Liver damage in bleomycin-induced pulmonary fibrosis in mice

Vásquez-Garzón, Verónica Rocío; Ramírez-Cosmes, Adriana; Reyes-Jiménez, Edilburga; Torres, Gustavo; Hernández-García, Sergio; Aguilar-Ruiz, Sergio Roberto; Torres-Aguilar, Honorio; Alpuche, Juan; Mayoral, Laura; Pina-Canseco, Socorro; Arellanes‐Robledo, Jaime; Villa‐Treviño, Saúl; Baltiérrez-Hoyos, Rafael

doi:10.1007/s00210-019-01690-7

Cited by 6 publications

(6 citation statements)

References 48 publications

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“…Endogenous lipid peroxidation strategically increases the PCCs formation in parallel with carbohydrate glycation processes (precursors of advanced glycation end products (AGEs)). The tissue proteins accumulation registers carbonyl stress during chronic induced disease [67,82,83], as in the IPF case. These our results are in complete agreement with previously reported studies [82,83], and demonstrated that in the BLM treated group there was a statistically significant twofold increase in PCC (Figure 4A), AGEs (Figure 4B) and delayed reduction in nitroxide protein distribution (Figure 4C), which leads to the IPF registration.…”

Section: Discussionmentioning

confidence: 99%

“…The tissue proteins accumulation registers carbonyl stress during chronic induced disease [67,82,83], as in the IPF case. These our results are in complete agreement with previously reported studies [82,83], and demonstrated that in the BLM treated group there was a statistically significant twofold increase in PCC (Figure 4A), AGEs (Figure 4B) and delayed reduction in nitroxide protein distribution (Figure 4C), which leads to the IPF registration. It is important to note that the combination treatment with BLM + L. minor significantly reduces these parameters.…”

Section: Discussionmentioning

confidence: 99%

“…Carbonyl stress induces complete protein dysfunctions and pathologically damages lung tissues, contributing to the acceleration of inflammation and the IPF development [82,83]. Cameli et al [67] found increased carbonylated oxidation of specific proteins or substrate accumulation of reactive dicarbonyls activated only in IPF patients.…”

Section: Discussionmentioning

confidence: 99%

“…Cameli et al [67] found increased carbonylated oxidation of specific proteins or substrate accumulation of reactive dicarbonyls activated only in IPF patients. Vásquez-Garzón et al [82] commented on irreversible protein oxidation, increased protein proliferation markers and inflammation, lipoperoxidation, and OS disorders induction in redox status of 35 days treated mice with 100 U/kg BLM. Endogenous lipid peroxidation strategically increases the PCCs formation in parallel with carbohydrate glycation processes (precursors of advanced glycation end products (AGEs)).…”

Section: Discussionmentioning

confidence: 99%

“…Takeshita et al [49], summarizes that once 5-MSL captures membrane albumin/protein, it leaves the maleimide group to react with the SH regions until alkylation, i.e., the rotational nitroxyl movement captures the weakened -SH regions of the corresponding amino acid. Based on these findings, we hypothesize that the L. minor therapeutic effect (120 mg/mL) is due to a modulated cellular response from the high polyphenol content [59,82], leading to a membrane albumin/protein reduction, • OH reduction and an amyloid protein aggregates neutralization.…”

Section: Discussionmentioning

confidence: 99%

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Pulmonary Protein Oxidation and Oxidative Stress Modulation by Lemna minor L. in Progressive Bleomycin-Induced Idiopathic Pulmonary Fibrosis

et al. 2022

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Bleomycin (BLM) administration is associated with multifunctional proteins inflammations and induction of idiopathic pulmonary fibrosis (IPF). Lemna minor L. extract, a free-floating monocot macrophyte possesses antioxidant and anti-inflammatory potential. The aim of the study was to examine the protective effect of L. minor extract on lung protein oxidation and oxidative stress modulation by BLM-induced pulmonary fibrosis in Balb/c mice. For this purpose, the protein carbonyl content, advanced glycation end product, nitroxide protein oxidation (5-MSL), and lipid peroxidation (as MDA and ROS), in lung cells were examined. The histological examinations, collagen deposition, and quantitative measurements of IL-1β, IL-6, and TNF in lung tissues and blood were investigated. Intraperitoneal, BLM administration (0.069 U/mL; 0.29 U/kg b.w.) for 33 days, caused IPF induction in Balb/c mice. Pulmonary combining therapy was administered with L. minor at dose 120 mg/mL (0.187 mg/kg b.w.). L. minor histologically ameliorated BLM induced IPF in lung tissues. L. minor significantly modulated (p < 0.05) BLM-alterations induced in lung hydroxyproline, carbonylated proteins, 5-MSL-protein oxidation. Oxidative stress decreased levels in antioxidant enzymatic and non-enzymatic systems in the lung were significantly regulated (p < 0.05) by L. minor. L. minor decreased the IL-1β, IL-6, and TNF-α expression in lung tissues and plasma. The L. minor improves the preventive effect/defense response in specific pulmonary protein oxidation, lipid peroxidation, ROS identifications, and cytokine modulation by BLM-induced chronic inflammations, and could be a good antioxidant, anti-inflammatory, and anti-fibrotic alternative or IPF prevention involved in their pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Pulmonary Protein Oxidation and Oxidative Stress Modulation by Lemna minor L. in Progressive Bleomycin-Induced Idiopathic Pulmonary Fibrosis

et al. 2022

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Systematic characterization of the components and molecular mechanisms of Jinshui Huanxian granules using UPLC-Orbitrap Fusion MS integrated with network pharmacology

