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30 results on '"Wang, Aimei"'

9. CD248 as a novel therapeutic target in pulmonary arterial hypertension

Author

Xu, Tao, Shao, Lei, Wang, Aimei, Liang, Rui, Lin, Yuhan, Wang, Guan, Zhao, Yan, Hu, Jing, and Liu, Shuangyue

Subjects
NOX4, CD248, pulmonary arterial hypertension, oxidative stress, PDGF‐BB, Research Articles, Research Article
Abstract

Pulmonary vascular remodeling is the most important pathological characteristic of pulmonary arterial hypertension (PAH). No effective treatment for PAH is currently available because the mechanism underlying vascular remodeling is not completely clear. CD248, also known as endosialin, is a transmembrane protein that is highly expressed in pericytes and fibroblasts. Here, we evaluated the role of CD248 in pulmonary vascular remodeling and the processes of PAH pathogenesis. Activation of CD248 in pulmonary artery smooth muscle cells (PASMCs) was found to be proportional to the severity of PAH. CD248 contributed to platelet‐derived growth factor‐BB (PDGF‐BB)‐induced PASMC proliferation and migration along with the shift to more synthetic phenotypes. In contrast, treatment with Cd248 siRNA or the anti‐CD248 therapeutic antibody (ontuxizumab) significantly inhibited the PDGF signaling pathway, obstructed NF‐κB p65‐mediated transcription of Nox4, and decreased reactive oxygen species production induced by PDGF‐BB in PAMSCs. In addition, knockdown of CD248 alleviated pulmonary vascular remodeling in rat PAH models. This study provides novel insights into the dysfunction of PASMCs leading to pulmonary vascular remodeling, and provides evidence for anti‐remodeling treatment for PAH via the immediate targeting of CD248., CD248 as a novel therapeutic target in pulmonary arterial hypertension. Expression of CD248 contributed to platelet‐derived growth factor‐BB (PDGF‐BB)‐induced PASMC proliferation and migration along with the shift to more synthetic phenotypes. Besides, treatment of human PASMCs with PDGF‐BB, to explore the PAH signaling, exhibited ERK and NF‐κB activation, enhanced NOX4 activity, and reactive oxygen species production.

Published
2020

30. Role of Eclipta prostrata extract in improving spatial learning and memory deficits in D-galactose-induced aging in rats.

Author

Xia X, Yu R, Wang X, Wei M, Li Y, Wang A, Ma Y, Zhang J, Ji Z, Li Y, and Wang Q

Subjects
Animals, Behavior, Animal drug effects, Behavior, Animal physiology, CA1 Region, Hippocampal drug effects, CA1 Region, Hippocampal pathology, CA1 Region, Hippocampal physiopathology, Catalase genetics, Dopamine metabolism, Gene Expression Regulation, Enzymologic drug effects, Glutathione Peroxidase genetics, Glutathione Reductase genetics, Male, Memory Disorders drug therapy, Memory Disorders metabolism, Nitric Oxide metabolism, Nitric Oxide Synthase Type II metabolism, Norepinephrine metabolism, Plant Extracts therapeutic use, RNA, Messenger genetics, Rats, Rats, Sprague-Dawley, Serotonin metabolism, Superoxide Dismutase genetics, Aging drug effects, Eclipta chemistry, Galactose adverse effects, Memory Disorders chemically induced, Memory Disorders physiopathology, Plant Extracts pharmacology, Spatial Learning drug effects
Abstract

Objective: To investigate the role of Eclipta prostrata (E. prostrata) extract in improving spatial learning and memory deficits in D-galactose-induced aging in rats., Methods: Rats were divided into five groups, with 10 animals in each group. Aging rats were produced by treatment with 100 mg·kg-1·d-1 of D-galactose for 6 weeks. Rats in the E. prostrata treatment groups received an aqueous extract of E. prostrata orally at a concentration of 50, 100, or 200 mg·kg-1·d-1 for 3 weeks. Animals in both the normal and model groups were treated with similar volumes of saline. Spatial memory performance was measured using the Morris water maze. The mRNA levels and enzyme activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) were analyzed using real-time quantitative PCR and spectrophotometry, respectively. The levels of induced nitric oxide synthase (iNOS), nitric oxide (NO), dopamine (DA), norepinephrine (NE), and serotonin (5-HT) were determined using enzyme-linked immunosorbent assay and spectrophotometry., Results: Compared with the normal group, rats in the D-galactose-treated model group exhibited significant memory loss. There was severe damage to the hippocampal CA1 area, and expression levels of SOD, CAT, GPx, and GR were significantly decreased in the model group compared with the normal group. In the model group, levels of iNOS and NO were significantly increased compared with the normal group. However, treatment with E. prostrata extract reversed the conditions caused by D-galactose-induced aging, especially in the groups with higher treatment concentrations. Compared with the normal group, the levels of DA, NE, and 5-HT were significantly lower in the D-galactose-treated model group. In the E. prostrata extract-treated groups, however, there was a dose-dependent upregulation of DA, NE, and 5-HT expression., Conclusion: Our results suggest that administration of E. prostrata extract can result in an improvement in the learning and memory impairments that are induced by D-galactose treatment in rats. This improvement may be the result of enhanced antioxidative ability, decreased iNOS and NO levels, and the induction of DA, NE, and 5-HT expression in the brain.

Published
2019

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