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"Yu, Chao"
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Angiogenesis after ischemic stroke
Owing to its high disability and mortality rates, stroke has been the second leading cause of death worldwide. Since the pathological mechanisms of stroke are not fully understood, there are few clinical treatment strategies available with an exception of tissue plasminogen activator (tPA), the only FDA-approved drug for the treatment of ischemic stroke. Angiogenesis is an important protective mechanism that promotes neural regeneration and functional recovery during the pathophysiological process of stroke. Thus, inducing angiogenesis in the peri-infarct area could effectively improve hemodynamics, and promote vascular remodeling and recovery of neurovascular function after ischemic stroke. In this review, we summarize the cellular and molecular mechanisms affecting angiogenesis after cerebral ischemia registered in PubMed, and provide pro-angiogenic strategies for exploring the treatment of ischemic stroke, including endothelial progenitor cells, mesenchymal stem cells, growth factors, cytokines, non-coding RNAs, etc.
Journal Article
In situ probing electrified interfacial water structures at atomically flat surfaces
Solid/liquid interfaces are ubiquitous in nature and knowledge of their atomic-level structure is essential in elucidating many phenomena in chemistry, physics, materials science and Earth science1. In electrochemistry, in particular, the detailed structure of interfacial water, such as the orientation and hydrogen-bonding network in electric double layers under bias potentials, has a significant impact on the electrochemical performances of electrode materials2–4. To elucidate the structures of electric double layers at electrochemical interfaces, we combine in situ Raman spectroscopy and ab initio molecular dynamics and distinguish two structural transitions of interfacial water at electrified Au single-crystal electrode surfaces. Towards negative potentials, the interfacial water molecules evolve from structurally ‘parallel’ to ‘one-H-down’ and then to ‘two-H-down’. Concurrently, the number of hydrogen bonds in the interfacial water also undergoes two transitions. Our findings shed light on the fundamental understanding of electric double layers and electrochemical processes at the interfaces.Interfacial water structures in electric double layers under bias potentials can impact the electrochemical performance of electrodes. Two structural transitions of interfacial water at electrified Au single-crystal electrode surfaces have now been identified.
Journal Article
Hollow MnO2 as a tumor-microenvironment-responsive biodegradable nano-platform for combination therapy favoring antitumor immune responses
Herein, an intelligent biodegradable hollow manganese dioxide (H-MnO
2
) nano-platform is developed for not only tumor microenvironment (TME)-specific imaging and on-demand drug release, but also modulation of hypoxic TME to enhance cancer therapy, resulting in comprehensive effects favoring anti-tumor immune responses. With hollow structures, H-MnO
2
nanoshells post modification with polyethylene glycol (PEG) could be co-loaded with a photodynamic agent chlorine e6 (Ce6), and a chemotherapy drug doxorubicin (DOX). The obtained H-MnO
2
-PEG/C&D would be dissociated under reduced pH within TME to release loaded therapeutic molecules, and in the meantime induce decomposition of tumor endogenous H
2
O
2
to relieve tumor hypoxia. As a result, a remarkable in vivo synergistic therapeutic effect is achieved through the combined chemo-photodynamic therapy, which simultaneously triggers a series of anti-tumor immune responses. Its further combination with checkpoint-blockade therapy would lead to inhibition of tumors at distant sites, promising for tumor metastasis treatment.
MnO
2
nanostructures are promising TME-responsive theranostic agents in cancer. Here, the authors develop a nano-platform based on hollow H-MnO
2
nanoshells able to modulate the tissue microenvironment, release a drug and inhibit tumor growth alone or in combination with check-point blockade therapy.