Yuan

Zhao

Liu

et al. 2022

Sci Rep

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Jinshui Huanxian granules (JSHX) is a clinical Chinese medicine formula used for treating pulmonary fibrosis (PF). However, the effective components and molecular mechanisms of JSHX are still unclear. In this study, a combination approach using ultra-high performance liquid chromatography-Orbitrap Fusion mass spectrometry (UPLC-Orbitrap Fusion MS) integrated with network pharmacology was followed to identify the components of JSHX and the underlying molecular mechanisms against PF. UPLC-Orbitrap Fusion MS was used to identify the components present in JSHX. On the basis of the identified components, we performed target prediction using the SwissTargetPrediction database, protein–protein interaction (PPI) analysis using STRING database, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis using Metascape and constructed a component-target-pathway network using Cytoscape 3.7.2. Molecular docking technology was used to verify the affinity between the core components and targets. Finally, the pharmacological activities of three potentially bioactive components were validated in transforming growth factor β1 (TGF-β1)-induced A549 cell fibrosis model. As a result, we identified 266 components, including 56 flavonoids, 52 saponins, 31 alkaloids, 10 coumarins, 12 terpenoids and 105 other components. Of these, 90 validated components were predicted to act on 172 PF-related targets and they exhibited therapeutic effects against PF via regulation of cell migration, regulation of the mitogen-activated protein kinase (MAPK) cascade, reduction of oxidative stress, and anti-inflammatory activity. Molecular docking showed that the core components could spontaneously bind to receptor proteins with a strong binding force. In vitro, compared to model group, hesperetin, ruscogenin and liquiritin significantly inhibited the increase of α-smooth muscle actin (α-SMA) and fibronectin (FN) and the decrease of e-cadherin (E-cad) in TGF-β1-induced A549 cells. This study is the first to show, using UPLC-Orbitrap Fusion MS combined with network pharmacology and experimental validation, that JSHX might exert therapeutic actions against PF by suppressing the expression of key factors in PF. The findings provide a deeper understanding of the chemical profiling and pharmacological activities of JSHX and a reference for further scientific research and clinical use of JSHX in PF treatment.

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Hepatic and immune modulatory effectiveness of lactoferrin loaded Selenium nanoparticles on bleomycin induced hepatic injury

Abdel-Wahhab,

Ashry,

Hassan

et al. 2024

Sci Rep

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This study aimed to estimate the hepatic and immune ameliorating potential of extracted bovine lactoferrin (LF), Selenium nanoparticles (SeNPs) or their combination (LF/SeNPs) against bleomycin (BLM) induced hepatic injury. Fifty adult male rats (160–200 g) were equally divided into five groups: (1) the saline control group, (2) BLM-injected (15 mg/kg twice a week, ip), and (3–5) groups treated orally with LF (200 mg/kg/day), SeNPs (0.0486 mg/kg/day) or LF/SeNPs combination (200.0486 mg/kg/day) for 6 weeks post BLM-intoxication. Blood and liver samples were subjected to biochemical, histopathological, and immunohistochemical analyses. The results revealed that BLM caused a significant increase in hepatic lipid peroxidation and nitric oxide, as well as serum markers of liver functions (AST, ALT and GGT activities), and levels of GM-CSF, CD4, TNF-α, IL-1β, TGF-β1, fibronectin, triglycerides, cholesterol and LDL-C. Additionally, hepatic glutathione, Na+/K+-ATPase, and glutathione peroxidase, as well as serum HDL-C, total protein and albumin levels were significantly reduced. Moreover, BLM injection resulted in marked histopathological alterations and severe expression of caspase 3. Post-treatment of BLM-intoxicated rats with LF, SeNPs or LF/SeNPs combination obviously improved the BLM-induced hepatic damages; this was achieved from the marked modulations in the mentioned parameters, besides improving the histopathological hepatic architecture. It is worth mentioning that LF/SeNPs exerted the greatest potency. In conclusion, the obtained results demonstrated that LF, SeNPs and LF/SeNPs succeeded in attenuating the BLM-induced hepatic dysfunction. Therefore, these supplements might be used to protect against drug-associated side effects.

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Liver damage in bleomycin-induced pulmonary fibrosis in mice

Cited by 6 publications

References 48 publications

Pulmonary Protein Oxidation and Oxidative Stress Modulation by Lemna minor L. in Progressive Bleomycin-Induced Idiopathic Pulmonary Fibrosis

Pulmonary Protein Oxidation and Oxidative Stress Modulation by Lemna minor L. in Progressive Bleomycin-Induced Idiopathic Pulmonary Fibrosis

Systematic characterization of the components and molecular mechanisms of Jinshui Huanxian granules using UPLC-Orbitrap Fusion MS integrated with network pharmacology

Hepatic and immune modulatory effectiveness of lactoferrin loaded Selenium nanoparticles on bleomycin induced hepatic injury

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