Idris Altun1, Ergül Belge Kurutaş2. 1. Department of Neurosurgery, Kahramanmaras Sutcu Imam University Medical Faculty, Kahramanmaras, Turkey. Electronic address: idrisaltun46@gmail.com. 2. Department of Biochemistry, Kahramanmaras Sutcu Imam University Medical Faculty, Kahramanmaras, Turkey.
Abstract
OBJECTIVE: To assess whether G protein-coupled estrogen receptor (GPER) levels were altered during crush-induced peripheral nerve injury in an experimental rat model. METHODS: Male Wistar rats (N = 80) were allocated to 1 sham and 6 study groups, and crush-type peripheral nerve injury was performed using a clamp on the sciatic nerves of study groups. In the sham group, the sciatic nerve was exposed only, and the wound was closed primarily without any surgical interventions. Peripheral nerve samples were obtained at 1 hour, 6 hours, 12 hours, 24 hours, 3 days, and 7 days. After analysis of nerve tissues by protein analysis and Western blotting, the groups were compared in terms of expression of GPER levels. RESULTS: The average levels of GPER in the sham group and study groups at 1 hour, 6 hours, 12 hours, 24 hours, 3 days, and 7 days were 15.06 ng/mL ± 2.91, 3.31 ng/mL ± 0.91, 4.06 ng/mL ± 0.87, 11.94 ng/mL ± 1.15, 10.76 ng/mL ± 1.76, 9.16 ng/mL ± 2.60, and 8.49 ng/mL ± 3.55. All study groups displayed significantly lower levels of GPER compared with the sham group. CONCLUSIONS: Our results demonstrate that a basal level of GPER expression occurs in peripheral nerve tissue. The lowest level was detected 1 hour after crush injury, and the highest levels of GPER were detected 12 hours and 24 hours after trauma. Further trials on larger series are required to elucidate the role of GPER in terms of protection and treatment after nerve injury.
OBJECTIVE: To assess whether G protein-coupled estrogen receptor (GPER) levels were altered during crush-induced peripheral nerve injury in an experimental rat model. METHODS: Male Wistar rats (N = 80) were allocated to 1 sham and 6 study groups, and crush-type peripheral nerve injury was performed using a clamp on the sciatic nerves of study groups. In the sham group, the sciatic nerve was exposed only, and the wound was closed primarily without any surgical interventions. Peripheral nerve samples were obtained at 1 hour, 6 hours, 12 hours, 24 hours, 3 days, and 7 days. After analysis of nerve tissues by protein analysis and Western blotting, the groups were compared in terms of expression of GPER levels. RESULTS: The average levels of GPER in the sham group and study groups at 1 hour, 6 hours, 12 hours, 24 hours, 3 days, and 7 days were 15.06 ng/mL ± 2.91, 3.31 ng/mL ± 0.91, 4.06 ng/mL ± 0.87, 11.94 ng/mL ± 1.15, 10.76 ng/mL ± 1.76, 9.16 ng/mL ± 2.60, and 8.49 ng/mL ± 3.55. All study groups displayed significantly lower levels of GPER compared with the sham group. CONCLUSIONS: Our results demonstrate that a basal level of GPER expression occurs in peripheral nerve tissue. The lowest level was detected 1 hour after crush injury, and the highest levels of GPER were detected 12 hours and 24 hours after trauma. Further trials on larger series are required to elucidate the role of GPER in terms of protection and treatment after nerve injury.