Deficiency of IKKɛ inhibits inflammation and induces cardiac protection in high-fat diet-induced obesity in mice

• DOI: 10.3892/ijmm.2014.1746
• Publication Date: 2014-04-25T09:40:13Z
• Authors: CHANGCHUN CAO; LIANGPENG LI; WEN CHEN; YIFAN ZHU; YONGCHAO QI; XIAODI WANG; XIN WAN; XIN CHEN
• Keywords: Inflammation; Male; Mice, Knockout; 0301 basic medicine; 2. Zero hunger; Myocardium; Cholesterol, HDL; Gene Expression; Cholesterol, LDL; Diet, High-Fat; Dietary Fats; I-kappa B Kinase; 3. Good health; Mice; 03 medical and health sciences; Apolipoproteins E; Animals; Female; Obesity; Triglycerides

Immune response and metabolic regulation have been recognized as a central homeostatic mechanism, the dysfunction of which can trigger cluster chronic disorders, particularly obesity, type Ⅱ diabetes cardio­vascular disease. Serine/threonine kinase IκB (IKK) ε is multifunctional regulator that participates in immune regulation, cell proliferation transformation, oncogenesis. In present study, we investigated role IKKε cardiovascular disorders using murine models apolipo­protein E‑deficient [ApoE(-/-)] mice ApoE/IKKε double‑knockout [ApoE(-/-)/IKKε(-/-)]mice, were fed normal diet (ND) high-fat (HFD) for 12 weeks, respectively. Results this study showed mouse obesity correlated vivo with an increased expression IKKε. Additionally, low‑grade inflammation cardiac tissue was evident ApoE(-/-) mice, but markedly reduced ApoE(-/-)/IKKε(-/-) mice. However, serum lipid levels group not significantly higher than those group. Furthermore, immunofluorescence western blot analysis demonstrated increases nuclear factor-κB (NF-κB) pathway components downstream factors group, while these blocked Taken together, data indicate deficiency prevented inflammatory hearts ND HFD, respectively, suggesting may play HFD-induced obese serve novel target treatment variety metabolism-associated diseases.