In Vitro Effect of Propofol on the Expression of Genes Involved in Inflammation and Apoptosis in Corneal Activated Keratocytes

Abstract

Purpose: We investigated the effect of propofol (0.5, 5, and 50 μM) on the gene expression of inflammatory cytokines [IL-1β, IL-6, transforming growth factor β (TGF-β), and LIF] and apoptosis process (BCL-2 and Bax) in corneal activated keratocytes (CAKs). Methods: CAKs (106 cells/10 cm2) were exposed to propofol at a concentration of 0.5, 5, and 50 μM for 24 hours at 37°C. The control group did not receive propofol at the same time or under the same condition. Ribonucleic acid (RNA) extraction, complementary DNA (cDNA) synthesis, and real-time polymerase chain reaction (PCR) were performed to quantify the relative expression of IL-1β, IL-6, TGF-β, LIF, BCL-2, and Bax expression in the treated versus control cells. Result: The results of this study showed that propofol treatment (0.5 and 5 μM) led to the downregulation of IL-1β and IL-6 gene expression in CAKs. TGF-β (with a role in fibrogenesis) was not changed in 0.5 and 5 μM propofol-treated CAKs, whereas CAKs treated with 50 μM propofol showed upregulation of the TGF-β gene. LIF (with a role in regeneration) was upregulated in 0.5 and 5 μM propofol-treated CAKs. The BCL-2/Bax ratio (as the antiapoptosis index) was increased in CAKs treated with 0.5 μM propofol and indicated the induction of an antiapoptotic effect. Conclusions: We showed that CAKs treatment with propofol, at concentrations of 0.5 and 5 μM, could decrease the expression of genes related to inflammation and enhance the genes associated with cell regeneration. While 50 μM propofol treatment might induce CAK fibrogenesis. This proof-of-concept study could preserve a groundwork for future drug design for the treatment of corneal stromal diseases and ocular regenerative medicine.