Abstract

Objective — To examine the morphometric parameters of neurons and the oxidative status of the Wistar rat brain tissues after administering proline-containing peptides, also known as glyprolines (Arg-Gly-Arg-Pro-Gly-Pro [RGRPGP] and Thr-Lys-Pro-Arg-Pro-Gly-Pro [WKPRPGP; Selank]), on a traumatic brain injury (TBI) model. Study subjects — Our study involved 26 mature male Wistar rats (2.5-3 mos. old, 220-300 g). The morphometric parameters of neurons and the oxidative status of animal brain tissues were studied. Material and Methods — Four experimental groups were formed. Group 1 included intact control animals. Animals in three other groups were subjected to TBI via free fall of a 50 g weight from a height of 50 cm on the second day of the experiment and received the following injections: 0.9% sodium chloride solution in Group 2; WKPRPGP peptide solution in Group 3; RGRPGP peptide solution in Group 4. Substances were administered intraperitoneally on a daily basis at a dose of 0.1 mg/kg from day 1 through day 5 of the experiment. Morphometric parameters of rat brain neurons were studied on paraffin sections stained with hematoxylin and eosin. The intensity of free radical processes in the brain tissue was investigated by chemiluminescence. Results — An analysis of morphometric parameters revealed significant increases in the neuronal cytoplasm area, nucleolar area, number of nucleoli, and nuclear-nucleolar index with the introduction of the RGRPGP peptide after TBI, compared with the WKPRPGP peptide under the same conditions. After TBI and peptide administration, we observed an oxidative stress in the neocortex of Wistar rats, and it was more pronounced in the group of animals treated with RGRPGP. Conclusion — After RGRPGP peptide administration, we observed an increase in the morphometric parameters of neurons in the closed TBI model: a larger area and a greater number of nucleoli. Chemiluminescence data implied that WKPRRPGP peptide better protected brain tissue in rats from the effects of oxidative stress caused by TBI.

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