Establishing a Severe Corneal Inflammation Model in Rats Based on Corneal Epithelium Curettage Combined with Corneal Sutures

Welcome to establishing a renewable model of number star cell deficiency, and we have successfully established a model of number star cell deficiency caused by severe information through corneal epithelium scraping combined with corneal suturing. Due to the fact that the thickness of a red cornea is only one third death of a human eye, suturing on the corneal surface can easily cause perforation, which poses a high demand on our surgical skill. The model induces corneal inflammation without directly damaging the limbo epithelial stem cells, thereby promoting research into the effects and mechanisms of corneal inflammation on limbo epithelial stem cells.

This helps to observe the impact of severe inflammation on the biological mechanisms of limbo stem cells. To begin, arrange the surgical instruments including sterilized corneal rust ring remover, skin sampling marker, needle holders, plate layer knives, ophthalmic surgical scissors, and forceps on a working platform, select the female Sprague dolly rats aged seven to eight weeks and verify the absence of ocular surface lesions under a slit lamp. After anesthetizing, the rat disinfect the skin and hair around the eyes using iota four.

To establish the inflammation model, position the rat in the lateral decubitus position. Expose the eyeball under an operating microscope. Next, center a two millimeter skin sampling marker around the central pupil.

Using a corneal tree fine and corneal epithelial scraper, Scrape the inner corneal epithelium. Using 10.0 nylon wire, needle holder, ophthalmic surgical scissors, and forceps, Place three 120 degree corneal sutures about three millimeters from the limbus. After suturing, apply ofloxacin eye ointment to prevent infection.

Observe and photograph the cornea on days one, three, and seven, post-operation under a slit lamp magnified 10x lens. Score the level of ciliary body congestion. Assign zero points for no congestion, one point for congestion, less than one millimeter, two points for hyperemia between one and two millimeters, and three points for hyperemia above two millimeters.

Next, score the central corneal edema. Assign zero points for no edema. One point for edema with clear iris visibility, two points for edema with unclear iris visibility, and three points for edema obscuring the iris.

Similarly, score the paracentral corneal edema. Calculate the inflammation index by summing all scores and dividing by nine. Using a slit lamp, observe the corneal neovascularization.

Analyze and process images using the slit lamp image processing software. Record the growth of corneal neovascularization at each observation time point, measuring the longest corneal neovascularization towards the central cornea with minimal curvature. Grade the extent of corneal neovascularization.

The healing of the corneal epithelium was impaired in the corneal central epithelium excision model with suturing as indicated by the incomplete healing by day seven, along with corneal limbal edema and neovascularization visible by day three. As inflammation progressed, corneal neovascularization and the inflammation index showed continuous increases.