Wogonin prevents lipopolysaccharide‐induced acute lung injury and inflammation in mice via peroxisome proliferator‐activated receptor gamma‐mediated attenuation of the nuclear factor‐kappaB pathway

Yao, Jing; Pan, Di; Zhao, Yue; Zhao, Li; Sun, Jie; Wang, Yu; Qin, You; Xi, Tao; Guo, Qinglong; Lu, Na

doi:10.1111/imm.12305

Cited by 80 publications

(51 citation statements)

References 67 publications

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“…The leakage of protein rich plasma into alveolar space due to the upregulation of pulmonary barrier permeability results in lung edema. In this study, we found that lung edema was induced by LPS and this result was similar to previous study (Yao et al, ). At the same time, Yao et al has also demonstrated that the increased protein concentration in BALF after intravascular administration of LPS for 24 h is inhibited by wogonin at 30 mg/kg.…”

Section: Discussionsupporting

confidence: 92%

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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Section: Discussionsupporting

confidence: 92%

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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“…Comparable anti-inflammatory actions have been previously reported in several in vivo models of endotoxemia when using flavonoid-rich plant extracts, as well as for isolated flavonoids or their metabolites [25], [26], [27], [28], [29]. Regarding the actions of ( − )-epicatechin, we have previously reported that in fructose-fed and in high fat-fed rats inflammatory markers were mostly normalized by the presence of (−)-epicatechin in the diet [30], [31].…”

Section: Discussionmentioning

confidence: 61%

LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats

et al. 2017

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This work investigated the capacity of (−)-epicatechin to prevent the renal damage induced by LPS administration in rats. Male Sprague Dawley rats were fed for 4 days a diet without or with supplementation with (−)-epicatechin (80 mg/kg BW/d), and subsequently i.p. injected with lipopolysaccharide (LPS). Six hours after injection, LPS-treated rats exhibited increased plasma creatinine and urea levels as indicators of impaired renal function. The renal cortex of the LPS-treated rats showed: i) increased expression of inflammatory molecules (TNF-α, iNOS and IL-6); ii) activation of several steps of NF-κB pathway; iii) overexpression of TLR4, and iv) higher superoxide anion production and lipid peroxidation index in association with increased levels of gp91phox and p47phox (NOX2) and NOX4. Pretreatment with dietary (−)-epicatechin prevented the adverse effects of LPS challenge essentially by inhibiting TLR4 upregulation and NOX activation and the consequent downstream events, e.g. NF-kB activation.

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“…The pieces of colonic tissue were used for ex vivo analysis. The histological analysis was performed as previously described [48]. …”

Section: Methodsmentioning

confidence: 99%

Wogonoside prevents colitis-associated colorectal carcinogenesis and colon cancer progression in inflammation-related microenvironment via inhibiting NF-κB activation through PI3K/Akt pathway

et al. 2016

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The inflammatory microenvironment has been reported to be correlated with tumor initiation and malignant development. In the previous studies we have found that wogonoside exerts anti-neoplastic and anti-inflammatory activities. In this study, we aimed to further investigate the chemopreventive effects of wogonoside on colitis-associated cancer and delineated the potential mechanisms. In the azoxymethane initiated and dextran sulfate sodium (AOM/DSS) promoted colorectal carcinogenesis mouse model, wogonoside significantly reduced the disease severity, lowered tumor incidence and inhibited the development of colorectal adenomas. Moreover, wogonoside inhibited inflammatory cells infiltration and cancer cell proliferation at tumor site. Furthermore, wogonoside dramatically decreased the secretion and expression of IL-1β, IL-6 and TNF-α as well as the nuclear expression of NF-κB in adenomas and surrounding tissues. In vitro results showed that wogonoside suppressed the proliferation of human colon cancer cells in the inflammatory microenvironment. Mechanistically, we found that wogonoside inhibited NF-κB activation via PI3K/Akt pathway. In conclusion, our results demonstrated that wogonoside attenuated colitis-associated tumorigenesis in mice and inhibited the progression of human colon cancer in inflammation-related microenvironment via suppressing NF-κB activation by PI3K/Akt pathway, indicating that wogonoside could be a promising therapeutic agent for colorectal cancer.

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Wogonin prevents lipopolysaccharide‐induced acute lung injury and inflammation in mice via peroxisome proliferator‐activated receptor gamma‐mediated attenuation of the nuclear factor‐kappaB pathway

Cited by 80 publications

References 67 publications

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

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

LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats

Wogonoside prevents colitis-associated colorectal carcinogenesis and colon cancer progression in inflammation-related microenvironment via inhibiting NF-κB activation through PI3K/Akt pathway

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