Journal Article
The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging
Oxidative stress, a term that describes the imbalance between oxidants and antioxidants, leads to the disruption of redox signals and causes molecular damage. Increased oxidative stress from diverse sources has been implicated in most senescence-related diseases and in aging itself. The Kelch-like ECH-associated protein 1- (Keap1-) nuclear factor-erythroid 2-related factor 2 (Nrf2) system can be used to monitor oxidative stress; Keap1-Nrf2 is closely associated with aging and controls the transcription of multiple antioxidant enzymes. Simultaneously, Keap1-Nrf2 signaling is also modulated by a more complex regulatory network, including phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), protein kinase C, and mitogen-activated protein kinase. This review presents more information on aging-related molecular mechanisms involving Keap1-Nrf2. Furthermore, we highlight several major signals involved in Nrf2 unbinding from Keap1, including cysteine modification of Keap1 and phosphorylation of Nrf2, PI3K/Akt/glycogen synthase kinase 3β, sequestosome 1, Bach1, and c-Myc. Additionally, we discuss the direct interaction between Keap1-Nrf2 and the mammalian target of rapamycin pathway. In summary, we focus on recent progress in research on the Keap1-Nrf2 system involving oxidative stress and aging, providing an empirical basis for the development of antiaging drugs.
Journal Article
Network pharmacology and experimental verification to decode the action of Qing Fei Hua Xian Decotion against pulmonary fibrosis
Pulmonary fibrosis (PF) is a common interstitial pneumonia disease, also occurred in post-COVID-19 survivors. The mechanism underlying the anti-PF effect of Qing Fei Hua Xian Decotion (QFHXD), a traditional Chinese medicine formula applied for treating PF in COVID-19 survivors, is unclear. This study aimed to uncover the mechanisms related to the anti-PF effect of QFHXD through analysis of network pharmacology and experimental verification.
The candidate chemical compounds of QFHXD and its putative targets for treating PF were achieved from public databases, thereby we established the corresponding \"herb-compound-target\" network of QFHXD. The protein-protein interaction network of potential targets was also constructed to screen the core targets. Furthermore, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were used to predict targets, and pathways, then validated by in vivo experiments.
A total of 188 active compounds in QFHXD and 50 target genes were identified from databases. The key therapeutic targets of QFHXD, such as PI3K/Akt, IL-6, TNF, IL-1β, STAT3, MMP-9, and TGF-β1 were identified by KEGG and GO analysis. Anti-PF effects of QFHXD (in a dose-dependent manner) and prednisone were confirmed by HE, Masson staining, and Sirius red staining as well as in vivo Micro-CT and immunohistochemical analysis in a rat model of bleomycin-induced PF. Besides, QFXHD remarkably inhibits the activity of PI3K/Akt/NF-κB and TGF-β1/Smad2/3.
QFXHD significantly attenuated bleomycin-induced PF via inhibiting inflammation and epithelial-mesenchymal transition. PI3K/Akt/NF-κB and TGF-β1/Smad2/3 pathways might be the potential therapeutic effects of QFHXD for treating PF.
Journal Article
A novel machine learning strategy for model selections - Stepwise Support Vector Machine (StepSVM)
An essential aspect of medical research is the prediction for a health outcome and the scientific identification of important factors. As a result, numerous methods were developed for model selections in recent years. In the era of big data, machine learning has been broadly adopted for data analysis. In particular, the Support Vector Machine (SVM) has an excellent performance in classifications and predictions with the high-dimensional data. In this research, a novel model selection strategy is carried out, named as the Stepwise Support Vector Machine (StepSVM). The new strategy is based on the SVM to conduct a modified stepwise selection, where the tuning parameter could be determined by 10-fold cross-validation that minimizes the mean squared error. Two popular methods, the conventional stepwise logistic regression model and the SVM Recursive Feature Elimination (SVM-RFE), were compared to the StepSVM. The Stability and accuracy of the three strategies were evaluated by simulation studies with a complex hierarchical structure. Up to five variables were selected to predict the dichotomous cancer remission of a lung cancer patient. Regarding the stepwise logistic regression, the mean of the C-statistic was 69.19%. The overall accuracy of the SVM-RFE was estimated at 70.62%. In contrast, the StepSVM provided the highest prediction accuracy of 80.57%. Although the StepSVM is more time consuming, it is more consistent and outperforms the other two methods.
