Effect of estrogen on recovering the injured nervous system.

Pakistan journal of pharmaceutical sciences

PubMedID: 26431647

Liu Z, Mu S, Wang X. Effect of estrogen on recovering the injured nervous system. Pak J Pharm Sci. 2015;28(4 Suppl):1471-5.
Estrogen plays an important role in the recovery of injured nervous system. This study aims to discuss the effect of estrogen on glial cells in spinal cord and apoptosis of neuron at different time points with a hope to lay theoretical basis on treating acute spinal cord injury (SCI) in clinic. Totally 72 adult rats were divided into a simple injury group and an estrogen group. Then several animal models with SCI were prepared. The estrogen group was treated with intramuscular injection of 100 µg/kg estrogen every day till the death of animal models, while the simple injury group was treated with intramuscular injection of 0. 5 mL saline every day. Then these animals were put to death in the 1st d, 3rd d, 5th d, 8th d, 14th d and 21st d after SCI respectively and tissue sections were prepared, followed by B-cell lymphoma-2 (Bcl-2) detection, Terminal Deoxynucleotidyl Transferase-mediated dUTP nick-end labeling (TUNEL) and detection of the cell apoptosis in animal models after SCI. In the 14th d after the injury of spinal cord nervous system, Gale grading and inclined plate maintenance tests were carried out. In the 1st d after SCI, there was a higher expression of Bcl-2 protein in the SCI tissues. Bcl-2 protein reached the peak in the 3rd d after SCI in the simple injured group, while the estrogen group reached the peak in the 8th d. At that time, Bcl-2 protein was both expressed in nerve cells, and in glial cells in a higher level. The expression began to decline in the 14th d after SCI, and with only a little expression in the 21st d after SCI (p<0. 05). TUNEL detection results showed that, positive cells dominated by glial cells emerged in simple injured group only 24th h later; they reached the peak after 3~8 days, and then began to reduce. In the 21st d, positive cells still existed, and there was less cell apoptosis after treated with estrogen (p<0. 05). Two weeks after SCI, Gale score and inclined plate maintenance rate were higher in the estrogen group than in the simple injured group (p<0. 01). Adverse effects that occurred in injury group included blood dryness, necrosis, cyst cavity and cavity, while in estrogen group, adverse effects included focal bleeding, hydropic degeneration of neuron, disappearance of partial nissl bodies and neuraxial edema. All these findings suggest that, estrogen used for treating SCI can effectively inhibit the apoptosis of early nerve cells and glial cells in injured spinal cord nervous system by improving the micro-circulation, enhancing the expression of Bcl-2 protein, removing the free radicals and inhibiting the antioxidation. Thus, it can reduce the secondary SCI and promote the recovery of injured spinal cord nervous functions.