MUC5AC Mucin Production Research Articles

Emodin Inhibited MUC5AC Mucin Gene Expression via Affecting EGFR-MAPK-Sp1 Signaling Pathway in Human Airway Epithelial Cells.

The aim of this study was to evaluate emodin, a natural trihydroxyanthraquinone compound found in the roots and barks of several plants including rhubarb and buckthorn, might attenuate epidermal growth factor (EGF)-induced airway MUC5AC mucin gene expression. The human pulmonary mucoepidermoid NCI-H292 cells were pretreated with for 30 min and then stimulated with EGF for the following 24 h. The effect of emodin on EGF-induced mitogen-activated protein kinase (MAPK) signaling pathway was examined. As a result, emodin blocked the expression of MUC5AC mucin mRNA and production of mucous glycoprotein via suppressing the phosphorylation of EGF receptor (EGFR), phosphorylation of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) 1 and 2 (MEK1/2), phosphorylation of p38 MAPK, phosphorylation of ERK 1/2 (p44/42), and the nuclear expression of specificity protein-1 (Sp1). These findings imply that emodin has a potential to mitigate EGF-stimulated mucin gene expression by inhibiting the EGFR-MAPK-Sp1 signaling pathway, in NCI-H292 cells.

Involvement of IKK/IkBα/NF-kB p65 Signaling into the Regulative Effect of Engeletin on MUC5AC Mucin Gene Expression in Human Airway Epithelial Cells.

In this study, we examined whether engeletin exerts an effect on the gene expression of MUC5AC mucin, in human pulmonary epithelial NCI-H292 cells. The cells were pretreated with engeletin for 30 min and stimulated with phorbol 12-myristate 13-acetate (PMA), for the following 24 h. The effect of engeletin on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also investigated. Engeletin suppressed the mRNA expression and production of MUC5AC mucin, induced by PMA through the inhibition of degradation of inhibitory kappa Bα (IkBα) and NF-kB p65 nuclear translocation. These results suggest engeletin inhibits the gene expression of mucin through regulation of NF-kB signaling pathway, in human airway epithelial cells.

Effects of Several Drugs for Metabolic Syndrome on Phorbol Ester- or Epidermal Growth Factor-induced Gene Expression and Production of Airway MUC5AC Mucin: Investigation of Potential Regulator for Hypersecretion of Airway Mucus using Drug Repositioning Strategy

We investigated whether rosiglitazone, metformin, thioctic acid, simvastatin, or glimepiride affects airway MUC5AC mucin gene transcription or protein expression induced by phorbol 12-myristate 13-acetate (PMA) or epidermal growth factor (EGF) in NCI-H292 cells. Cells were pretreated with each agent for 30 min, then stimulated with PMA or EGF for 24 h. Of the five agents, rosiglitazone inhibited PMA-induced gene transcription and production of MUC5AC mucin in NCI-H292 cells. This result suggests that rosiglitazone, an antidiabetic peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist, can inhibit PMA-induced mucin expression at mRNA and protein levels, through directly acting on airway epithelial cells.

Eriodictyol Inhibits the Production and Gene Expression of MUC5AC Mucin via the IκBα-NF-κB p65 Signaling Pathway in Airway Epithelial Cells.

In this study, we investigated whether eriodictyol exerts an effect on the production and gene expression of MUC5AC mucin in human pulmonary epithelial NCI-H292 cells. The cells were pretreated with eriodictyol for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h. The effect of eriodictyol on PMA-induced nuclear factor kappa B (NF-κB) signaling pathway was also investigated. Eriodictyol suppressed the MUC5AC mucin production and gene expression induced by PMA via suppression of inhibitory kappa Bα degradation and NF-κB p65 nuclear translocation. These results suggest that eriodictyol inhibits mucin gene expression and production in human airway epithelial cells via regulation of the NF-κB signaling pathway.

Kaempferol Regulates the Expression of Airway MUC5AC Mucin Gene via IκBα-NF-κB p65 and p38-p44/42-Sp1 Signaling Pathways.

