Diabetes mellitus (DM) often causes ocular disorders leading to vision loss.
Metformin is commonly prescribed for
type 2 diabetes. This study assessed the effect of
metformin on hyperglycemic histopathological
eye abnormalities and some possible pathways involved. Male rats were divided into 3 groups (N = 6), namely, healthy control, hyperglycemic non-treated control, and hyperglycemic rats treated with 200 mg/kg
metformin. Two weeks after diabetes induction by an intraperitoneal
streptozotocin (60 mg
streptozotocin (STZ)/kg) injection, the rats develop ocular abnormalities, and
metformin (200 mg/kg) treatment was administered daily. Rats underwent dilated
retinal digital ophthalmoscope examination and graded for
diabetic retinopathy. Rats were sacrificed at 12 weeks, and the cornea, lens, sclera, ciliary body, iris, conjunctiva,
retinal, and optic nerve were examined histologically. Rats' fasting
blood glucose and
body weight were monitored. Serum
tumor necrosis factor-α (TNF-α),
vascular endothelial growth factor (
VEGF),
claudin-1, and
glutathione/
malondialdehyde ratios were analyzed.
Metformin significantly attenuated diabetes-related histopathological ocular deteriorations in the cornea, lens, sclera, ciliary body, iris, conjunctiva, retina, and optic nerve partly by restoring serum TNF-α,
VEGF,
claudin-1, and
glutathione/
malondialdehyde ratios without significantly affecting the fasting
blood glucose levels or
body weight in these hyperglycemic rats.
Metformin attenuated
hyperglycemia-associated histopathological eye deteriorations, possibly partly by ameliorating vascular leakage, oxidative stress,
inflammation, and neovascularization, without affecting the fasting
blood glucose levels or
body weights in these STZ-induced diabetic rats.