The effects of phycocyanin on bleomycin-induced pulmonary fibrosis and the intestinal microbiota in C57BL/6 mice

Xie, Yuanyuan; Li, Wenjun; Lu, Chenyang; Zhu, Limeng; Qin, Song; Du, Zhimin

doi:10.1007/s00253-019-10018-7

Cited by 22 publications

(13 citation statements)

References 34 publications

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“…In addition, chest irradiation can lead to disorders of the lung and intestinal flora, while PC intervention significantly alleviated the disorder of the flora. This result is very similar to our previous report on the effects of phycocyanin on bleomycin-induced pulmonary fibrosis and the intestinal microbiota in C57BL/6 mice [ 10 ].…”

Section: Discussionsupporting

confidence: 92%

“…It has been reported that PC can alleviate paraquat-induced lung injury in rats [ 8 ]. Research found that in the bleomycin-induced mouse lung fibrosis model, PC could regulate TLR2-MyD88-NF-κB signaling pathways alleviate pulmonary fibrosis [ 9 ], and in addition, could significantly reduce bacteria that associated with inflammation, thereby alleviating pulmonary fibrosis [ [10] , [11] , [12] ].…”

Section: Introductionmentioning

confidence: 99%

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Effects of phycocyanin on pulmonary and gut microbiota in a radiation-induced pulmonary fibrosis model

Li¹,

Lu²,

Liu³

et al. 2020

Biomedicine & Pharmacotherapy

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Objective Radiation pneumonia and fibrosis are major clinical complications of radiotherapy for thoracic tumor patients, and may significantly reduce survival and quality of life. At present, no safe and effective radiation protection measures have been approved for clinical use. Phycocyanin, a protein responsible for photosynthesis from Spirulina , has been shown to have a variety of biological activities and to be beneficial for a variety of diseases, including pulmonary fibrosis. However, the preventive and protective effects of phycocyanin on radiation-induced pulmonary fibrosis have not been studied. Design X-ray single dose irradiation was used on the chest of mice to prepare a mouse model of pulmonary fibrosis, from which the effect of phycocyanin on pulmonary histopathologic change, pulmonary fibrosis, the microbiota in lung and gut, LPS, TNF-α, and IL-6 at different time after irradiation were evaluated. Results Phycocyanin alleviated the radiation-induced lung injury and reduced the level of inflammatory factors. Thorax irradiation led to the disorder in microbiota of the lung and gut. The variation trend of the diversity of the two tissues was opposite, but that of the microbiota composition was similar. The phycocyanin intervention regulated the composition of the lung and gut microbiota, transformed them into normal state, and reduced the level of LPS, which significantly reduced the abundance of inflammation-related bacteria, and increased the abundance of probiotics that produce short-chain fatty acids. Conclusion Phycocyanin could regulate the radiation-induced disorder in lung and gut microbiota of mice, and reduce the radiation-induced lung inflammation and fibrosis.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Effects of phycocyanin on pulmonary and gut microbiota in a radiation-induced pulmonary fibrosis model

Li¹,

Lu²,

Liu³

et al. 2020

Biomedicine & Pharmacotherapy

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“…It is of possible relevance that taurine administration has been shown to exert anti-inflammatory activity when the lungs of rodents have been challenged with endotoxin or various other pro-inflammatory agents [256][257][258]. Similar effects have been reported with phycocyanin, glucosamine, berberine, lipoic and ferulic acids, melatonin, and N-acetylcysteine [259][260][261][262][263][264][265].…”

