Ginsenoside Rb1 improves brain, lung, and intestinal barrier damage in middle cerebral artery occlusion/reperfusion (MCAO/R) micevia the PPARγ signaling pathway.
10.1016/S1875-5364(22)60204-8
- Author:
Lin-Jie SU
1
;
Yu-Chuan REN
1
;
Zhuo CHEN
1
;
Hui-Fen MA
1
;
Fan ZHENG
1
;
Fang LI
1
;
Yuan-Yuan ZHANG
1
;
Shuai-Shuai GONG
2
;
Jun-Ping KOU
3
Author Information
1. Jiangsu Key Laboratory of TCM Evaluation and Translational Research, Department of Pharmacology of Chinese Materia Medica, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China.
2. Jiangsu Key Laboratory of TCM Evaluation and Translational Research, Department of Pharmacology of Chinese Materia Medica, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China. Electronic address: 331864602@qq.com.
3. Jiangsu Key Laboratory of TCM Evaluation and Translational Research, Department of Pharmacology of Chinese Materia Medica, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China. Electronic address: junpingkou@cpu.edu.cn.
- Publication Type:Journal Article
- Keywords:
Brain/lung/intestinal barriers;
Focal ischemic stroke;
Ginsenoside Rb1;
PPARγ
- MeSH:
Animals;
Brain;
Brain Ischemia;
Ginsenosides;
Infarction, Middle Cerebral Artery;
Lung;
Mice;
NF-kappa B;
Neuroprotective Agents;
PPAR gamma;
Reperfusion;
Reperfusion Injury;
Signal Transduction
- From:
Chinese Journal of Natural Medicines (English Ed.)
2022;20(8):561-571
- CountryChina
- Language:English
-
Abstract:
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 PPARγ signaling 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, PPARγ and 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 PPARγ antagonist GW9662 reversed the barrier-protective effect of GRb1. These findings indicated that GRb1 can improve stroke-induced brain/lung/intestinal barrier damagevia the PPARγ pathway.
