Chitosan aerosol inhalation alleviates lipopolysaccharide- induced pulmonary fibrosis in rats

Zhou, Lulu; He, Xing‐Ying; Xu, Fei; Du, Bin; Zou, Zui; Shi, Xueyin

doi:10.3109/01902148.2014.948231

Cited by 7 publications

(3 citation statements)

References 32 publications

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“…The histopathology of lung tissue sections in animals pre-treated with Ch-NPs showed a normal appearance. Our findings agreed with those of Zhou et al (2014) who suggested that chitosan exhibited potent antifibrotic activities by reducing fibroblast proliferation, decreasing extracellular matrix deposition and collagen synthesis levels. In addition, chitosan was shown to stimulate reepithelialization in experimental wounds ( Lee et al 2016a, b).…”

Section: Discussionsupporting

confidence: 93%

The targeted delivery of chitosan nanoparticles to treat indoxacarb: induced lung fibrosis in rats

et al. 2022

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Background This study evaluated the effects of chitosan nanoparticles (Ch-NPs) on indoxacarb (INDOX)-induced pulmonary fibrosis in in vivo and in vitro models. In in vivo studies, 40 male albino rats were randomly divided into four groups (10 rats/group): Group 1, normal control; Group 2, INDOX (600 mg/kg b.w.); Group 3, Ch-NPs (2 mg/kg b.w.); and Group 4, Ch-NPs + INDOX. Characterization of Ch-NPs was done measuring dynamic light scattering, zeta potential, Fourier-transform infrared spectroscopy, transmission electron microscopy, and antioxidant activity studies after various Ch-NPs treatments. From in vitro studies, the impact of Ch-NPs on A549 lung carcinoma cell proliferation was also examined. Results Our data indicated that INDOX provoked considerable lung damage as indicated by decreased antioxidant enzyme levels of superoxide dismutase and glutathione peroxidase, increased production of nitric oxide and malondialdehyde serum levels, elevated myeloperoxidase activity, increased hydroxyproline and cytokeratin-19 serum levels, and significantly upregulated matrix metallopeptidase-9 and microRNA-101 gene expression levels when compared with controls. Furthermore, histopathological and immunohistochemical investigations of cyclooxygenase-2 in the lung tissue revealed marked inflammation, severe fibrosis, and neutrophil infiltration. Critically, Ch-NPs treatment significantly reversed INDOX-induced changes in lung biochemical, histopathological, and immunohistochemical outcomes. Conclusion Therefore, Ch-NPs may function as potential therapeutic drugs for lung fibrosis owing to their antioxidant, anti-inflammatory, and antifibrotic activities with neutrophil infiltration.

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Section: Discussionsupporting

confidence: 93%

The targeted delivery of chitosan nanoparticles to treat indoxacarb: induced lung fibrosis in rats

et al. 2022

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“…While fibrosis progression is characterised by extracellular matrix (ECM) accumulation and fibroblast proliferation, chitosan is known to inhibit the latter with potent effects on collagen synthesis and ECM production (4,15). TGF-β reportedly plays a crucial role in idiopathic PF and animal models of lung fibrosis (16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

Oral Administration of Chitosan Attenuates Bleomycin-induced Pulmonary Fibrosis in Rats

Kim

Youn

et al. 2019

In Vivo

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Background/Aim: Idiopathic pulmonary fibrosis (PF) is a fatal disorder of unknown aetiology with limited treatment options. Chitosan has antibacterial, antifungal, antioxidant, antitumour, and anti-inflammatory effects. This study aimed to investigate the effects of chitosan administration on bleomycin (BLM)-induced PF in rats. Materials and Methods: A PF rat model was established by endotracheal instillation of 5 mg/kg BLM; then, chitosan was administered in drinking water for 3 weeks. Histology, cell counts, and cytokine responses in the bronchoalveolar lavage fluid (BALF) and weight measurements (body and lung) were analyzed to assess its therapeutic effects. Results: Chitosan administration tended to reduce transforming growth factor (TGF)-β1 and interferon (IFN)-γ levels in BALF, and histopathological examination confirmed that chitosan attenuated the degree of inflammation and fibrosis in the lung. Conclusion: This study revealed that oral chitosan exhibits potential antifibrotic effects, as measured by decreased proinflammatory cytokine levels and histological evaluation, in a BLM-induced PF rat model.

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“…It has been documented that chitosan decreases the levels of BUN and CRE and elevates the activities/levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in an adenine-induced rat model of CRF [ 9 ]. Moreover, chitosan exerts potent anti-fibrosis activity by inhibiting tissue inhibitor of metalloproteinase-1 (TIMP-1) [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Combination therapy of chitosan, gynostemma, and motherwort alleviates the progression of experimental rat chronic renal failure by inhibiting STAT1 activation

Bai

Wang

et al. 2018

Oncotarget

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This study aimed to investigate the effect of single and combination therapy using chitosan (K), gynostemma (J), and motherwort (Y) on an experimental rat model of chronic renal failure (CRF) induced by adenine and the underlying mechanisms. CRF rats were treated with individual or combinational therapy with two or three of these agents. Biochemical indicators showed that the levels of blood urea nitrogen, creatinine and uric acid decreased and the levels of albumin and hemoglobin increased by single or combination therapy of these drugs. Drug treatment also decreased oxidative stress damage of renal tissues in CRF rats. Histopathological lesions were attenuated in each drug treatment group by various degrees. Additionally, drug treatment affected the expression of extracellular matrix (ECM) proteins including plasminogen activator inhibitor 1, collagen I, matrix metalloprotease-1, and tissue inhibitor of metalloproteinases 1. In particular, the combination therapy of K, J, and Y was superior to the respective monotherapy, which supported the prescription of KJY combination. We further studied the inhibitory effect of KJY on LPS-induced inflammation in RAW264.7 macrophages. The results showed that KJY inhibited LPS-induced secretion of inflammatory cytokines (Interferon-gamma, Interleukin-1 Beta, chemokine (C-X-C motif) ligand 10, cyclooxygenase-2 and Tumor necrosis factor-α in RAW264.7 macrophages. Combination therapy of KJY suppressed the protein expression of Cyclooxygenase-2 and inducible nitric oxide synthase in vivo and in vitro. Further study indicated that KJY inhibited STAT1 activation by down regulating p-STAT1 to exert anti-inflammatory effect and improve renal function in rats with chronic renal failure.

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Chitosan aerosol inhalation alleviates lipopolysaccharide- induced pulmonary fibrosis in rats

Abstract: Our findings show that chitosan aerosol inhalation inhibits the expression of MMP-3 and TIMP-1, and ameliorates LPS-induced pulmonary remodeling and fibrosis in rats.

Cited by 7 publications

References 32 publications

The targeted delivery of chitosan nanoparticles to treat indoxacarb: induced lung fibrosis in rats

The targeted delivery of chitosan nanoparticles to treat indoxacarb: induced lung fibrosis in rats

Oral Administration of Chitosan Attenuates Bleomycin-induced Pulmonary Fibrosis in Rats

Combination therapy of chitosan, gynostemma, and motherwort alleviates the progression of experimental rat chronic renal failure by inhibiting STAT1 activation

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