高脂血症
内分泌学
内科学
心脏病学
医学
病态的
生理学
糖尿病
出处
期刊:Oral Diseases
[Wiley]
日期:2022-06-29
卷期号:29 (8): 3640-3653
被引量:3
摘要
We explored whether hyperlipidemia or combination of hyperlipidemia and E2 could induce TMJOA.Four groups of female rats were treated with normal diet, normal diet with E2, high-fat diet, and high-fat diet with E2 (HFD/E2), respectively, to induce TMJOA till 8 weeks. Another three groups were then used for COX2 inhibitor celecoxib to block the induction of TMJOA. Primary condylar chondrocytes were treated with combination of E2, ox-LDL, and corresponding inhibitors for evaluating expressions of related molecules.Condylar cartilage proliferation with plenty of chondrocyte apoptosis and increased staining for LOX1, nuclear NF-κB, IL-1β, and COX2 at 4 weeks and decreased condylar cartilage and increased subchondral bone density at 8 weeks were observed only in the HFD/E2 group. Celecoxib significantly alleviated the cartilage proliferation and apoptosis in the HFD/E2 group. Serum ox-LDL increased in both high-fat diet groups, while serum IL-1β increased only in the HFD/E2 group. Combination of E2 and ox-LDL synergistically induced expressions of LOX1, phosphorylated NF-κB, IL-1β, and COX2, while LOX1 inhibitor blocked the induction of phosphorylated NF-κB, and NF-κB inhibitor the induction of IL-1β, and IL-1β inhibitor the induction of COX2.Combination of hyperlipidemia and E2-induced TMJOA-like pathological changes through LOX1/NF-κB/IL-1β/COX2-signaling pathway.
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