Department of Ophthalmology, Xiang'an Hospital of Xiamen University, Xiamen, Fujian, China.
Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Xiamen, Fujian, China.
Invest Ophthalmol Vis Sci. 2021 Aug 2;62(10):13. doi: 10.1167/iovs.62.10.13.
To determine if a high-fat diet (HFD) induces meibomian gland (MG) inflammation in mice.
Male C57BL/6J mice were fed a standard diet (SD), HFD, or HFD supplemented with the peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist rosiglitazone for various durations. Body weight, blood lipid levels, and eyelid changes were monitored at regular intervals. MG sections were subjected to hematoxylin and eosin staining, LipidTox staining, TUNEL assay, and immunostaining. Quantitative RT-PCR and western blot analyses were performed to detect relative gene expression and signaling pathway activation in MGs.
MG acinus accumulated more lipids in the mice fed the HFD. Periglandular CD45-positive and F4/80-positive cell infiltration were more evident in the HFD mice, and they were accompanied by upregulation of inflammation-related cytokines. PPAR-γ downregulation accompanied activation of the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways in the HFD mice. There was increased acini cell apoptosis and mitochondria damage in mice fed the HFD. MG inflammation was ameliorated following a shift to the standard diet and rosiglitazone treatment in the mice fed the HFD.
HFD-induced declines in PPAR-γ expression and MAPK and NF-κB signaling pathway activation resulted in MG inflammation and dysfunction in mice.
确定高脂肪饮食（HFD）是否会引起小鼠的睑板腺（MG）炎症。
雄性 C57BL/6J 小鼠分别喂食标准饮食（SD）、HFD 或 HFD 补充过氧化物酶体增殖物激活受体γ（PPAR-γ）激动剂罗格列酮，持续不同时间。定期监测体重、血脂水平和眼睑变化。对 MG 切片进行苏木精和伊红染色、脂质染色、TUNEL 检测和免疫染色。进行定量 RT-PCR 和 Western blot 分析，以检测 MGs 中的相对基因表达和信号通路激活情况。
HFD 喂养的小鼠中，MG 腺泡内积累了更多的脂质。HFD 组小鼠的围腺 CD45 阳性和 F4/80 阳性细胞浸润更为明显，同时伴有炎症相关细胞因子的上调。HFD 组小鼠中 PPAR-γ 下调伴随着丝裂原活化蛋白激酶（MAPK）和核因子 kappa B（NF-κB）信号通路的激活。HFD 喂养的小鼠中，腺泡细胞凋亡和线粒体损伤增加。HFD 喂养的小鼠转为标准饮食和罗格列酮治疗后，MG 炎症得到改善。
HFD 诱导的 PPAR-γ 表达下降以及 MAPK 和 NF-κB 信号通路的激活导致了小鼠的 MG 炎症和功能障碍。
