|
|
|
| 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.
|
|
|
|
|
|
[1] 熊英.新生儿缺血缺氧性脑病研究进展[J].系统医学，2020，5（12）：196-198.
[2] 郭江波，袁天明.新生儿缺氧缺血性脑病的发病机制及诊治研究进展[J].医学综述，2021，27（13）：2624-2629.
[3] 吴静静，包蕾.新生儿缺氧缺血性脑病的发病机制及相关治疗进展[J].现代医药卫生，2019，35（20）：3172-3175.
[4] 兰雪，崔艳芳，陈国萍，等.血清生物标志物在缺血缺氧性脑病新生儿中的研究进展[J].标记免疫分析与临床，2021，28（2）：353-357.
[5] 李艺.新生儿窒息诊断与治疗新进展[J].临床医学，2021， 41（2）：121-124.
[6] 李艳伟，赵晋英，李琳.GLP-1类药物防治神经退行性疾病的研究进展[J].广东医学，2017，38（15）：2407-2411， 2415.
[7] 董文彬，文婷婷，王文波，等.胰高血糖素样肽-1受体激动剂抗脑缺血损伤作用研究进展[J].中南药学，2020，18（12）：2019-2026.
[8] Prado R，Ginsberg MD，Dietrich WD，et al. Hyperglycemia increases infarct size in collaterally perfused but not end-arterial vascular territories [J]. J Cere Blood Flow Metab，1988，8（2）：186-192.
[9] 刘玉琴，刘元涛.胰高血糖素样肽-1及其相关药物与神经保护[J].青岛大学学报：医学版，2018，54（4）：483-486.
[10] 吴灵灵，孙李丹.胰高血糖素样肽-1及其类似物对细胞氧化应激的研究进展[J].中国药科大学学报，2020， 51（1）：114-120.
[11] Müller TD，Finan B，Bloom SR，et al. Glucagon-like peptide 1（GLP-1）[J]. Mol Metab，2019，30：72-130.
[12] 周刚，吴辉，刘滴，等.GLP-1及其受体激动剂在缺血再灌注损伤中的研究进展[J].生命的化学，2021，41（4）：799-803.
[13] 弥婉军，王晓娟.胰高血糖素样肽-1蛋白对帕金森病氧化应激损伤的保护作用及机制研究[J].陕西医学杂志，2021，50（4）：395-397，402.
[14] 杨晓燕，郑辑英.GLP-1受体激动剂对缺血性卒中神经保护作用机制的研究进展[J].世界最新医学信息文摘，2018，18（38）：68-70.
[15] 孙艳丽，邓伟，沈静.胰高血糖素样肽1受体激动剂在缺血性脑卒中治疗中的研究进展[J].实用老年医学，2020，34（5）：502-505.
[16] 张翼鸿，徐明艳，冯琨，等.胰高糖素样肽-1对糖尿病合并阿尔兹海默症大鼠腺苷酸化蛋白激酶-哺乳动物雷帕霉素靶蛋白介导的细胞自噬的影响[J].中华糖尿病杂志，2019，11（10）：671-676.
[17] 曹义坡，姚旻，刁云锋，等.胰高血糖素样肽-1受体激动剂对颅脑创伤小鼠神经功能的影响及可能机制[J].中华实用诊断与治疗杂志，2020，34（7）：660-665.
[18] 杨扬，田晔，王芹，等.脑缺血大鼠皮质区TNF-α及NF-κB的表达研究[J].潍坊医学院学报，2019，41（5）：361-363，394.
[19] 王力娜，刘莹，季辉，等.HMGB1/NF-κB通路在脑梗死治疗中的调控研究[J].脑与神经疾病杂志，2021，29（6）：335-340.
[20] 张瑶，谢家钊，胡军，等.利拉鲁肽通过p38 MAPK通路改善高同型半胱氨酸血症诱导的大鼠海马氧化应激及炎症损伤[J].中国病理生理杂志，2018，34（11）：2025-2030.
[21] 曹晓红，徐勇，陈平.GLP-1类似物利拉鲁肽对糖尿病神经病变大鼠坐骨神经PARP-1/NF-κB表达的影响[J/OL].重庆医科大学学报：1-9[2021-12-13]. https://kns.cnki.net/kcms/detail/detail.aspx?dbcode=CAPJ&dbname=CAPJ LAST&filename=ZQYK20201123001&uniplatform=NZKP T&v=OQbLDJFQG-2uRyw__zan7PxpYsOx1NO8phiclca NS3glpF54pTc9QGZ_gl-Hmm1Q
[22] 姜一弘，张丹，张天择，等.核因子κB（NF-κB）信号通路在炎症与肿瘤中作用的研究进展[J].细胞与分子免疫学杂志，2018，34（12）：1130-1135.
[23] 李彦辰，郭元虎.NF-κB介导的炎症通路与消化道肿瘤相关研究进展[J].智慧健康，2020，6（24）：28-29.
[24] 史丙科，李守林.NF-κB/iNOS-NO信号转导通路的临床研究进展[J].医学理论与实践，2020，33（24）：4081-4083.
[25] 阴雪研，郭哨恺，谭军，等.腺苷预处理对大鼠脑缺血-再灌注损伤后脑内肿瘤坏死因子α和核因子κB表达的影响[J].解剖学报，2020，51（6）：839-847.
[26] 庞艳利，许二妮，尉娜，等.腺苷预处理对大鼠脑缺血再灌注损伤后Caspase-3的表达及细胞凋亡的影响[J].山东医药，2020，60（13）：42-45. |
|
|
|
