Background Hyperglycemia in brain and spinal cord could aggravate neurologic impairment. Recent studies showed that L-lysine monohydrochlonde （LMH） could increase the insulin secretion and regulate the blood glucose...Background Hyperglycemia in brain and spinal cord could aggravate neurologic impairment. Recent studies showed that L-lysine monohydrochlonde （LMH） could increase the insulin secretion and regulate the blood glucose level. The aim of the present study was to investigate the effects of LMH on pancreatic islet B cells, the levels of endogenous insulin and blood glucose in spinal cord injured rats.Methods Forty male Wistar rats were divided into four groups, namely, normal control group, model group, high-dose LMH group （621.5 mg/kg equal to LMH 1/8 LD50）, and low-dose LMH group （310.8 mg/kg equal to LMH 1/16 LD50）. The model of spinal cord injured rat was established by hemi-transection at the lower right thoracic spinal cord. LMH was administered via intraperitoneal injection once spinal cord injury was produced in rats. All rats were sacrificed 48 hours after spinal cord injured. The effects of LMH on pancreatic islet B cells, the content of endogenous insulin, end the level of blood glucose were observed with immunohistochemical method, radioimmunoassay method, end biochemical analyzer, respectively. Results The insulin immunohistochemical intensities of islet B cells were significantly weaker in model group then those in normal control group （P 〈0.01）. The levels of endogenous insulin were significantly lower and the blood glucose levels were significantly higher in model group than those in normal control group （P 〈0.01）. The insulin immunohistochemical intensities of islet B cells were significantly stronger in high-dose LMH group then those in model group （P〈0.05）. In addition, we found that the levels of endogenous insulin were significantly higher and the blood glucose levels were significantly lower in high-dose LMH group then those in model group （P 〈0.05）. There were no significant differences in the insulin immunohistochemical intensities of islet B cells, the levels of endogenous insulin and the blood glucose between low-dose LMH group and model group （P 〉0.05）. Conclusion LMH, but dose-dependent, might participate in the regulation of pancreatic islet B cells, and then reduce the blood glucose levels in the spinal cord injured rats.展开更多
文摘Background Hyperglycemia in brain and spinal cord could aggravate neurologic impairment. Recent studies showed that L-lysine monohydrochlonde （LMH） could increase the insulin secretion and regulate the blood glucose level. The aim of the present study was to investigate the effects of LMH on pancreatic islet B cells, the levels of endogenous insulin and blood glucose in spinal cord injured rats.Methods Forty male Wistar rats were divided into four groups, namely, normal control group, model group, high-dose LMH group （621.5 mg/kg equal to LMH 1/8 LD50）, and low-dose LMH group （310.8 mg/kg equal to LMH 1/16 LD50）. The model of spinal cord injured rat was established by hemi-transection at the lower right thoracic spinal cord. LMH was administered via intraperitoneal injection once spinal cord injury was produced in rats. All rats were sacrificed 48 hours after spinal cord injured. The effects of LMH on pancreatic islet B cells, the content of endogenous insulin, end the level of blood glucose were observed with immunohistochemical method, radioimmunoassay method, end biochemical analyzer, respectively. Results The insulin immunohistochemical intensities of islet B cells were significantly weaker in model group then those in normal control group （P 〈0.01）. The levels of endogenous insulin were significantly lower and the blood glucose levels were significantly higher in model group than those in normal control group （P 〈0.01）. The insulin immunohistochemical intensities of islet B cells were significantly stronger in high-dose LMH group then those in model group （P〈0.05）. In addition, we found that the levels of endogenous insulin were significantly higher and the blood glucose levels were significantly lower in high-dose LMH group then those in model group （P 〈0.05）. There were no significant differences in the insulin immunohistochemical intensities of islet B cells, the levels of endogenous insulin and the blood glucose between low-dose LMH group and model group （P 〉0.05）. Conclusion LMH, but dose-dependent, might participate in the regulation of pancreatic islet B cells, and then reduce the blood glucose levels in the spinal cord injured rats.
