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Ginsenoside Rb1 improves brain,lung,and intestinal barrier damage in middle cerebral artery occlusion/reperfusion(MCAO/R)micevia the PPARγsignaling pathway

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Chinese Journal of Natural Medicines 2022年第8期20卷 561-571页

作者： SU Lin-Jie REN Yu-Chuan CHEN Zhuo MA Hui-Fen ZHENG Fan LI Fang ZHANG Yuan-Yuan GONG Shuai-Shuai KOU Jun-Ping Jiangsu Key Laboratory of TCM Evaluation and Translational Research Department of Pharmacology of Chinese Materia MedicaSchool of Traditional Chinese PharmacyChina Pharmaceutical UniversityNanjing 211198China

ischemic stroke causes brain inflammation and multi-organ injury,which is closely associated with the peroxisome proliferator-activated receptor-gamma(PPARγ)signaling pathway.Recent studies have indicated that ginsenoside Rb1(GRb1)can protect the integrity of the blood-brain barrier after stroke.In the current study,a mouse model of middle cerebral artery occlusion/reperfusion(MCAO/R)was established to determine whether GRb1 can ameliorate brain/lung/intestinal barrier damage via the PPARγsignaling pathway.Staining(2,3,5-triphenyltetrazolium chloride,hematoxylin,and eosin)and Doppler ultrasonography were employed to detect pathological changes.Endothelial breakdown was investigated with the leakage of Evans Blue dye and the expression of TJs(tight junctions)and AJs(adherent junctions).Western blot and immunofluorescence were used to determine the levels of cell junction proteins,PPARγand NF-κB.Results showed that GRb1 significantly mitigated multi-organ injury and increased the expression of cerebral microvascular,pulmonary vascular,and intestinal epithelial connexins.In brain,lung,and intestinal tissues,GRb1 activated PPARγ,decreased the levels of phospho-NF-κB p65,and inhibited the production of proinflammatory cytokines,thereby maintaining barrier permeability.However,co-treatment with GRb1 and the PPARγantagonist GW9662 reversed the barrier-protective effect of GRb1.These findings indicated that GRb1 can improve stroke-induced brain/lung/intestinal barrier damagevia the PPARγpathway.

关键词： focal ischemic stroke Brain/lung/intestinal barriers Ginsenoside Rb1 PPARγ

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Physiopathology of ischemic stroke and its modulation using memantine:evidence from preclinical stroke

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Neural Regeneration Research 2021年第3期16卷 433-439页

作者： Hilda Martínez-Coria Isabel Arrieta-Cruz María-Esther Cruz Héctor E.López-Valdés División de Investigación Facultad de MedicinaUniversidad Nacional Autónoma de México(UNAM)Ciudad de MéxicoMéxico Laboratorio Experimental de Enfermedades Neurodegenerativas Facultad de MedicinaUNAM/Instituto Nacional de Neurología y NeurocirugíaCiudad de MéxicoMéxico Departamento de Investigación Básica Instituto Nacional de GeriatríaCiudad de MéxicoMéxico Unidad de Investigación en Biología de la Reproducción Laboratorio de NeuroendocrinologíaFacultad de Estudios Superiores ZaragozaUNAMCiudad de MéxicoMéxico Unidad Periférica de Neurociencia Facultad de MedicinaUNAM/Instituto Nacional de Neurología y NeurocirugíaCiudad de MéxicoMéxico

ischemic stroke is the most common type of cerebrovascular disease and is caused by an interruption of blood flow in the brain.In this disease,two different damage areas are identifying:the lesion core,in which cells quickly die;and the penumbra(surrounding the lesion core),in which cells are functionally weakened but may recover and restore their functions.The currently approved treatments for ischemic stroke are the recombinant tissue plasminogen activator and endovascular thrombectomy,but they have a short therapeutic window(4.5 and 6 hours after stroke onset,respectively)and a low percentage of stroke patients actually receive these treatments.Memantine is an approved drug for the treatment of Alzheimer's disease.Memantine is a noncompetitive,low affinity and use-dependent antagonist of N-methyl-D-aspartate glutamate receptor.Memantine has several advantages over developing a new drug to treat focal ischemic stroke,but the most important is that it has sufficient safe probes in preclinical models and humans,and if the preclinical studies provide more evidence about pharmacological actions in tissue protection and repair,this could help to increase the number of clinical trials.The present review summarizes the physiopathology of isquemic stroke and the pharmacological actions in neuroprotection and neuroplasticity of memantine in the post stroke stage of preclinical stroke models,to illustrate their potential to improve functional recovery in human patients.

关键词： focal ischemic stroke memantine neuroplasticity neuroprotection stroke therapy

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