Acanthopanax senticosus attenuates inflammation in lipopolysaccharide-induced acute lung injury by inhibiting the NF-κB pathway

Fei, X J; Zhu, Lei; Xia, Li; Peng, Wei-Jung; Wang, Q

doi:10.4238/2014.december.12.16

Cited by 21 publications

(13 citation statements)

References 19 publications

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“…NF-κB pathway is considered as the prototype pro-inflammatory pathway mainly because of its role on expression of cytokines, and chemokines [ 34 ]. Similar to our findings, Fei XJ and colleagues shown in their study that Acanthopanax senticosus , a common medicine in Oriental medicine protected murine lung cells from LPS-induced injury via inactivation of NF-κB pathway [ 35 ]. Furthermore, it was found that the protective action of Smad7 against LPS-induced cell damage is mediated by inactivation of NF-κB pathway as estimated by western blot.…”

Section: Discussionsupporting

confidence: 91%

MicroRNA-17-5p aggravates lipopolysaccharide-induced injury in nasal epithelial cells by targeting Smad7

Huang

Wang

et al. 2018

BMC Cell Biol

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BackgroundGlobally, rhinitis is one of the most common chronic disorders. Despite availability of drugs to manage the symptomatology of rhinitis, researchers still focus on identification of novel molecular targets for better management. MicroRNAs are implicated in many biological and pathological processes. However, the role of miR-17-5p in rhinitis remains unexplored. This study aimed to explore the role of miR-17-5p in lipopolysaccharide (LPS)-induced injury of nasal epithelial RPMI2650 cells and to elucidate the possible underlying molecular mechanism.ResultsLPS damaged RPMI2650 cells by inhibiting cell proliferation, promoting apoptosis, and stimulating the release of inflammatory cytokines. miR-17-5p expression was significantly increased in RPMI2650 cells following treatment with LPS. Furthermore, it was found that overexpression of miR-17-5p led to aggravation of LPS-induced injury. miR-17-5p negatively regulated expression of Smad7; overexpression of Smad7 protected the RPMI2650 cells by inactivating NF-κB and Wnt/β catenin pathways and vice versa.ConclusionsOverexpression of miR-17-5p aggravated LPS-induced damage of RPMI2650 cells. Expression of Smad7 was negatively regulated by miR-17-5p; Smad7 expression inactivated NF-κB and Wnt/β catenin pathways.

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Section: Discussionsupporting

confidence: 91%

MicroRNA-17-5p aggravates lipopolysaccharide-induced injury in nasal epithelial cells by targeting Smad7

Huang

Wang

et al. 2018

BMC Cell Biol

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“…Herbal extracts (e.g., seaweed extract, borneol oil, ciwujia dried roots) have been reported to be enhancers (Leonard et al, 2012) and attenuators (Juhás et al, 2008;Fei et al, 2014) of immune responses. Further, essential oils (e.g., oregano and thymol) (Jang et al, 2007;Levkut et al, 2011) and dietary spices (black pepper, piperine, red pepper, capsaicin, and ginger) (Prakash and Srinivasan, 2010) have been shown to modulate IAP activity.…”

Section: Discussionmentioning

confidence: 99%

“…The phytochemical properties of these natural anti-inflammatory substances suggest that they can be used as potential therapeutic agents to attenuate unwanted immune responses (Fei et al, 2014). For example, essential oil extracted from Brazilian red pepper (EO) (Schinus terebinthifolius Raddi) has been shown to promote gut health (Gois et al, 2016) by acting as an antioxidant (Bendaoud et al, 2010), antimicrobial (de Lima et al, 2006, anti-inflammatory (Barbosa et al, 2007), and anti-ulcerogenic agent (Carlini et al, 2010, Carvalho et al, 2013.…”

