Abstract
The aim of this study was to assess the anti-inflammatory and anti-apoptotic effects of KIOM-2015EW, the hot-water extract of maple leaves in hyperosmolar stress (HOS)-induced human corneal epithelial cells (HCECs). HCECs were exposed to hyperosmolar medium and exposed to KIOM-2015EW with or without the hyperosmolar media. Tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 production and apoptosis were observed, and the activation of mitogen-activated protein kinases (MAPKs) including extracellular signal regulated kinase (ERK), p38 and c-JUN N-terminal kinase (JNK) signaling and nuclear factor (NF)-κB was confirmed. Compared to isomolar medium, the induction of cell cytotoxicity significantly increased in HCECs exposed to hyperosmolar medium in a time-dependent manner. KIOM-2015EW-treatment significantly reduced the mRNA and protein expression of pro-inflammatory mediators and apoptosis. KIOM-2015EW-treatment inhibited HOS-induced MAPK signaling activation. Additionally, the HOS-induced increase in NF-κB phosphorylation was attenuated by KIOM-2015EW. The results demonstrated that KIOM-2015EW protects the ocular surface by suppressing inflammation in dry eye disease, and suggest that KIOM-2015EW may be used to treat several ocular surface diseases where inflammation plays a key role.
Highlights
Dry eye syndrome (DES) is a common ocular surface disease attributable to disorders of the tear film and ocular surface [1]
Assay; (B) human corneal epithelial cells (HCECs) were exposed to 450 milliosmoles F-12/ Dulbecco’s Modified Eagle Medium for 24 h, and cell viability measured by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium (DMEM) serum-free media for the indicated time, and cell viability measured by cell counting kit Bromide) assay; (B) HCECs were exposed to 450 milliosmoles F-12/ Dulbecco’s Modified (CCK)-8 assay
IL-6 were significantly by orientin, isoorientin and vitexin
Summary
Dry eye syndrome (DES) is a common ocular surface disease attributable to disorders of the tear film and ocular surface [1]. Inadequate tear secretion and increased tear evaporation are the two major causes of DES. The two common mechanisms underlying the pathogenesis of ocular surface injury in DES are ocular surface inflammation and increased tear hyperosmolarity [1,2,3,4,5,6]. An in vitro dry eye model induced by hyperosmotic stress (HOS) has been developed to investigate. HOS can result from decreased tear secretion or increased tearevaporation [1,15]
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