Protective effect of rutin on LPS-induced acute lung injury via down-regulation of MIP-2 expression and MMP-9 activation through inhibition of Akt phosphorylation

Chen, Wenying; Huang, Yi-Chun; Yang, Ming-Ling; Lee, Chien‐Ying; Chen, Chun‐Jung; Yeh, Chung‐Hsin; Pan, Pin-Ho; Horng, Chi‐Ting; Kuo, Wu‐Hsien; Kuan, Yu‐Hsiang

doi:10.1016/j.intimp.2014.07.026

Cited by 53 publications

(42 citation statements)

References 31 publications

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“…Cells as well as body fluids participate in the inflammatory response (24). Cells participating in inflammation include polymorphonuclear neutrophil (PMN), alveolar epithelial cells, vascular endothelial cells, pulmonary vascular endothelial cells, alveolar macrophages, pulmonary interstitial macrophages and pulmonary intravascular macrophages, among which PMN and pulmonary intravascular macrophageshave a pivotal role in lung injury (25).…”

Section: Discussionmentioning

confidence: 99%

Salvianolic acid B attenuates lipopolysaccharide-induced acute lung injury in rats through inhibition of apoptosis, oxidative stress and inflammation

Zhao

Liu

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The present study was performed to assess the protective effect of salvianolic acid B on lipopolysaccharide (LPS)-induced acute lung injury (ALI). Sprague Dawley rats were injected with 100 µg/kg LPS through a 24-gauge catheter. One group of rats was pre-treated with salvianolic acid B (1 mg/ml; 20 ml/kg body weight) 1 h prior to LPS challenge, then 20 ml/kg salvianolic acid B every 2 days for 4 weeks thereafter. Salvianolic acid B attenuated LPS-induced increases in the lung wet/dry weight rate and lung tissue injury in ALI model rats. LPS-induced changes in the content of caspase-3, malondialdehyde, superoxide dismutase, catalase, glutathione peroxidase, tumor necrosis factor-α and interleukin-6 in ALI model rats were attenuated by treatment with salvianolic acid B. Furthermore, treatment with salvianolic acid B inhibited the protein expression of type I collagen I, endogenous transforming growth factor-β1 production and α-smooth muscle actin in ALI model rats. These findings indicated that salvianolic acid B attenuates LPS-induced ALI through inhibition of apoptosis, oxidative stress and inflammation in rats and therefore exertsa protective effect against ALI.

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Section: Discussionmentioning

confidence: 99%

Salvianolic acid B attenuates lipopolysaccharide-induced acute lung injury in rats through inhibition of apoptosis, oxidative stress and inflammation

Zhao

Liu

et al. 2017

Experimental and Therapeutic Medicine

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“…One of the most important characteristics of the initial innate immune response in the lung against bacterial infection or BLE is the vigorous recruitment of neutrophils [23]. In ALI, neutrophils are the earliest immune cells which recruited to the site of injury and express multiple cytotoxic products.…”

Section: Discussionmentioning

confidence: 99%

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Tao

Wang

et al. 2015

International Immunopharmacology

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“…BALF was centrifuged at 800 g for 10 min at 4°C. The levels of protein in the BALF supernatants were measured by Bradford protein assay (Chen et al, ).…”

Section: Methodsmentioning

confidence: 99%

Protective effect of wogonin on endotoxin‐induced acute lung injury via reduction of p38 MAPK and JNK phosphorylation

Wei

Sun

Yang

et al. 2016

Environmental Toxicology

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Acute lung injury (ALI) is a serious inflammatory disorder which remains the primary cause of incidence and mortality in patients with acute pulmonary inflammation. However, there is still no effective medical strategy available clinically for the improvement of ALI. Wogonin, isolated from roots of Scutellaria baicalensis Georgi, is a common medicinal herb which presents biological and pharmacological effects, including antioxidation, anti-inflammation, and anticancer. Preadministration of wogonin inhibited not only lung edema but also protein leakage into the alveolar space in murine model of lipopolysaccharide (LPS)-induced ALI. Moreover, wogonin not only reduced the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 but also inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) induced by LPS. We further found wogonin inhibited the phosphorylation of p38 MAPK and JNK at a concentration lower than ERK. In addition, inhibition of lung edema, protein leakage, expression of iNOS and COX-2, and phosphorylation of p38 MAPK and JNK were all observed in a parallel concentration-dependent manner. These results suggest that wogonin possesses potential protective effect against LPS-induced ALI via downregulation of iNOS and COX-2 expression by blocking phosphorylation of p38 MAPK and JNK. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 397-403, 2017.

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Protective effect of rutin on LPS-induced acute lung injury via down-regulation of MIP-2 expression and MMP-9 activation through inhibition of Akt phosphorylation

Cited by 53 publications

References 31 publications

Salvianolic acid B attenuates lipopolysaccharide-induced acute lung injury in rats through inhibition of apoptosis, oxidative stress and inflammation

Salvianolic acid B attenuates lipopolysaccharide-induced acute lung injury in rats through inhibition of apoptosis, oxidative stress and inflammation

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Protective effect of wogonin on endotoxin‐induced acute lung injury via reduction of p38 MAPK and JNK phosphorylation

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