2023
DOI: 10.1016/j.phymed.2022.154545
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Xuanfei Baidu formula alleviates impaired mitochondrial dynamics and activated NLRP3 inflammasome by repressing NF-κB and MAPK pathways in LPS-induced ALI and inflammation models

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Cited by 42 publications
(20 citation statements)
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“…A mouse model of pulmonary fibrosis bleomycin treated with Xuanfei Baidu decoction showed that this medicine could effectively protect the alveolar structure, reduce the cellular changes of lung, improve the infiltration of inflammatory cells, and inhibit the thickening of the blood vessel wall and collagen deposition; furthermore, after network pharmacology and protein-protein interaction analysis, we found that the above effects were related to inhibition of the activation of interleukin (IL)-6/STAT3 signaling pathway, preventing the differentiation of M2 macrophages, and downregulating the overexpression of inflammatory factors such as IL-6 and transforming growth factor (TGF)-β [14] . The model of acute lung injury induced by lipopolysaccharide LPS showed that Xuanfei Baidu decoction can improve the pathological changes of lung tissue in mice, downregulate the levels of inflammatory factors IL-6, tumor necrosis factor (TNF)-α, and IL-1β in serum and alveolar lavage fluid of mice, and also inhibit the infiltration of macrophages and neutrophils [15][16][17] . Its mechanism is related to the inhibition of programmed death (PD)-1/IL17A pathways [15] and the polarization of proinflammatory macrophages by increasing mitochondrial fusion and inhibiting the activation of NLRP3 inflammatory bodies mediated by nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways [16][17] .…”
Section: Discussionmentioning
confidence: 99%
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“…A mouse model of pulmonary fibrosis bleomycin treated with Xuanfei Baidu decoction showed that this medicine could effectively protect the alveolar structure, reduce the cellular changes of lung, improve the infiltration of inflammatory cells, and inhibit the thickening of the blood vessel wall and collagen deposition; furthermore, after network pharmacology and protein-protein interaction analysis, we found that the above effects were related to inhibition of the activation of interleukin (IL)-6/STAT3 signaling pathway, preventing the differentiation of M2 macrophages, and downregulating the overexpression of inflammatory factors such as IL-6 and transforming growth factor (TGF)-β [14] . The model of acute lung injury induced by lipopolysaccharide LPS showed that Xuanfei Baidu decoction can improve the pathological changes of lung tissue in mice, downregulate the levels of inflammatory factors IL-6, tumor necrosis factor (TNF)-α, and IL-1β in serum and alveolar lavage fluid of mice, and also inhibit the infiltration of macrophages and neutrophils [15][16][17] . Its mechanism is related to the inhibition of programmed death (PD)-1/IL17A pathways [15] and the polarization of proinflammatory macrophages by increasing mitochondrial fusion and inhibiting the activation of NLRP3 inflammatory bodies mediated by nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways [16][17] .…”
Section: Discussionmentioning
confidence: 99%
“…The model of acute lung injury induced by lipopolysaccharide LPS showed that Xuanfei Baidu decoction can improve the pathological changes of lung tissue in mice, downregulate the levels of inflammatory factors IL-6, tumor necrosis factor (TNF)-α, and IL-1β in serum and alveolar lavage fluid of mice, and also inhibit the infiltration of macrophages and neutrophils [15][16][17] . Its mechanism is related to the inhibition of programmed death (PD)-1/IL17A pathways [15] and the polarization of proinflammatory macrophages by increasing mitochondrial fusion and inhibiting the activation of NLRP3 inflammatory bodies mediated by nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways [16][17] . In addition, Xuanfei Baidu decoction can also improve weight loss, spleen index, disease activity index, TNF-α level, and colon tissue injury of mice with acute colitis.…”
Section: Discussionmentioning
confidence: 99%
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“…Once NF-κB is activated, the secretions of a large number of inflammatory cytokines will aggravate secondary damage and induce cell apoptosis in sepsis ( 13 , 14 ). In many disease models, inhibition of NF-κB activation also has been shown to effectively reduce cell apoptosis ( 8 , 13 , 15 17 ). Therefore, NF-κB is considered as an important therapeutic target for sepsis and inflammatory diseases.…”
Section: Introductionmentioning
confidence: 99%
“…COVID-19 is a global pandemic disease that has affected hundreds of millions of people worldwide. Most patients with COVID-19 may have mild to moderate symptoms such as cough and shortness of breath in the first week, and some patients may show extensive pneumonia, ultimate organ failure and diffuse intravascular coagulation in approximately three weeks ( Fenollar et al, 2021 ; Li et al, 2023 ). The main cause of death from COVID-19 is acute lung injury (ALI).…”
Section: Introductionmentioning
confidence: 99%