Corneal diseases exhibit a high prevalence and are prone to cause blindness; 
furthermore, maintaining the morphology and ionic transporter expression in 
corneal endothelial cells (CECs) is crucial for treatment of these diseases. 
This study aimed to investigate the effects of the novel Rho associated 
coiled-coil containing protein kinase (ROCK) inhibitor, 
thiazovivin (2,4‑disubstituted thiazole, TZV), on human corneal 
endothelial‑to‑mesenchymal transition/epithelial‑to‑mesenchymal 
transition (EndMT/EMT), cell morphology, junction proteins and ionic transporter 
expression in human CECs (HCECs) in vitro and then to clarify the mechanisms of 
action of TZV. In the present study, primary HCECs were cultured in vitro and 
passaged. The expression levels of adhesion proteins (E‑cadherin and 
N‑cadherin), the EndMT/EMT marker, α smooth muscle  actin (α‑SMA), the tight 
junction protein, Zonula occludens-1 (ZO‑1), and the ionic transporter, 
Na+/K+‑ATPase, were detected by immunofluorescence. The proliferative ability of 
the HCECs was determined by CCK-8 assay. The mRNA expression of the 
EndMT/EMT‑inducing gene, Snail, was examined by RT‑PCR. The protein expression 
levels of ROCK1/2 were evaluated by western blot analysis. The HCECs were 
cultured with TZV at various concentrations (2, 4, or 6 µM) for different 
periods of time (24 or 48 h). We found that the the cell states of the HCECs 
co‑cultured with 4 µM TZV for 48 h reached the optimum, and corneal EndMT/EMT 
was inhibited, as evidenced by the significantly upregulated expression of ZO‑1 
and E‑cadherin, and the markedly downregulated expression of N‑cadherin and 
α‑SMA. Furthermore, the cells exhibited a normal, tightly connected hexagonal or 
pentagonal morphology. Additionally, the protein expression of ROCK1/2 and the 
mRNA expression of Snail were significantly decreased. However, there was no 
significant difference between the TZV‑treated and the control groups as regards 
HCEC proliferative ability. These findings suggested that the ROCK inhibitor, 
TZV (4 µM), was effective in improving the morphology, cell junctions and ionic 
transporter expression of HCECs by inhibiting EndMT/EMT, but had no effect on 
HCEC proliferation.