Therapeutic targets of vitamin C on liver injury and associated biological mechanisms: A study of network pharmacology

Su, Min; Guo, Chao; Liu, Meizhen; Liang, Xiaoliu; Yang, Bin

doi:10.1016/j.intimp.2018.11.048

Cited by 82 publications

(72 citation statements)

References 22 publications

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“…Vitamin C (VC) is a pharmacologically bioactive monomer, characterized by potent antioxidative, antiaging effects, tumor prevention, and detoxification . Recently, our previous study reveals the therapeutic biotargets and molecular mechanisms of VC for treating liver injury by using the network pharmacological assay . A pharmacological study demonstrates that VC inhibits the cyclophosphamide (CPS)‐induced hemorrhagic cystitis in rats, and the underlying mechanism behind this anticystitis effect is associated with blocking the release of toxic‐free radicals .…”

Section: Introductionmentioning

confidence: 99%

Network analysis, and human and animal studies disclose the anticystitis glandularis effects of vitamin C

Guo

Liang

et al. 2019

BioFactors

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Background Our present study aimed to unravel the therapeutic biotargets of vitamin C (VC) against cystitis glandularis (CG), and to elucidate the molecular mechanisms for VC treating CG. Methods Network pharmacology was used to predict therapeutic targets of VC against CG, and to identify molecular mechanisms. In addition, further human and animal studies were designed to validate the bioinformatic findings through biochemical tests, computerized tomography scans, and immunostaining assays. Results In bioinformatic analyses, pathogenic targets of CG and putative targets of VC were identified, respectively. An interaction network between biological target and functional protein was produced before screening and collecting the key therapeutic targets of VC against CG, biological processes, and signaling pathways. In addition, ingenuity pathway analysis with cloud platform indicated that anti‐CG mechanisms of VC were achieved through modulating a cluster of molecular pathways, such as tumor necrosis factor (TNF) pathway. Meanwhile, 18 core targets of VC against CG were identified, and the most important TNF, interleukin‐6 (IL6), and Jun biotargets were obtained, respectively. In further validation in human study, cellular TNF‐α, IL6, and c‐Jun expressions in patient's CG samples were elevated significantly, accompanied with detectable urinary tract infection. Beneficially, VC‐dosed CG mice resulted in downregulated expressions of endogenous TNF‐α, IL6, and c‐Jun in blood and bladder samples. Conclusion Collectively, these bioinformatic findings and experimentative data uncover the therapeutic targets and biological mechanisms of VC for treating CG, in which the key biomarkers of TNF‐α, IL6, and c‐Jun may be the potential molecules for treating CG in clinical application.

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Section: Introductionmentioning

confidence: 99%

Network analysis, and human and animal studies disclose the anticystitis glandularis effects of vitamin C

Guo

Liang

et al. 2019

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“…The experimental arm that received vitamin C showed less hepatocyte damage, with similar histological patterns described by Awadalla in 2012 (23).In this study Vitamin C administration attenuated the morphological damages induced by PQ in the liver of experimental animals; being these results were attributed to vitamin C's ability to capture free radicals from paraquat-induced stress and anti-apoptosis activity. Preclinical studies in liver injury show that the benefits of Vitamin C were principally implicated in regulating signaling pathways, such as inflammation-associated TNF signaling pathway, NF-κB signaling pathway (24,25). These studies give arguments to evaluate the protective role against acute liver injury that can occur in patients with acute intoxication especially in those with high doses of ingestion which have the highest risk of developing acute liver disease and placing the patient's life at risk.…”

Section: Discussionmentioning

confidence: 99%

Comparison of four pharmacological strategies aimed to prevent the lung inflammation and paraquat-induced alveolar damage

Rodriguez

Castro

Vela

et al. 2019

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Objective : The aim of this study was to compare in vivo effect of five pharmacological options on inflammation and pulmonary fibrosis induced by paraquat. Methods: 54 Wistar SPF rats were used. After 2 hours post-intoxication with paraquat ion, groups of 9 animals were randomly assigned to : (1) cyclophosphamide plus dexamethasone (2) low molecular weight heparin (3) unfractionated heparin (4) vitamin C every 24 h , (v) atorvastatin or (vi) placebo with intraperitoneal saline .Lung inflammation, alveolar injury, hepatocyte damage, hepatic regeneration, acute tubular necrosis and kidney congestion were evaluated. Results: In the control group 100% of animals presented moderate and severe lung inflammation, while in the groups with atorvastatin and intratracheal heparin this proportion was lower (55.5% ; CI 26.6 – 81.3%) (p = 0.025). A lower degree of moderate or severe hepatic regeneration was evident in the treatment groups with atorvastatin (p = 0.009). In this study was demonstrated that statins and heparin may have a protective effect in the paraquat-induced destructive phase. More evidence are needed to evaluated of dose response effects of these drugs before to study in clinical trials.

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“…After FunRich test, all key targets of calycosin managing OS were entered a database of Functional Annotation Bioinformatics Microarray Analysis (DAVID) for creating available biological processes and signalling pathways of calycosin managing OS. According to the -Log p-value, a three-dimensional bar chart of biological processes and signalling pathways of calycosin managing OS was drew [15][16].…”

Section: Enriched Determination Of Molecular Functions and Pathways Omentioning

confidence: 99%

Systematic and experimental approaches to indicate anti-tumor biotargets and molecular mechanisms of calycosin against osteosarcoma

Tan¹,

Xiong²,

Liu³

et al. 2020

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BackgroundCalycosin is reported to pharmacologically combat cancer cells, however, the detailed anti-osteosarcoma (OS) mechanisms remain unclear. By using systemic method of network pharmacology, the present study purposed to reveal the anti-OS biotargets and molecular mechanisms played by calycosin. Moreover, human and animal experiments were used to verify the key biotargets of calycosin combating OS. ResultsIn OS findings, the blood parameters showed increased tumor markers and OS sections resulted in negatively expressed proteins of tumor protein p53 (TP53), Caspase-3 (CASP3), X-linked Inhibitor of Apoptosis Protein (XIAP). To feature the pharmacological biotargets in a cell line study, calycosin-treated OS cells showed reduced cell proliferation, and promoted cell apoptosis. In TUNEL stains, calycosin resulted in elevated apoptotic cells. As showed in immunostaining, calycosin-treated OS cells suggested elevated TP53, CASP3, XIAP protein expressions. ConclusionsOverall, our present human and cell culture data manifest all candidate and key biotargets, molecular functions and pathways of calycosin combating OS. Attractively, these top biotargets may be used for pharmacological hallmarks to combat OS.

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Therapeutic targets of vitamin C on liver injury and associated biological mechanisms: A study of network pharmacology

Cited by 82 publications

References 22 publications

Network analysis, and human and animal studies disclose the anticystitis glandularis effects of vitamin C

Network analysis, and human and animal studies disclose the anticystitis glandularis effects of vitamin C

Comparison of four pharmacological strategies aimed to prevent the lung inflammation and paraquat-induced alveolar damage

Systematic and experimental approaches to indicate anti-tumor biotargets and molecular mechanisms of calycosin against osteosarcoma

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