Background Diabetic rats are more sensitive to nerve entrapment. This study was conducted to evaluate nerve function and histological changes in diabetic rats after nerve compression and subsequent decompression. Methods A total of 35 Wistar rats were included. The experimental group was divided into diabetic sciatic nerve compression group (DSNC, n = 5) and diabetic sciatic nerve decompression group (DSND, n = 20). The DSNC model was created by wrapping a silicone tube circumferentially around the nerve for 4 weeks, and then the DSND group accepted nerve decompression and was followed up to 12 weeks. The DSND group was equally divided into DSND 3 weeks (DSND3), 6 weeks (DSND6), 9 weeks (DSND9), and 12 weeks (DSND12) groups. Five rats were taken as normoglycemic control group (CR, n = 5), and another 5 rats as diabetic control group (DM, n = 5). The mechanical hyperalgesia of rats was detected by Semmes-Weinstein nylon monofilaments (SWMs) and by motor nerve conduction velocity (MNCV). These 2 physiological indicators and histology of sciatic nerves were compared among different groups. Results The SWM measurements improved toward normal values after decompression. The SWM value was significantly lower (more normal) in the DSNC groups than in the DSND group (P < 0.05). The MNCV was 53.7 ± 0.8 m/s in the CR group, whereas it was 28.4 ± 1.0 m/s in the DSNC group (P < 0.001). Six weeks after decompression, the MNCV was significantly faster than that in the DSNC group (P < 0.001). Histological examination demonstrated chronic nerve compression, which responded toward normal after decompression, but with degree of myelination never recovering to normal. Conclusions Chronic compression of the diabetic sciatic nerve has measureable negative effects on sciatic nerve motor nerve function, associated with a decline of touch/pressure threshold and degeneration of myelin sheath and axon. Nerve decompression surgery can reverse these effects and partially restore nerve function.

Our study suggests that additional silicone tube wrapping on the SCN of rat with diabetes closely mimics the course and pathologic findings of human DPN. Further studies are needed to verify the effectiveness of this rat model of DPN and elucidate the roles of the individual genes in the progression of DPN.