Section: Pertinence To the Management Of Covid-19mentioning

confidence: 83%

Nutraceutical Strategies for Suppressing NLRP3 Inflammasome Activation: Pertinence to the Management of COVID-19 and Beyond

et al. 2020

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Inflammasomes are intracellular protein complexes that form in response to a variety of stress signals and that serve to catalyze the proteolytic conversion of pro-interleukin-1β and pro-interleukin-18 to active interleukin-1β and interleukin-18, central mediators of the inflammatory response; inflammasomes can also promote a type of cell death known as pyroptosis. The NLRP3 inflammasome has received the most study and plays an important pathogenic role in a vast range of pathologies associated with inflammation—including atherosclerosis, myocardial infarction, the complications of diabetes, neurological and autoimmune disorders, dry macular degeneration, gout, and the cytokine storm phase of COVID-19. A consideration of the molecular biology underlying inflammasome priming and activation enables the prediction that a range of nutraceuticals may have clinical potential for suppressing inflammasome activity—antioxidants including phycocyanobilin, phase 2 inducers, melatonin, and N-acetylcysteine, the AMPK activator berberine, glucosamine, zinc, and various nutraceuticals that support generation of hydrogen sulfide. Complex nutraceuticals or functional foods featuring a number of these agents may find utility in the prevention and control of a wide range of medical disorders.

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“…ALI is characterised by diffused pulmonary interstitial and alveolar oedema, which leads to acute hypoxic respiratory insufficiency and pulmonary fibrosis, posing a significant health threat to individuals. 22,23 However, the precise molecular mechanism behind the development of pulmonary fibrosis after ALI remains unclear. During epithelial injury repair, alveolar type II epithelial cells act as stem cells and undergo transdifferentiation to alveolar type I epithelial cells, thus ensuring the renewal of the latter.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of lipopolysaccharide-mediated induction of epithelial-mesenchymal transition of alveolar type II epithelial cells in absence of other inflammatory cells

Xue

et al. 2021

Eur J Inflamm

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Several studies have shown that gram-negative bacilli infection can cause acute lung injury, and that consequent pulmonary fibrosis is caused when alveolar type-II epithelial cells undergo epithelial-mesenchymal transition (EMT). However, the mechanism underlying this change remains unclear. This study aimed to elucidate whether the main toxin of gram-negative bacteria, lipopolysaccharide (LPS), can induce EMT in human alveolar epithelial cells, and the underlying molecular mechanisms. Human alveolar type-II epithelial cells (A549) were used in EMT induction experiments. Cells were collected after LPS exposure, and changes in the expression levels of epithelial and mesenchymal cell markers were determined. Further, the effect of LPS exposure on the expression of Toll-like Receptor 4 (TLR4), Transforming Growth Factor-beta 1 (TGF-β1) and Smad2/3 was assessed. The expression level of a mesenchymal cell marker was also assessed after pharmacological inhibition of TLR4 and TGF-β1 prior to addition of LPS, to identify downstream pathways involved in EMT induction. Results showed that LPS exposure caused significant downregulation of epithelial marker E-cadherin, and upregulation of mesenchymal marker vimentin, together with increased expression of TGF-β1 and activation of the TGF-β1/Smad2/3 pathway. Furthermore, pretreatment with TGF-β1 and TLR4 inhibitors suppressed EMT, and treatment with the latter also reduced the expression level of TGF-β1. Overall, we conclude that LPS directly induces EMT in A549 cells through upregulation of TLR4 and activation of the TGF-β1/Smad2/3 signalling pathway. Our results suggest that LPS-mediated pulmonary fibrosis may occur in ALI patients even if the LPS-induced inflammatory response is inhibited.

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The effects of phycocyanin on bleomycin-induced pulmonary fibrosis and the intestinal microbiota in C57BL/6 mice

Cited by 22 publications

References 34 publications

Effects of phycocyanin on pulmonary and gut microbiota in a radiation-induced pulmonary fibrosis model

Effects of phycocyanin on pulmonary and gut microbiota in a radiation-induced pulmonary fibrosis model

Nutraceutical Strategies for Suppressing NLRP3 Inflammasome Activation: Pertinence to the Management of COVID-19 and Beyond

Mechanism of lipopolysaccharide-mediated induction of epithelial-mesenchymal transition of alveolar type II epithelial cells in absence of other inflammatory cells

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