Effect of glucagon-like peptide-1 on cerebral ischemic-reperfusion injury in neonatal rats#br#
LI Chengyan1 ZHOU Xuan2 TANG Lanfen1 MO Bo1 CHEN Yinhui1 CHEN Qiaomei1 YAN Xingyu1 AO Dang1
1.Department of Pediatrics, Affiliated Hospital of Guangdong Medical University, Guangdong Province, Zhanjiang 524000, China;
2.Department of Pediatrics, Sichuan Academy of Medical Sciences · Sichuan Provincial People’s Hospital, Sichuan Province, Chengdu 610000, China
Abstract：Objective To study the neuroprotective effect and mechanism of glucagon-like peptide-1 (GLP-1) on cerebral ischemia-reperfusion injury in neonatal rats. Methods Eighteen 7-day-old SD neonatal rats were divided into control group, model group， and treatment group, with six rats in each group. After anesthesia, the left common carotid artery was dissected in the neck of neonatal rats, while only the left common carotid artery was exposed in the control group, the blood flow of model group and treatment group was recovered after clipping the left common carotid artery for 60 min. After operation, treatment group was given Liraglutide Injection intraperitoneal injection, and control group and model group were given the same amount of normal saline intraperitoneal injection. Longa method was used to score neurobehavioral disorder in neonatal rats; TUNEL assay was used to detect the number of apoptotic cells in hippocampal neurons; the number of nuclear factor κB(NF-κB) positive cells in hippocampus was detected by immunohistochemistry; the expressions of NF-κB, tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), and Caspase-3 protein in hippocampus tissues were detected by Western blot. Results The neurobehavioral disorder score, the number of apoptotic cells in hippocampal neurons, the number of NF-κB positive cells, and the levels of TNF-α, iNOS, and Caspase-3 protein in model group were higher than those in control group, the neurobehavioral disorder score, the number of apoptotic cells in hippocampal neurons, the number of NF-κB positive cells, and the levels of TNF-α, iNOS, and Caspase-3 protein in treatment group were lower than those in model group, and the differences were statistically significant (P < 0.05). In model group, the level of intranuclear p-NF-κB protein level was higher than that in cytoplasmic NF-κB protein level; and in treatment group, the intranuclear p-NF-κB p65 protein level was lower than the cytoplasmic NF-κB protein level, and the differences were statistically significant (P < 0.05). Conclusion GLP-1 can reduce apoptosis of hippocampal neurons in ischemia-reperfusion neonatal rats by inhibiting NF-κB mediated inflammatory response.
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