Effects of transforming growth factor-beta1 on tumor necrosis factor-alpha expression of corneal allografts during acute immunological rejection in rats

ABSTRACT

BACKGROUND:

Al ogeneic penetrating keratoplasty is the most effective method for treating corneal blindness. However, the incidence of rejections is high after keratoplasty, so it is urgent to develop an immunosuppressive drug with high efficacy and low toxicity.

To establish al ogeneic penetrating keratoplasty models and monitor the expression of tumor necrosis factor-αin blank control group and after transforming growth factor-β1 eyedrop during acute rejection period of corneal grafts.

Al ogeneic penetrating keratoplasty models were established and were randomly divided into blank control group, ciclosporin A group (1%ciclosporin A), and transforming growth factor-β1 group (1μg/ml transforming growth factor-β1 eyedrop). The medications from each group commenced at 1 day after surgery, one eyedrop once, three eyedrops per day. Al the operated eyes were given 0.3%ofloxacin ophthalmic solutions and 0.5%tropicaide ophthalmic solution, three times per day, for 12 days. The corneal grafts were harvested for hematoxylin-eosin staining and immunihistochemical staining (SABC method), to detect tumor necrosis factor-αexpression in corneal grafts. RESULTS AND

Hematoxylin-eosin staining showed that, corneal grafts were significantly thickened, a large number of histoleucocytes and lymphocytes infiltrated in the blank control group;corneal grafts showed normal thickness and no inflammatory cel s infiltrated in the transforming growth factor-β1 group. Immunohistochemical staining showed that, there were less cel s positive for tumor necrosis factor-αin the transforming growth factor-β1 group compared with the blank control group (P<0.05). Transforming growth factor-β1 eyedrops can reduce the expression of tumor necrosis factor-αin the corneal grafts during acute rejection period, and reduce the inflammatory cel s infiltration in the corneal grafts, which is probably the mechanism of transforming growth factor-β1 to prevent and treat corneal al ograft rejection.