Abstract
The effects of each subtype-selective peroxisome proliferator activated receptor (PPAR) agonist (α, β/δ, γ) on corneal epithelial wound healing were investigated using a rat corneal alkali burn model. After the alkali burn, each PPAR agonist or vehicle ophthalmic solution was instilled topically onto the rat’s cornea. Corneal epithelial healing processes were evaluated by fluorescein staining. Pathological analyses and real-time reverse transcription polymerase chain reactions were performed to evaluate Ki67 (proliferative maker) expression and inflammatory findings. The area of the corneal epithelial defect at 12 h and 24 h after the alkali burn was significantly smaller in each PPAR group than in the vehicle group. Ki67 mRNA expression was increased in the PPARβ/δ group, whereas mRNA expressions of inflammatory cytokines were suppressed in all of the PPAR agonist groups. Nuclear factor kappa B (NF-κB) was the most suppressed in the PPARγ group. The accelerated corneal epithelial healing effects of each PPAR ligand were thought to be related to the promotion of proliferative capacity and inhibition of inflammation.
Highlights
The peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptors belonging to the steroid hormone receptor superfamily [1,2,3]
Corneal epithelial defects were created by an alkali burn, and the vehicle ophthalmic solution or one of each PPAR agonist
The involvement of PPARs in wound healing has often been reported in the field of dermatology [16]
Summary
The peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptors belonging to the steroid hormone receptor superfamily [1,2,3]. PPARs consist of three main subtypes: α, β/δ, and γ [1]. The PPARs are involved in glucose and lipid metabolism in humans [1,2]. PPAR agonists play important roles in adipocyte differentiation and lipid metabolism [4]. Whereas PPARα and PPARγ agonists are widely recognized as drugs for dyslipidemia and diabetes [5,6], several studies have reported that PPARs have roles in the transcriptional regulation of metabolism, and in inflammation, angiogenesis, and fibrotic reactions [7,8]. Activation of all subtypes of PPARs has been reported to suppress inflammation via inhibition of NF-κB [9,10].
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