Cornea absorbs most of daily ultraviolet (UV) light. An excess of UV damages results in not only keratopathy and cataract but also maculopathy. It has been reported that thymosin beta-4 (Tβ 4) promotes wound healing, decreases inflammatory response and prevents apoptosis of corneal epithelial cells. However, it is not clear whether Tβ 4 protects UVB-induced corneal injury, particularly in corneal endothelial cells because of its non-proliferation in nature. The purpose of this study is to compare the protective effects of Tβ 4 on bovine corneal endothelial (BCE) cells from low- and high-dose UVB damage. In this study, 1 μg/ml of Tβ 4 was added to BCE cells 2 h before low (12.5 mj/cm 2) or high dosage (100 mj/cm 2) UVB exposure. Using a fluorogenic substrate cleavage assay, we found that Tβ 4 diminished the reactive oxygen species level in BCE cells elicited by UVB. However, the protection of viability by Tβ 4 could only be detected under low-dose UVB exposure. Moreover, both caspase-9 activity and annexin V/propidium iodine staining demonstrated that Tβ 4 only protected BCE cells from low-dose UVBinduced apoptosis but not high-dose UVB-induced necrosis. Together, Tβ 4 protected corneal endothelial cells from UVB-induced oxidative stress and apoptosis after low-dose UVB exposure. The results support further investigation towards topical use or anterior chamber injection of this small hydrophilic peptide in treating and preventing UVB-induced corneal endothelial damage.
ASJC Scopus subject areas
- Physiology (medical)