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

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 (10 6 cells/10 cm 2 ) 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.