AAA incidence increased from 47 to 85% in AngII-infused mice administered PCB77. Adipose tissue in close proximity to AAAs from mice administered PCB77 exhibited increased mRNA abundance of proinflammatory cytokines and elevated expression of components of the renin-angiotensin system (angiotensinogen, angiotensin type 1a receptor (AT1aR)). These results demonstrate that PCB77 augments AngII-induced atherosclerosis and AAA formation.
Previous research in experimental animals suggests that PUFA may improve resolution of periodontitis by inhibiting inflammation and modulating alveolar bone loss, but human data are limited. In the present study 65 patients with chronic periodontitis (mean age 43.9 ± 10.9, 37.8% female and 71.9% Caucasian) were randomized to receive 3 g of PUFA or placebo (PL). In addition, all patients received oral health instruction at weeks 0 and 16. Clinical periodontal measures (pocket depth, bleeding on probing, attachment loss and plaque index) and blood samples for serum and red blood cell fatty acids (FA), were collected at weeks 0, 8, 16 and 28 with data presented for weeks 0,8 and 16. PUFA subjects had significantly greater amounts of DHA and total PUFA in serum at week 8 and 16 when compared to week 0 or to PL at the corresponding time. Similar changes were seen with EPA, DHA and total PUFA in RBC membranes. Despite significant effects of PUFA supplementation on serum and RBC FA content, clinical measures were not significantly associated with lipid changes. These results suggest that PUFA administration may not enhance oral health outcomes in humans with periodontitis, or their effect is dwarfed by the impact of oral hygiene. This research was supported by NIH‐NCRR grant P20RR020145 and GCRC grant #M01RR02602.
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