电针减弱的脑缺血损伤与增加的葡萄糖消耗和海马体GLUT1/3表达升高相关
Ri Xu1, Xu Ma2, Minya Zhou1
1Department of Rehabilitation Medicine, Lishui Second People's Hospital Affiliated with Wenzhou Medical University Lishui 323000, Zhejiang, China.
American journal of translational research
|July 17, 2025
概括
电针 (EA) 通过增强葡萄糖代谢和升调海马中的葡萄糖转运基因GLUT1和GLUT3来缓解大脑缺血/再输液 (I/R) 损伤. 这种治疗改善了神经功能,并减少了心脏病发作量.
科学领域:
- 神经科学是一个神经科学.
- 整合和补充医学是整合和补充医学.
- 生物化学 生物化学
背景情况:
- 大脑缺血性中风 (IS) 带来了重大的健康风险,缺血/反 (I/R) 损伤加剧了损伤.
- 电针 (EA) 在减轻I/R损伤方面表现有前途,但其对葡萄糖代谢的影响尚不清楚.
- 葡萄糖载体基因的升级与I/R期间大脑细胞的能量恢复有关.
研究的目的:
- 研究EA在大脑I/R过程中调节葡萄糖代谢中的作用.
- 阐明EA在脑I/R损伤的背景下影响葡萄糖运输的分子机制.
主要方法:
- 使用中脑动脉阻塞 (MCAO) 确立的大脑I / R损伤的老鼠模型.
- 在Baihui和Shenting的针点进行了EA的管理.
- 评估脑梗塞体积 (MRI),海马体葡萄糖吸收 (PET/CT),神经学缺陷 (评分和莫里斯水迷宫),以及GLUT1和GLUT3基因的表达 (西部斑,ELISA).
主要成果:
- 治疗EA显著降低了神经缺陷和脑梗塞的数量.
- 在I/R受伤的老鼠的海马中,EA增强了葡萄糖的吸收和代谢.
- 在海马体中,EA提高了葡萄糖转运基因GLUT1和GLUT3的表达.
结论:
- 在Baihui和Shenting针点的EA有效地改善了大脑I/R损伤.
- 通过对海马GLUT1和GLUT3基因表达进行上调,EA促进葡萄糖的吸收和新陈代谢.
相关概念视频
01:16Hormones Regulating Blood Glucose
Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
In addition to accelerating glucose uptake and utilization, insulin has...
01:15Hypoglycemia and Glucagon
Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
01:29Hyperglycemia
Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...
01:27Diabetic Retinopathy
DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...
01:28Diabetic Nephropathy
Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
01:22Diabetic Neuropathy
DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...