Journal Article
Magnesium galvanic cells produce hydrogen and modulate the tumor microenvironment to inhibit cancer growth
Hydrogen can be used as an anti-cancer treatment. However, the continuous generation of H
2
molecules within the tumor is challenging. Magnesium (Mg) and its alloys have been extensively used in the clinic as implantable metals. Here we develop, by decorating platinum on the surface of Mg rods, a Mg-based galvanic cell (MgG), which allows the continuous generation of H
2
in an aqueous environment due to galvanic-cell-accelerated water etching of Mg. By implanting MgG rods into a tumor, H
2
molecules can be generated within the tumor, which induces mitochondrial dysfunction and intracellular redox homeostasis destruction. Meanwhile, the Mg(OH)
2
residue can neutralize the acidic tumor microenvironment (TME). Such MgG rods with the micro-galvanic cell structure enable hydrogen therapy to inhibit the growth of tumors, including murine tumor models, patient-derived xenografts (PDX), as well as VX
2
tumors in rabbits. Our research suggests that the galvanic cells for hydrogen therapy based on implantable metals may be a safe and effective cancer treatment.
The production of hydrogen inside cells can stimulate cell death. Here, the authors made magnesium galvanic rods that continuously produce hydrogen and result in tumor inhibition in vitro and in vivo.
Journal Article
Network pharmacology and molecular docking analyses on Lianhua Qingwen capsule indicate Akt1 is a potential target to treat and prevent COVID‐19
Objectives Coronavirus disease 2019 (COVID‐19) is rapidly spreading worldwide. Lianhua Qingwen capsule (LQC) has shown therapeutic effects in patients with COVID‐19. This study is aimed to discover its molecular mechanism and provide potential drug targets. Materials and Methods An LQC target and COVID‐19–related gene set was established using the Traditional Chinese Medicine Systems Pharmacology database and seven disease‐gene databases. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis and protein‐protein interaction (PPI) network were performed to discover the potential mechanism. Molecular docking was performed to visualize the patterns of interactions between the effective molecule and targeted protein. Results A gene set of 65 genes was generated. We then constructed a compound‐target network that contained 234 nodes of active compounds and 916 edges of compound‐target pairs. The GO and KEGG indicated that LQC can act by regulating immune response, apoptosis and virus infection. PPI network and subnetworks identified nine hub genes. The molecular docking was conducted on the most significant gene Akt1, which is involved in lung injury, lung fibrogenesis and virus infection. Six active compounds of LQC can enter the active pocket of Akt1, namely beta‐carotene, kaempferol, luteolin, naringenin, quercetin and wogonin, thereby exerting potential therapeutic effects in COVID‐19. Conclusions The network pharmacological strategy integrates molecular docking to unravel the molecular mechanism of LQC. Akt1 is a promising drug target to reduce tissue damage and help eliminate virus infection. A Lianhua Qingwen capsule (LQC) target and COVID‐19 related gene set is established to construct compound‐target pharmacology network. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis indicate the regulating effect of LQC on apoptosis, antivirus, immune defense, and inflammatory response. Protein‐protein interaction network and critical subnetworks are constructed to identify hub gene target. The most significant gene, Akt 1, is selected to perform molecular docking with active compounds of LQC. Six compounds are finally recognized as potential anti‐COVID‐19 agents.
Journal Article
LncRNA SNHG14 promotes inflammatory response induced by cerebral ischemia/reperfusion injury through regulating miR-136-5p /ROCK1
Recently, long non-coding RNAs (lncRNAs) are considered as critical regulators in pathogenesis progression of cerebral ischemia. In present study, lncRNA-small nucleolar RNA host gene 14 (SNHG14) was found upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) treated brain tissues and oxygen-glucose deprivation and reoxygenation (OGD/R) treated PC-12 cells. Interference of SNHG14 by shRNA vector enhanced neuron survival and suppressed inflammation in response to OGD/R insult. SNHG14 positively regulated the expression of Rho-associated coiled-coil-containing protein kinase 1 (ROCK1) via acting as a sponge of microRNA (miR)-136–5p. SNHG14 promoted neurological impairment and inflammatory response through elevating the expression of ROCK1 while decreasing miR-136–5p level in OGD/R induced damage. Collectively, we illustrated that SNHG14 could be a novel strategy for treatment ischemia stoke.
Journal Article