<i>Astragalus polysaccharides</i> alleviates LPS‐induced inflammation via the NF‐κB/MAPK signaling pathway

Dong, Na; Li, Xinran; Xue, Chenyu; Zhang, Lei; Wang, Chensi; Xu, Xinyao; Shan, Anshan

doi:10.1002/jcp.29452

Cited by 131 publications

(84 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The DSS model is regarded as a useful tool for the experimental model of ulcerative colitis [ 26 ]. In the model, the colon length shortened, and the DAI score, spleen weight, and histology score increased significantly [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Sodium Butyrate Alleviates Mouse Colitis by Regulating Gut Microbiota Dysbiosis

Dou

Gao

Yan

et al. 2020

Animals

Self Cite

View full text Add to dashboard Cite

Inflammatory bowel disease (IBD) develops as a result of complicated interactions between genetic susceptibility, excessive innate immunity, and environmental factors, which are mainly related to the gut microbiota. The present study aimed to elucidate the protective effects and underlying mechanisms of a short-chain fatty acid salt, sodium butyrate, on colonic inflammation induced by dextran sulfate sodium (DSS) in mice. Pretreatment with sodium butyrate attenuated colitis, as demonstrated by the decreased disease activity index (DAI), colon length shortening, spleen tumidness, and histopathology scores, while maintaining intestinal barrier integrity, as observed by H&E staining and electron microscopy. 16S rRNA sequence analysis revealed that sodium butyrate caused a remarkable alteration of the gut microbiota. Bacteroides, Lachnospiraceae, the Lachnospiraceae NK4A136 group, and Ruminiclostridium 6 presented dramatic differences after sodium butyrate supplementation. This work verifies that sodium butyrate can improve mouse colitis via microbe–host interactions by regulating the microbial community. Taken together, the findings demonstrate that sodium butyrate shows great potential as a probiotic agent for ameliorating colitis.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Briefly, dietary NaB can alleviate inflammatory response in DSS-induced colitis by maintaining gut microbiota dysbiosis, which is evidenced by the increasing abundance of beneficial bacteria, the decreasing abundance of harmful bacteria, and the minimized impact of DSS-induced inflammation [ 26 , 33 ].…”

Section: Discussionmentioning

confidence: 99%

Sodium Butyrate Alleviates Mouse Colitis by Regulating Gut Microbiota Dysbiosis

Dou

Gao

Yan

et al. 2020

Animals

Self Cite

View full text Add to dashboard Cite

show abstract

“…The NF-kB pathway has an active role during inflammation (Wu et al, 2020) though factors such as p65, whose levels can reflect the extent of inflammation . P65 can aggravate inflammation by interacting with other signaling pathways such as the NF-kB/MAPK signaling pathway (Dong et al, 2020). The activation of NF-k B may be a key step in the inflammatory cascade, which can induce the expression of IL-6 (Quay et al, 1998) TNF-a (Lee et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Gehua Jiecheng Decoction Inhibits Diethylnitrosamine-Induced Hepatocellular Carcinoma in Mice by Improving Tumor Immunosuppression Microenvironment

et al. 2020

View full text Add to dashboard Cite

Gehua Jiecheng Decoction (GHJCD), a famous traditional Chinese medicine, has been used in the prevention and treatment of precancerous lesion of liver cancer, but its active mechanism has not been reported. This study aimed to evaluate the therapeutic effect of GHJCD on diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC) in mice and the mechanism of this effect. We found that GHJCD effectively inhibited the occurrence of liver cancer and reduced the tumor area. The ratio of regulatory cells (Tregs), tumorassociated macrophages (TAMs), and myeloid-derived suppressor cells (MDSCs) in HCC microenvironment was down-regulated, whereas that of CD8 T and effective CD8 T cells was up-regulated. In addition, the expression levels of inflammatory factors IL-6, IL-10, TNF-a, and CCL-2 in the liver were inhibited, whereas those of the angiogenesis related molecules CD31 and VEGF were decreased. Moreover, WNT1, b-catenin, NF-kB, p-MAPK, p-AKT, and p-SRC content in the liver decreased, whereas APC content increased. These results suggested that GHJCD exerted a good inhibitory effect on liver cancer induced by DEN and thus may have a multi-target effect; GHJCD not only antagonized the immunosuppressive effect of the microenvironment of liver cancer but also exerted strong anti-inflammatory and antiangiogenesis effects.

show abstract

“…Activation of the NF-κB signaling pathway can induce expression of the proinflammatory cytokines IL-6 [13], TNF-α, and IL-1β [14], and these proinflammatory factors can further activate NF-κB, thus aggravating inflammation [15]. IL-6, TNF-α and IL-1β are important cytokines secreted by cells used to evaluate the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Geniposide, a component of Gardenia jasminoides Ellis, inhibits NF-ĸB to attenuate LPS-induced injury in intestinal epithelial cells

Cui¹,

Qiao²,

Qiu-ju³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: The nuclear factor-ĸB (NF-ĸB) transcriptional system is a major effector pathway involved in inflammatory responses. Previous studies found that a Gardenia decoction (GD) inhibited the expression of NF-κB in a lipopolysaccharide (LPS)-stimulated mouse intestinal injury model. Herein, we hypothesized that geniposide (GE), a component of Gardenia jasminoides Ellis, also exerts anti-inflammatory effects and inhibits NF-ĸB activity in LPS-induced intestinal epithelial cells (IEC-6). IEC-6 cells were stimulated with LPS, following which the effects of GE on NF-ĸB signaling in the IEC-6 cells were examined by western blotting to detect IĸB phosphorylation/degradation. The expression of NF-κB was determined by immunofluorescence assay (IFA). Enzyme-linked immunosorbent assay (ELISA) was used to detect the inhibitory effect of GE on the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) activated by LPS in IEC-6 cells. In addition, the migration ability of IEC-6 cells was observed by the scratch method. Results: These results showed that GE dose-dependently downregulated levels of the proinflammatory cytokines TNF-α, IL-6 and IL-1β that had been upregulated by LPS and suppressed the phosphorylation of IĸB and NF-ĸB induced by LPS. Our findings indicated that GE could reduce LPS-induced NF-ĸB signaling and proinﬂammatory expression in IEC-6 cells and significantly enhance the migration of IEC-6 cells. Moreover, GE inhibited the expression of NF-κB, nuclear transfer, and transcriptional activity in IEC-6 cells. Conclusion: GE could block the synthesis of inflammatory factors of IEC-6 cells by inhibiting activation of the IĸB/NF-κB signaling pathway induced by LPS.

show abstract

Astragalus polysaccharides alleviates LPS‐induced inflammation via the NF‐κB/MAPK signaling pathway

Cited by 131 publications

References 54 publications

Sodium Butyrate Alleviates Mouse Colitis by Regulating Gut Microbiota Dysbiosis

Sodium Butyrate Alleviates Mouse Colitis by Regulating Gut Microbiota Dysbiosis

Gehua Jiecheng Decoction Inhibits Diethylnitrosamine-Induced Hepatocellular Carcinoma in Mice by Improving Tumor Immunosuppression Microenvironment

Geniposide, a component of Gardenia jasminoides Ellis, inhibits NF-ĸB to attenuate LPS-induced injury in intestinal epithelial cells

Contact Info

Product

Resources

About