Abstract
This study was done to investigate the histopathological Changes in a Rat Model of Diabetic Neuropathy. The 24 male rats used in this investigation were split into two groups of 12 animals. The first group (G1), which consisted of healthy individuals, was given standard saline. Normal saline was administered after G2 (STZ group) received STZ at a dosage of 60 mg/kg. After rats were starved overnight, a single intraperitoneal injection of 60 mg/kg of freshly produced STZ was given to induce diabetes. (0.1 M, pH 4.5) Sodium Citrate Buffer was used to dissolve STZ. On the third day after the injection of STZ, a digital glucometer was used to measure the blood glucose levels of 12-hour fasting rats; hyperglycemia was defined as values greater than 250 mg/dl. In order to assess neuropathic pain, cold allodynia was calculated by counting the number of times the foot withdrew in response to cold stimuli applied to the back of the hand. The sciatic nerve was carefully removed after the sacrifice (after 2 months) and preserved in 10% formalin for histopathological study. Normal blood glucose levels were maintained in the control rats throughout the study. However, G2 exhibited much greater FBG levels than healthy animals. In the 2-month study, the G2 maintained FBG levels above 250 mg/dl. The score for severity of STZ on sciatic nerves showed a significant difference between treated group as compared with G1. No paw reactions were seen when intact animals were subjected to plantar surface acetone. The experimental groups did not show any notable reactions to acetone on the tenth day after the diagnosis of diabetes. On days 20, 30, 40, 50 and 60 after diabetes confirmation, there were significant differences in paw withdrawal frequency between the G1 and G2 (p<0.001). Within the control group, nerve fibres were found to be regularly arranged and there was no evidence of axonal swelling. However, in the G2 group, nerve fibres were found to be significantly disorganised, and there was a notable increase in the number of Schwann cells in the sciatic nerves, suggesting damage, in comparison to the control group.
In conclusion, potentially via antinociceptive, antihyperglycemic, antioxidant, and neuro-regeneration boosting pathways in STZ-induced diabetic peripheral disease.

Key words: Histopathology, Rat, Diabetes, Neuropathy