Abstract
Ghrelin, a 28-amino acid peptide, is mainly secreted by the stomach. Ghrelin has been shown to have neuroprotective effects. However, whether ghrelin protects the spinal cord from ischemia/reperfusion (I/R) injury is unknown. To investigate this, 60 rats were randomly divided into three different groups: the sham group (n = 20), the vehicle group (n = 20), and the Ghrelin group (100 μg/kg, n = 20). Rats were sacrificed 12, 24, 48 and 72 h after ischemia. After the evaluation of neurologic function (48 h), the spinal cords were immediately removed for the determination of myeloperoxidase (MPO) activity (12–72 h). Apoptosis was quantitatively measured using the terminal transferase UTP nick end-labeling (TUNEL) method (24 h). The expression of bax and bcl-2 were evaluated by Western blot analysis (1 h), and GHSR-1a mRNA expression was detected using reverse transcriptase polymerase chain reaction (24 h). The neurological motor function was evaluated by ‘Tarlov’s score’. The neurologic outcomes in the ghrelin-group were significantly better than those in the vehicle group (p < 0.05). Serum tumor necrosis factor (TNF-α) levels were assessed in the peripheral venous blood. Ghrelin decreased the serum TNF-α levels and ameliorated the down regulation of spinal cord MPO activity. The expression of ghrelin receptors (GHSR-1a) in the rat spinal cord was decreased by I/R injury and increased by ghrelin. Ghrelin reduced the TUNEL-positive rate. Greater bcl-2, HSP27, HSP70, and attenuated bax expression were observed in the ghrelin-treated rats. Our results suggest that ghrelin administration may inhibit spinal I/R injury. Moreover, the improvement of neurologic function in rats was increased after the ghrelin treatment.
Highlights
Ischemic spinal cord injury is a serious complication of thoraco-abdominal aortic surgery and can cause paraplegia in approximately 40% of patients [1]
Compared with the sham group, the I/R group showed significantly reduced growth hormone secretagogue receptor-1a (GHSR-1a) mRNA expression (* p < 0.01) that is reversed by ghrelin (** p < 0.05). These results suggest that the GHSR-1a level is affected by both the ischemia and ghrelin treatment
Recent studies have revealed that ghrelin receptor gene expression in the spinal cord can be detected by PCR and in situ hybridization [22]
Summary
Ischemic spinal cord injury is a serious complication of thoraco-abdominal aortic surgery and can cause paraplegia in approximately 40% of patients [1]. This complication has been attributed, at least in part, to temporary or permanent ischemia of the spinal cord caused by interruption of the blood supply during aortic cross-clamping [2]. Several studies have shown that ghrelin has anti-apoptotic and protective effects on various cell types subjected to I/R injury [16,17]. The neuroprotective effects of ghrelin on the spinal cord are explored in an I/R rat model
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