In the present study, kaempferol, a flavonoidal natural compound found in Polygonati Rhizoma, was investigated for its potential effect on the gene expression and production of airway MUC5AC mucin. A human respiratory epithelial NCI-H292 cells was pretreated with kaempferol for 30 min and stimulated with epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA), for the following 24 h. The effect on PMA-induced nuclear factor kappa B (NF-κB) signaling pathway or EGF-induced mitogen-activated protein kinase (MAPK) signaling pathway was investigated. Kaempferol suppressed the production and gene expression of MUC5AC mucins, induced by PMA through the inhibition of degradation of inhibitory kappa Bα (IκBα), and NF-κB p65 nuclear translocation. Also, kaempferol inhibited EGF-induced gene expression and production of MUC5AC mucin through regulating the phosphorylation of EGFR, phosphorylation of p38 MAPK and extracellular signal-regulated kinase (ERK) 1/2 (p44/42), and the nuclear expression of specificity protein-1 (Sp1). These results suggest kaempferol regulates the gene expression and production of mucin through regulation of NF-κB and MAPK signaling pathways, in human airway epithelial cells.

Diclofenac Inhibits Phorbol Ester-Induced Gene Expression and Production of MUC5AC Mucin via Affecting Degradation of IkBα and Translocation of NF-kB p65 in NCI-H292 Cells

In this study, diclofenac, a non-steroidal anti-inflammatory drug, was investigated for its potential effect on the gene expression and production of airway MUC5AC mucin. The human respiratory epithelial NCI-H292 cells were pretreated with diclofenac for 30 min and stimulated with phorbol 12-myristate 13-acetate (PMA), for the following 24 h. The effect of diclofenac on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also investigated. Diclofenac suppressed the production and gene expression of MUC5AC mucins, induced by PMA through the inhibition of degradation of inhibitory kappa Bα (IkBα) and NF-kB p65 nuclear translocation. These results suggest diclofenac regulates the gene expression and production of mucin through regulation of NF-kB signaling pathway, in human airway epithelial cells.

Growth Factor- and Phorbol Ester-induced Production and Gene Expression of MUC5AC Mucin in Human Airway Epithelial NCI-H292 Cells Were Inhibited by Afzelin and Natural Products Derived from Houttuynia Cordata

Growth Factor- and Phorbol Ester-induced Production and Gene Expression of MUC5AC Mucin in Human Airway Epithelial NCI-H292 Cells Were Inhibited by Afzelin and Natural Products Derived from <i>Houttuynia Cordata</i>

Effects of Natural Products Derived from Persicae Semen including Daucosterol on gene Expression and Production of Respiratory Mucin induced by Growth Factor and Phorbol Ester

Persicae semen was used as folk remedy for regulating pulmonary inflammatory diseases in traditional oriental medicine. In the prersent study, we investigated whether prunasin, erucic acid or daucosterol derived from Persicae semen affects airway MUC5AC mucin gene expression and production, induced by phorbol 12-myristate 13-acetate (PMA) or epi-dermal growth factor (EGF) from NCI-H292 cells. Confluent cells were pretreated with each agent for 30 min and then stim-ulated with PMA or EGF for 24h. The MUC5AC mucin gene expression was measured by RT-PCR (Reverse Transcription-Polymerase Chain Reaction). Production of MUC5AC mucin protein was measured by enzyme-linked immunosorbent assay (ELISA). The results were as follows: (1) Erucic acid inhibited the gene expression and production of MUC5AC mucin from NCI-H292 cells; (2) Daucosterol also inhibited the gene expression and production of MUC5AC mucin from NCI-H292 cells. This result suggests that erucic acid or daucosterol can inhibit the production and gene expression of mucin induced by PMA or EGF, through directly acting on airway epithelial cells.

