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Your search keyword '"Zhou, Zheyi"' showing total 3 results
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3 results on '"Zhou, Zheyi"'

1. Neuroprotective effects of exosomes derived from bone marrow mesenchymal stem cells treated by Musk Ketone on ischemic stroke.

Author

Chen C, Feng D, Lu F, Qin J, Dun L, Liao Z, Tao J, and Zhou Z

Subjects
Animals, Male, Cells, Cultured, Microglia drug effects, Microglia pathology, Microglia metabolism, Recovery of Function, Neurons drug effects, Neurons pathology, Neurons metabolism, Neuroprotective Agents pharmacology, Inflammation Mediators metabolism, Brain pathology, Brain drug effects, Brain metabolism, Behavior, Animal drug effects, Macrophage Activation drug effects, Exosomes transplantation, Exosomes metabolism, Disease Models, Animal, Apoptosis drug effects, Infarction, Middle Cerebral Artery pathology, Infarction, Middle Cerebral Artery therapy, Infarction, Middle Cerebral Artery physiopathology, Infarction, Middle Cerebral Artery metabolism, Mesenchymal Stem Cells metabolism, Mesenchymal Stem Cells drug effects, Rats, Sprague-Dawley, Ischemic Stroke metabolism, Ischemic Stroke physiopathology, Ischemic Stroke therapy, Ischemic Stroke pathology, Ischemic Stroke drug therapy, Mesenchymal Stem Cell Transplantation
Abstract

Objectives: Ischemic stroke (IS) is a leading cause of morbidity and mortality globally. This study aimed to investigate the role of exosomes (Exo) derived from bone marrow mesenchymal stem cells (BMSCs) treated with Musk Ketone (Mus treated-Exo) in the development of IS injury., Methods: BMSCs were pretreated with 10 μM Mus for 36 h, and Exo derived from these Mus-treated BMSCs (Mus-treated Exo) were extracted. Rats with middle cerebral artery occlusion (MCAO) were administered either 2 mg/kg of control Exo (Ctrl-Exo), 2 mg/kg of Mus treated-Exo, or 10 μM Mus. Neurological deficit and cerebral infarction in the MCAO rats were assessed utilizing neurological scores and TTC staining. Neuronal apoptosis, activation of microglia/macrophages, and inflammation were evaluated through TUNEL staining, immunofluorescence staining, and western blot analysis, respectively., Results: Our findings revealed that Mus-treated Exo possessed a more pronounced neuroprotective effect on MCAO rats when compared to Ctrl-Exo and Mus treatment alone. Specifically, Mus treated-Exo effectively ameliorated neurological function, reduced the volume of cerebral infarction, and diminished hemispheric swelling in MCAO rats. Moreover, it inhibited neuronal apoptosis and activation of microglia/macrophages, promoted the expression of the anti-apoptotic protein Bcl-2 while decreasing the expression of pro-apoptotic protein Bax, Cleaved-caspase 3, and pro-inflammatory factors IL-6 and COX-2., Conclusions: The findings imply that Mus treated-Exo could confer neuroprotection in rats affected by IS, potentially by attenuating apoptosis and neuroinflammation. The underlying mechanisms, however, warrant further investigation. Mus treated-Exo shows potential as a new therapeutic strategy for IS., Competing Interests: Declaration of competing interest The all authors declare that there are no conflicts of interest regarding the publication of this paper., (Copyright © 2024. Published by Elsevier Inc.)

Published
2024
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2. Suppression of lncRNA RMRP ameliorates oxygen-glucose deprivation/re-oxygenation-induced neural cells injury by inhibiting autophagy and PI3K/Akt/mTOR-mediated apoptosis.

Author

Zhou Z, Xu H, Liu B, Dun L, Lu C, Cai Y, and Wang H

Subjects
Cell Cycle Checkpoints genetics, Cell Proliferation genetics, Gene Expression Regulation genetics, Gene Knockdown Techniques, Glucose metabolism, Humans, Neurons metabolism, Neurons pathology, Oxygen metabolism, Phosphatidylinositol 3-Kinases genetics, Proto-Oncogene Proteins c-akt genetics, Proto-Oncogene Proteins c-bcl-2 genetics, RNA, Long Noncoding antagonists & inhibitors, RNA, Small Interfering genetics, RNA-Binding Proteins genetics, Reperfusion Injury metabolism, Reperfusion Injury pathology, Signal Transduction, TOR Serine-Threonine Kinases genetics, Apoptosis genetics, Autophagy genetics, RNA, Long Noncoding genetics, Reperfusion Injury genetics
Abstract

