Puerarin prevents LPS-induced acute lung injury via inhibiting inflammatory response

Wang, Xinye; Yan, Jian; Xu, Xiaohong; Duan, Chunyan; Xie, Zheng; Su, Zheqian; Ma, Hongxia; Ma, Hui; Wei, Xing; Du, Xiaochun

doi:10.1016/j.micpath.2018.03.033

Cited by 60 publications

(40 citation statements)

References 27 publications

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“…Cinnamic acid was shown to decrease the production of inflammatory mediators such as NO, prostaglandin E2, IL-6, and TNF-α in LPS-stimulated RAW264.7 cells [ 26 ]. Puerarin and glycyrrhizin inhibited inflammatory responses in an LPS-induced acute lung injury model and an imiquimod-induced psoriasis-like skin model, respectively [ 27 , 28 ]. In addition, paeoniflorin has shown anti-inflammatory properties in various experimental models such as collagen-induced rheumatoid arthritis, high-fat diet-induced atherosclerosis, and LPS-induced acute lung injury [ 29 , 30 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

Galgeun-tang Attenuates Cigarette Smoke and Lipopolysaccharide Induced Pulmonary Inflammation via IκBα/NF-κB Signaling

et al. 2018

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Galgeun-tang water extract (GGWE) is used to treat various diseases such as the common cold, eczema and asthma in China and Korea. In this study, we investigated the anti-inflammatory effect of GGWE using a cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced induced pulmonary inflammation mouse model. The mice were exposed to CS for a total of seven days (eight cigarettes per day for 1 h) and LPS was administered intranasally to mice on day 4. GGWE was administered by oral gavage at doses of 50 mg/kg or 100 mg/kg 1 h before exposure to CS. GGWE decreased inflammatory cell counts, and expression of inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α) in bronchoalveolar lavage fluid (BALF) from mice exposed to CS and LPS. GGWE reduced the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the phosphorylation of inhibitor of kappa-B subunit alpha (IκBα) and nuclear factor kappa-B (NF-κB) in CS- and LPS-exposed mice. Histological examinations revealed that GGWE suppressed inflammatory cell infiltration into lung tissue compared to untreated CS- and LPS-exposed mice. In conclusion, GGWE effectively suppressed CS- and LPS-induced pulmonary inflammation. Our results indicate that GGWE may be used as a protective drug to control pulmonary inflammation diseases such as chronic obstructive pulmonary disease.

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Section: Discussionmentioning

confidence: 99%

Galgeun-tang Attenuates Cigarette Smoke and Lipopolysaccharide Induced Pulmonary Inflammation via IκBα/NF-κB Signaling

et al. 2018

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“…OA is a common joint disease with persistent, low-degree inflammation in the synovium (3). Puerarin has been reported to exhibit anti-inflammatory effects in various mouse models of inflammatory disease, including ischemia/reperfusion, atopic dermatitis, mastitis and collagen antibody-induced arthritis (11,16,28,29). Puerarin treatment inhibits chronic inflammation induced by lipopolysaccharide or pro-inflammatory mediators, such as IL-1β, in various types of cells (9,19,30).…”

Section: Discussionmentioning

confidence: 99%

Puerarin alters the function of monocytes/macrophages and exhibits chondroprotection in mice

et al. 2019

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Recent studies have suggested that puerarin may impede osteoclastogenesis and facilitate bone regeneration, in addition to attenuating tissue inflammation. The present study investigated the therapeutic effects of puerarin on inflammatory responses and monocyte recruitment in in vitro and in vivo osteoarthritis (OA) models. Puerarin treatment increased the proliferation of OA chondrocytes, as determined by Cell Counting Kit-8 assay. In addition, the present results suggested that puerarin suppressed the interleukin-1β-induced production of inflammatory cytokines in OA chondrocytes and monocytes/macrophages, as assessed by ELISA. In a mouse model of mono-iodoacetate-induced OA, the present histological analyses suggested that administration with puerarin attenuated the inflammatory profile of OA joints and reduced cartilage destruction. Using flow cytometry, a decreased number of myeloid-derived CC chemokine receptor 2 + /lymphocyte Ag 6C + monocytes was identified in the blood of OA mice treated with puerarin compared with control OA mice. Furthermore, quantitative real-time polymerase chain reaction analysis suggested that puerarin treatment decreased CC chemokine ligand 2 expression in arthritic tissues. Collectively, the results suggested that puerarin treatment limited the recruitment of inflammatory monocytes. In summary, the present study provided pre-clinical evidence that puerarin may serve as a potential target in the treatment of OA.

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“…Sepsis is the immune response of the organism to invading microbes (Wu et al, 2016). Sepsis can cause multiple organ dysfunction in the body and the most affected organ is lung, so acute lung injury (ALI) is one of the common complications of sepsis (Wang et al, 2018; Zhang et al, 2015). Study showed that the incidence of lung injury in sepsis patients was 21.98% and the fatality rate was 66.7% in China (Wang et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Flufenamic acid alleviates sepsis‐induced lung injury by up‐regulating CBR1

Jiang

Chen

Jiang

2020

Drug Development Research

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Investigate the effect of flufenamic acid (FFA) on lung injury of sepsis rats. Rat sepsis model was established using cecal ligation and puncture (CLP). The pathomorphology of lung tissue was detected by Hematoxylin–eosin (H&E) staining. The expression levels of tumor necrosis factor alpha (TNF‐α), interleukin‐6 (IL‐6), and high mobility group box‐1 (HMGB‐1) in serum and TNF‐α, IL‐6, malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) in lung tissues. The viability of RLE‐6TN cells was detected by CCK‐8 assay. The expression of carbonyl reductase 1 (CBR1) in RLE‐6TN cells was analyzed by Western blot analysis and reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR) analysis. The inflammatory response was obviously enhanced in CLP‐constructed sepsis rats and alleviated by FFA treatment. Sepsis induced the increase of W/D ratio, promoted the levels of TNF‐α, IL‐6, HMGBR1, and MDA and inhibited the levels of SOD and GSH. FFA could effectively alleviate the sepsis‐induced lung injury. The viability of RLE‐6TN cells induced by LPS was improved with the treatment of FFA. CBR1 expression in LPS‐induced RLE‐6TN cells was decreased and FFA could up‐regulate the CBR1 expression. In addition, LPS‐induced lung injury promoted the inflammatory response in lung tissues, increased the W/D ratio and levels of TNF‐α, IL‐6, HMGBR1, and MDA while inhibited the levels of SOD and GSH. FFA could effectively improve the LPS‐induced lung injury while the effect of FFA on LPS‐induced lung injury was alleviated by CBR1 interference. FFA may alleviate sepsis‐induced lung injury by up‐regulating CBR1.

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Puerarin prevents LPS-induced acute lung injury via inhibiting inflammatory response

Cited by 60 publications

References 27 publications

Galgeun-tang Attenuates Cigarette Smoke and Lipopolysaccharide Induced Pulmonary Inflammation via IκBα/NF-κB Signaling

Galgeun-tang Attenuates Cigarette Smoke and Lipopolysaccharide Induced Pulmonary Inflammation via IκBα/NF-κB Signaling

Puerarin alters the function of monocytes/macrophages and exhibits chondroprotection in mice

Flufenamic acid alleviates sepsis‐induced lung injury by up‐regulating CBR1

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