Piscroside C inhibits TNF-α/NF-κB pathway by the suppression of PKCδ activity for TNF-RSC formation in human airway epithelial cells

Lee, Su Ui; Lee, Seoghyun; Ro, Hyunju; Choi, Jihee; Ryu, Hyung Won; Kim, Mun-Ock; Yuk, Heung Joo; Lee, Jinhyuk; Hong, Sung-Tae; Oh, Sei‐Ryang

doi:10.1016/j.phymed.2018.01.012

Cited by 19 publications

(20 citation statements)

References 33 publications

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“…To evaluate the levels of IL-6, IL-8 and MUC5AC in the human NCI-H292 cells, the presence of cytokines in the supernatant was analyzed using human IL-6 and IL-8 ELISA kits (BD Biosciences, Franklin Lakes, NJ, USA), according to the manufacturer's protocols. Human MUC5AC protein levels were measured by modified ELISA assay using anti-MUC5AC (Abcam, Cambridge, MA, USA), as previously described (29). The absorbance was measured at 450 nm using a Spark™ 10 M multimode microplate reader (Tecan Science and Technology Co., Ltd., Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

Pistacia weinmannifolia ameliorates cigarette smoke and lipopolysaccharide‑induced pulmonary inflammation by inhibiting interleukin‑8 production and NF‑κB activation

et al. 2019

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Pistacia weinmannifolia (PW) has been used in traditional Chinese medicine to treat headaches, dysentery, enteritis and influenza. However, PW has not been known for treating respiratory inflammatory diseases, including chronic obstructive pulmonary disease (COPD). The present in vitro analysis confirmed that PW root extract (PWRE) exerts anti-inflammatory effects in phorbol myristate acetate- or tumor necrosis factor α (TNF-α)-stimulated human lung epithelial NCI-H292 cells by attenuating the expression of interleukin (IL)-8, IL-6 and Mucin A5 (MUC5AC), which are closely associated with the pulmonary inflammatory response in the pathogenesis of COPD. Thus, the aim of the present study was to evaluate the protective effect of PWRE on pulmonary inflammation induced by cigarette smoke (CS) and lipopoly-saccharide (LPS). Treatment with PWRE significantly reduced the quantity of neutrophils and the levels of inflammatory molecules and toxic molecules, including tumor TNF-α, IL-6, IL-8, monocyte chemoattractant protein-1, neutrophil elastase and reactive oxygen species, in the bronchoalveolar lavage fluid of mice with CS- and LPS-induced pulmonary inflammation. PWRE also attenuated the influx of inflammatory cells in the lung tissues. Furthermore, PWRE downregulated the activation of nuclear factor-κB and the expression of phosphodiesterase 4 in the lung tissues. Therefore, these findings suggest that PWRE may be a valuable adjuvant treatment for COPD.

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Section: Methodsmentioning

confidence: 99%

Pistacia weinmannifolia ameliorates cigarette smoke and lipopolysaccharide‑induced pulmonary inflammation by inhibiting interleukin‑8 production and NF‑κB activation

et al. 2019

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“…PF is one of the major constituents isolated from the root of Paeonia lactiflora Pall. PF inhibits the NF‐κB pathway by suppression of protein kinase Cδ (PKCδ) activity [ 137 ] and PKCδ interacts with NF‐κB and upregulates transcription of several inflammation markers such as IL‐6 and TNF‐α [ 138 ] (Figure 4). The PF appears to have the potential for a protective effect on rotenone‐induced neurotoxicity in PC12 cells.…”

Section: Protective Effects Of Natural Compounds Against Rotenone‐indmentioning

confidence: 99%

The protective effect of natural compounds against rotenone‐induced neurotoxicity

Yarmohammadi

Hayes

Najafi

et al. 2020

J Biochem & Molecular Tox

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Rotenone is a widely used organic pesticide; its serious side effect for off-target species is neurotoxicity. The primary mechanism of rotenone toxicity is inhibition of the mitochondrial complex I. Oxidative stress, apoptosis, and reduction of autophagy are key outcomes of the inhibition of complex I. Numerous in vitro and in vivo studies have shown antioxidant, anti-apoptotic, and autophagy enhancement of a variety of natural compounds (NCs). In this manuscript, we reviewed several NCs, which have protective effects against rotenone-induced neurotoxicity.

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“…Various ligands and environmental stimuli regulate inflammatory responses in the human airway (Bonser and Erle, 2017). Several factors, such as EGF, TNF-α, Acrolein, PMA, LPS, IL-1β, CSC, or TGFβ are reported to modulate mucin production and secretion in NCI-H292 mucoepidermoid carcinoma cells derived from human lungs (Hewson et al, 2004;Kanai et al, 2015;Lee et al, 2018;Voynow and Rubin, 2009). However, the molecular mechanisms regulating mucin pro- duction and secretion in the airway cells are not fully understood.…”

Section: Tgfβ1 Negatively Regulates Muc5ac Expression In Nci-h292 Cellsmentioning

confidence: 99%

Transforming Growth Factor β Inhibits MUC5AC Expression by Smad3/HDAC2 Complex Formation and NF-κB Deacetylation at K310 in NCI-H292 Cells

et al. 2021

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Airway mucus secretion is an essential innate immune response for host protection. However, overproduction and hypersecretion of mucus, mainly composed of the gelforming MUC5AC protein, are significant risk factors for patients with asthma and chronic obstructive pulmonary disease (COPD). The transforming growth factor β (TGFβ) signaling pathway negatively regulates MUC5AC expression; however, the underlying molecular mechanism is not fully understood. Here, we showed that TGFβ significantly reduces the expression of MUC5AC mRNA and its protein in NCI-H292 cells, a human mucoepidermoid carcinoma cell line. This reduced MUC5AC expression was restored by a TGFβ receptor inhibitor (SB431542), but not by the inhibition of NF-κB (BAY11-7082 or Triptolide) or PI3K (LY294002) activities. TGFβ-activated Smad3 dose-dependently bound to MUC5AC promoter. Notably, TGFβ-activated Smad3 recruited HDAC2 and facilitated nuclear translocation of HDAC2, thereby inducing the deacetylation of NF-κB at K310, which is essential for a reduction in NF-κB transcriptional activity. Both TGFβ-induced nuclear translocation of Smad3/HDAC2 and deacetylation of NF-κB at K310 were suppressed by a Smad3 inhibitor (SIS3). These results suggest that the TGFβ-activated Smad3/HDAC2 complex is an essential negative regulator for MUC5AC expression and an epigenetic regulator for NF-κB acetylation. Therefore, these results collectively suggest that modulation of the TGFβ1/Smad3/HDAC2/NF-κB pathway axis can be a promising way to improve lung function as a treatment strategy for asthma and COPD.

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Piscroside C inhibits TNF-α/NF-κB pathway by the suppression of PKCδ activity for TNF-RSC formation in human airway epithelial cells

Cited by 19 publications

References 33 publications

Pistacia weinmannifolia ameliorates cigarette smoke and lipopolysaccharide‑induced pulmonary inflammation by inhibiting interleukin‑8 production and NF‑κB activation

Pistacia weinmannifolia ameliorates cigarette smoke and lipopolysaccharide‑induced pulmonary inflammation by inhibiting interleukin‑8 production and NF‑κB activation

The protective effect of natural compounds against rotenone‐induced neurotoxicity

Transforming Growth Factor β Inhibits MUC5AC Expression by Smad3/HDAC2 Complex Formation and NF-κB Deacetylation at K310 in NCI-H292 Cells

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