The aberrant expression of lncRNAs has been inferred to be closely related with the progression of neural ischemia/reperfusion (I/R) injury. RMRP is an lncRNA associated with I/R injury. In order to determine the role of RMRP in I/R injury, the effects of RMRP knockdown on oxygen-glucose deprivation/re-oxygenation (OGD/R)-induced injury in SH-SY5Y cells were evaluated. The effect of OGD/R administration on the expression of RMRP and apoptosis in SH-SY5Y cells, and the effect of RMRP suppression by siRNA on the impairments of cells proliferation and mobility potential due to OGD/R administration were assessed in the current study. At the molecular level, the current study detected the expressions of indicators involved in autophagy and PI3K/Akt/mTOR-mediated apoptosis pathways. The OGD/R administration induced the expression of RMRP and apoptosis in SH-SY5Y cells. After RMRP knockdown, the proliferation potential of SH-SY5Y cells was restored, and apoptosis and cell cycle arrest were inhibited. Moreover, RMRP inhibition also increased the invasion and migration of SH-SY5Y cells which were treated with OGD/R. The effects of RMRP suppression on the phenotypes of SH-SY5Y were associated with the inhibition of LC3II, p-PI3K, p-Akt, and p-mTOR as well as the induction of P62 and Bcl-2. Inhibition of RMRP contributed to the improvement of OGD/R-induced neuronal injury, which might be mediated through the inhibition of autophagy and apoptosis pathways., (© 2019 The Author(s).)

Published
2019
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3. Silencing of PTGS2 exerts promoting effects on angiogenesis endothelial progenitor cells in mice with ischemic stroke via repression of the NF‐κB signaling pathway

Author

Shuhui Meng, Zhou Zheyi, Hong Xu, Changjun Lu, Nannan Yin, An Hongwei, Guocheng Liu, Linglu Dun, and Yefeng Cai

Subjects
Male, 0301 basic medicine, Physiology, Angiogenesis, Clinical Biochemistry, Neovascularization, Physiologic, Apoptosis, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Cell Movement, Animals, Gene Silencing, Angiogenic Proteins, Progenitor cell, Cells, Cultured, Cell Proliferation, Endothelial Progenitor Cells, NF-kappa B, Brain, Infarction, Middle Cerebral Artery, Cell Cycle Checkpoints, Cell Biology, Cell cycle, Vascular endothelial growth factor, Disease Models, Animal, 030104 developmental biology, chemistry, Cyclooxygenase 2, 030220 oncology & carcinogenesis, Cancer research, Ectopic expression, Tumor necrosis factor alpha, Inflammation Mediators, Signal transduction, Apoptosis Regulatory Proteins, Signal Transduction
Abstract

The objective of the current study is to investigate the effect of PTGS2 on proliferation, migration, angiogenesis and apoptosis of endothelial progenitor cells (EPCs) in mice with ischemic stroke through the NF-κB signaling pathway. Middle cerebral artery occlusion (MCAO) model was established in mice. EPCs were identified, in which ectopic expression and depletion experiments were conducted. The mRNA and protein expression of related factors in tissues and cells were measured. Besides, proliferation, migration, angiogenesis, and apoptosis, as well as cell cycle distribution, of cells were determined. MCAO mice showed overexpression of interleukin-6 (IL-6), IL-17, and IL-23, and increased positive protein expression of PTGS2, as well as expression of PTGS2, nuclear factor-κB (NF-κB), tumor suppressor region 1 (TSP-1) and Bcl-2-associated X protein (Bax), but underexpression of vascular endothelial growth factor (VEGF), S-phase kinase associated protein 2 (Skp2), and B-cell lymphoma 2 (Bcl-2). Moreover, ectopic expression of tumor necrosis factor-α significantly elevated the expression of PTGS2, NF-κB, TSP-1, and Bax, as well as cell apoptosis and cell cycle arrest, but decreased the expression of VEGF, Skp2, and Bcl-2, as well as proliferation, migration and angiogenesis of EPCs, and the PTGS2-siRNA group showed an opposite trend. Taken together, we conclude that the specific knockdown of PTGS2 expression could repress the NF-κB signaling pathway, thereby inhibits apoptosis and promotes proliferation, migration and angiogenesis of EPCs, providing protective effect on mice with ischemic stroke.

Published
2019
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