Section: Introductionmentioning

confidence: 99%

Intestinal alkaline phosphatase and sodium butyrate may be beneficial in attenuating LPS-induced intestinal inflammation

et al. 2016

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ABSTRACT. In this study, we evaluated the effect of intestinal alkaline phosphatase (IAP) and sodium butyrate (NaBu) on lipopolysaccharide (LPS)-induced intestinal inflammation. Intestinal alkaline phosphatase and RelA/p65 (NF-κB) gene expressions in porcine jejunum explants were evaluated following exposure to sodium butyrate (NaBu) and essential oil from Brazilian red pepper (EO), alone or in combination with NaBu, as well as exogenous IAP with or without LPS challenge. Five piglets weighing approximately 20 kg each were sacrificed, and their jejunum were extracted. The tissues were segmented into 10 parts, which were exposed to 10 treatments. Gene expressions of IAP and RelA/p65 (NF-κB) in jejunal explants were evaluated via RT-PCR. We found that EO, NaBu, and exogenous IAP were able to up-regulate endogenous IAP and enhance RelA/p65 (NF-κB) gene expression. However, only NaBu and exogenous IAP down-regulated LPSinduced inflammatory response via RelA/p65 (NF-κB). In conclusion, we demonstrated that exogenous IAP and NaBu may be beneficial in attenuating LPS-induced intestinal inflammation.

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“…Fei et al [39] found that Acanthopanax could attenuate acute lung inflammation via blocking NF- κ B signaling pathway. Intervention of the NF- κ B signaling pathway has proved to be a target for the treatment of AP [40].…”

Section: Discussionmentioning

confidence: 99%

Acanthopanaxversus3-Methyladenine Ameliorates Sodium Taurocholate-Induced Severe Acute Pancreatitis by Inhibiting the Autophagic Pathway in Rats

Wang

Zhou

et al. 2016

Mediators of Inflammation

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Objectives. To observe the therapeutic effects of Acanthopanax and 3-methyladenine against severe acute pancreatitis (SAP). Methods. Sodium taurocholate-induced SAP rats were equally randomized into a SAP group, an Acanthopanax group, and a 3-methyladenine group. Serum amylase levels were determined by ELISA; protein and mRNA expression levels of nucleus nuclear factor kappa B (NF-κB) p65, light chain 3II (LC3-II), and Beclin-1 and mRNA expression levels of Class III phosphatidylinositol 3-kinase (PI3K-III) in pancreas tissue were detected by Western blot and quantitative real-time PCR, respectively; mortality and pathological change of the pancreas were observed at 3, 12, and 24 h after operation. Results. There was no significant difference in mortality between SAP group and both treatment groups (P > 0.05). Serum amylase levels, protein, and mRNA expression levels of nucleus NF-κB p65, LC3-II, and Beclin-1 protein, mRNA expression levels of PI3K-III, and pathological score of the pancreas in both treatment groups were significantly lower than those in SAP group at 12 and 24 h after operation (P < 0.05 or 0.01). The number of autophagosomes and autophagolysosomes of pancreatic acinar cells in both treatment groups was smaller than that in SAP group at 12 and 24 h. Conclusions. Acanthopanax and 3-methyladenine had similar therapeutic effects against SAP in rats. The mechanism may be through inhibiting abnormal autophagy activation of pancreatic acinar cells.

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Acanthopanax senticosus attenuates inflammation in lipopolysaccharide-induced acute lung injury by inhibiting the NF-κB pathway

Cited by 21 publications

References 19 publications

MicroRNA-17-5p aggravates lipopolysaccharide-induced injury in nasal epithelial cells by targeting Smad7

MicroRNA-17-5p aggravates lipopolysaccharide-induced injury in nasal epithelial cells by targeting Smad7

Intestinal alkaline phosphatase and sodium butyrate may be beneficial in attenuating LPS-induced intestinal inflammation

Acanthopanaxversus3-Methyladenine Ameliorates Sodium Taurocholate-Induced Severe Acute Pancreatitis by Inhibiting the Autophagic Pathway in Rats

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