Dataset Information

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

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.

SUBMITTER: Hyun SW

PROVIDER: S-EPMC6384987 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:To reveal the accumulation pattern of cyanogenic glycosides (amygdalin and prunasin) in bitter apricot kernels to further understand the metabolic mechanisms underlying differential accumulation during kernel development and ripening and explore the association between cyanogenic glycoside accumulation and the physical, chemical and biochemical indexes of fruits and kernels during fruit and kernel development, dynamic changes in physical characteristics (weight, moisture content, linear dimensions, derived parameters) and chemical and biochemical parameters (oil, amygdalin and prunasin contents, β-glucosidase activity) of fruits and kernels from ten apricot (Prunus armeniaca L.) cultivars were systematically studied at 10 day intervals, from 20 days after flowering (DAF) until maturity. High variability in most of physical, chemical and biochemical parameters was found among the evaluated apricot cultivars and at different ripening stages. Kernel oil accumulation showed similar sigmoid patterns. Amygdalin and prunasin levels were undetectable in the sweet kernel cultivars throughout kernel development. During the early stages of apricot fruit development (before 50 DAF), the prunasin level in bitter kernels first increased, then decreased markedly; while the amygdalin level was present in quite small amounts and significantly lower than the prunasin level. From 50 to 70 DAF, prunasin further declined to zero; while amygdalin increased linearly and was significantly higher than the prunasin level, then decreased or increased slowly until full maturity. The cyanogenic glycoside accumulation pattern indicated a shift from a prunasin-dominated to an amygdalin-dominated state during bitter apricot kernel development and ripening. β-glucosidase catabolic enzyme activity was high during kernel development and ripening in all tested apricot cultivars, indicating that β-glucosidase was not important for amygdalin accumulation. Correlation analysis showed a positive correlation of kernel amygdalin content with fruit dimension parameters, kernel oil content and β-glucosidase activity, but no or a weak positive correlation with kernel dimension parameters. Principal component analysis (PCA) showed that the variance accumulation contribution rate of the first three principal components totaled 84.56%, and not only revealed differences in amygdalin and prunasin contents and β-glucosidase activity among cultivars, but also distinguished different developmental stages. The results can help us understand the metabolic mechanisms underlying differential cyanogenic glycoside accumulation in apricot kernels and provide a useful reference for breeding high- or low-amygdalin-content apricot cultivars and the agronomic management, intensive processing and exploitation of bitter apricot kernels.

Project description:Sjögren syndrome (SS) is an autoimmune condition that targets the salivary and lacrimal glands, with cardinal clinical signs of dry eye (keratoconjunctivitis sicca, KCS) and dry mouth. The conjunctiva of SS patients is often infiltrated by immune cells that participate in the induction and maintenance of local inflammation. The purpose of this study was to investigate immune-related molecular pathways activated in the conjunctiva of SS patients. Female SS patients (n=7) and controls (n=19) completed a series of oral, ocular surface exams. Symptom severity scores were evaluated using validated questionnaires (OSDI and SANDE). All patients fulfilled the ACR/EULAR criteria for SS and the criteria for KCS. Fluorescein and lissamine green dye staining evaluated tear-break-up time (TBUT), corneal and conjunctival disease, respectively. Impression cytology of the temporal bulbar conjunctiva was performed to collect cells lysed and subjected to gene expression analysis using the NanoString Immunology Panel. 53/594 differentially expressed genes (DEGs) were observed between SS and healthy controls; 49 DEGs were upregulated, and 4 were downregulated (TRAF5, TGFBI, KLRAP1, and CMKLRI). The top 10 DEGs in descending order were BST2, IFITM1, LAMP3, CXCL1, IL19, CFB, LY96, MX1, IL4R, CDKN1A. Twenty pathways had a global significance score greater or equal to 2. Spearman correlations showed that 29/49 upregulated DEGs correlated with either TBUT (inverse) or OSDI or conjunctival staining score (positive correlations). Venn diagrams identified that 26/29 DEGs correlated with TBUT, 5/26 DEGs correlated with OSDI, and 16/26 correlated with conjunctival staining scores. Five upregulated DEGs (CFB, CFI, IL1R1, IL2RG, IL4R) were uniquely negatively correlated with TBUT. These data indicate that the conjunctiva of SS patients exhibits a phenotype of immune activation, although some genes could be inhibitory. Some of the DEGs and pathways overlap with previous DEGs in salivary gland biopsies, but new DEGs were identified, and some of these correlated with symptoms and signs of dry eye. Our results indicate that gene analysis of conjunctiva imprints is a powerful tool to understand the pathogenesis of SS and develop new therapeutic targets.

Project description:Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM2.5 (<2.5 μm) and ozone exposures have been shown to associate with carotid intima media thickness in humans. Animal studies support a causal relationship between air pollution and atherosclerosis and identified adverse PM effects on HDL functionality. We aimed to determine whether brief exposures to PM2.5 and/or ozone could induce effects on HDL anti-oxidant and anti-inflammatory capacity in humans.Subjects were exposed to fine concentrated ambient fine particles (CAP) with PM2.5 targeted at 150 μg/m(3), ozone targeted at 240 μg/m(3) (120 ppb), PM2.5 plus ozone targeted at similar concentrations, and filtered air (FA) for 2 h, on 4 different occasions, at least two weeks apart, in a randomized, crossover study. Blood was obtained before exposures (baseline), 1 h after and 20 h after exposures. Plasma HDL anti-oxidant/anti-inflammatory capacity and paraoxonase activity were determined. HDL anti-oxidant/anti-inflammatory capacity was assessed by a cell-free fluorescent assay and expressed in units of a HDL oxidant index (HOI). Changes in HOI (ΔHOI) were calculated as the difference in HOI from baseline to 1 h after or 20 h after exposures.There was a trend towards bigger ΔHOI between PM2.5 and FA 1 h after exposures (p = 0.18) but not 20 h after. This trend became significant (p <0.05) when baseline HOI was lower (<1.5 or <2.0), indicating decreased HDL anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM2.5 on the change in HOI at both time points. The change in HOI due to PM2.5 showed a positive trend with particle mass concentration (p = 0.078) and significantly associated with the slope of systolic blood pressure during exposures (p = 0.005).Brief exposures to concentrated PM2.5 elicited swift effects on HDL anti-oxidant/anti-inflammatory functionality, which could indicate a potential mechanism for how particulate air pollution induces harmful cardiovascular effects.

Dataset Information

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

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets