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杏仁核提取物和苦杏仁苷抑制城市颗粒物诱导的干燥性角膜结膜炎。

Apricot Kernel Extract and Amygdalin Inhibit Urban Particulate Matter-Induced Keratoconjunctivitis Sicca.

机构信息

Herbal Medicine Research Division, Korea Institute of Oriental Medicine, Daejeon 34054, Korea.

Department of Oral Pathology, School of Dentistry, Chonbuk National University, Jeonju 54896, Korea.

出版信息

Molecules. 2019 Feb 12;24(3):650. doi: 10.3390/molecules24030650.

DOI:10.3390/molecules24030650
PMID:30759852
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6384987/
Abstract

Exposure to particulate matter is a risk factor for various ocular surface diseases, including keratoconjunctivitis sicca (KCS). In this study, we investigated the protective effects of apricot kernel extract (AKE) and its bioactive compound, amygdalin, on KCS induced by exposure to urban particulate matter (UPM). In the in vivo experiments, eye drops containing 0.5 mg/mL AKE (AKE-0.5) or 1 mg/mL AKE (AKE-1) were administered directly into the eyes of female rats after UPM exposure. Additionally, the effect of AKE and amygdalin on matrix metalloproteinases (MMPs) activity and the expressions of inflammatory factors, including tumor necrosis factor (TNF)-α and interleukin (IL)-6, was investigated in conjunctival epithelial cells in vitro. Topical administration of AKE-1 attenuated UPM exposure-induced reduction of tear secretion. Both AKE-0.5 and AKE-1 inhibited UPM exposure-induced corneal epithelial damage and irregularity. AKE also protected against UPM exposure-induced disruption of the mucin-4 layer on the ocular surface. In addition, AKE and amygdalin prevented UPM-induced activation of MMPs and upregulation of TNF-α and IL-6 in conjunctival epithelial cells. Therefore, AKE may have protective effects against UPM exposure-induced KCS via the inhibition of MMPs and inflammation. The pharmacological activities of AKE may be in part due to its bioactive compound, amygdalin.

摘要

颗粒物暴露是各种眼表疾病的一个风险因素，包括干眼症（KCS）。在这项研究中，我们研究了杏仁核提取物（AKE）及其生物活性化合物苦杏仁苷对暴露于城市颗粒物（UPM）引起的 KCS 的保护作用。在体内实验中，在 UPM 暴露后，直接将含有 0.5mg/mL AKE（AKE-0.5）或 1mg/mL AKE（AKE-1）的眼药水滴入雌性大鼠的眼睛中。此外，还研究了 AKE 和苦杏仁苷对体外结膜上皮细胞中基质金属蛋白酶（MMPs）活性和炎症因子，包括肿瘤坏死因子（TNF）-α和白细胞介素（IL）-6 的表达的影响。局部给予 AKE-1 可减轻 UPM 暴露引起的泪液分泌减少。AKE-0.5 和 AKE-1 均可抑制 UPM 暴露引起的角膜上皮损伤和不规则。AKE 还可防止 UPM 暴露引起的眼表面黏蛋白-4 层的破坏。此外，AKE 和苦杏仁苷可防止 UPM 诱导的 MMPs 激活以及 TNF-α和 IL-6 在结膜上皮细胞中的上调。因此，AKE 可能通过抑制 MMPs 和炎症对 UPM 暴露引起的 KCS 具有保护作用。AKE 的药理学活性可能部分归因于其生物活性化合物苦杏仁苷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/04d776886452/molecules-24-00650-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/23388cf10226/molecules-24-00650-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/a90ee144e5db/molecules-24-00650-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/82f1bf0d512e/molecules-24-00650-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/3d284b54c6f5/molecules-24-00650-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/d561a0f0bffa/molecules-24-00650-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/04d776886452/molecules-24-00650-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/23388cf10226/molecules-24-00650-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/a90ee144e5db/molecules-24-00650-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/82f1bf0d512e/molecules-24-00650-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/3d284b54c6f5/molecules-24-00650-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/d561a0f0bffa/molecules-24-00650-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3590/6384987/04d776886452/molecules-24-00650-g006a.jpg

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