Effects of Natural products including Tussilagonone on gene Expression and Production of MUC5AC Mucin from human airway Epithelial Cells

Effects of Natural products including Tussilagonone on gene Expression and Production of MUC5AC Mucin from human airway Epithelial Cells

Effects of natural products derived from Acanthopanax divaricatus var. albeofructus including coniferin on gene expression and production of MUC5AC mucin from human airway epithelial cells

We investigated whether coniferin, tortoside A, eleutheroside E or salvadoraside derived from Acanthopanax divaricatus var. albeofructus affects airway MUC5AC mucin gene expression and production induced by epidermal growth factor(EGF) from NCI-H292 cells. Cells were pretreated with each agent for 30 min and then stimulated with EGF for 24h.&nbsp;The four compounds inhibited the gene expression and production of MUC5AC mucin from NCI-H292 cells. This result suggests that the four compounds can inhibit the production and gene expression of mucin induced by EGF, through directly acting on airway epithelial cells.

Year in review 2017: Chronic obstructive pulmonary disease and asthma.

Year in review 2017: Chronic obstructive pulmonary disease and asthma.

Tussilagone suppressed the production and gene expression of MUC5AC mucin via regulating nuclear factor-kappa B signaling pathway in airway epithelial cells

In the present study, we investigated whether tussilagone, a natural product derived from Tussilago farfara, significantly affects the production and gene expression of airway MUC5AC mucin. Confluent NCI-H292 cells were pretreated with tussilagone for 30 min and then stimulated with EGF (epidermal growth factor) or PMA (phorbol 12-myristate 13-acetate) for 24 h or the indicated periods. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. To elucidate the action mechanism of tussilagone, effect of tussilagone on PMA-induced NF-κB signaling pathway was investigated by western blot analysis. Tussilagone significantly inhibited the production of MUC5AC mucin protein and down-regulated the expression of MUC5AC mucin gene, induced by EGF or PMA. Tussilagone inhibited PMA-induced activation (phosphorylation) of inhibitory kappa B kinase (IKK), and thus phosphorylation and degradation of inhibitory kappa Ba (IκBα). Tussilagone inhibited PMA-induced phosphorylation and nuclear translocation of nuclear factor kappa B (NF-κB) p65. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. These results suggest that tussilagone can regulate the production and gene expression of mucin by acting on airway epithelial cells through regulation of NF-κB signaling pathway.

Mulberry leaf extract fermented with Lactobacillus acidophilus A4 ameliorates 5-fluorouracil-induced intestinal mucositis in rats.

Our results suggest that fermented mulberry leaf extract (ME) may provide synergistic therapeutic benefits of both probiotics and natural plant extracts in prevention of 5-fluorouracil-induced mucositis. These impacts are particularly significant given the induction of MUC2 and MUC5AC gene expressions for production of mucins and the reduction of pro-inflammatory cytokine interleukin-1β in gut environments. Therefore, we proposed that enhanced functionality of ME by fermentation of Lactobacillus acidophilus A4 can be applied as food-grade adjuncts for mucositis therapy and prevention in food industry.

Effects of Homogentisic Acid and Natural Products Derived from Pinellia ternata on Secretion, Production and Gene Expression of MUC5AC Mucin from Cultured Airway Epithelial Cells

In this study, we investigated whether adenosine, adenine, uridine and homogentisic acid derived from Pinellia ternata affect the secretion, production and gene expression of MUC5AC mucin from airway epithelial cells. Confluent NCI-H292 cells were pretreated with adenosine, adenine, uridine or homogentisic acid for 30 min and then stimulated with PMA (phorbol 12-myristate 13-acetate) for 24 h. The MUC5AC mucin gene expression, mucin protein production and secretion were measured by RT-PCR and ELISA, respectively. The results were as follows: (1) Adenine and homogentisic acid decreased PMA-induced MUC5AC mucin gene expression, although adenosine and uridine did not affect the mucin gene expression; (2) Adenosine, adenine, uridine and homogentisic acid inhibited PMA-induced MUC5AC mucin production; (3) Homogentisic acid inhibited the secretion of MUC5AC mucin from NCI-H292 cells. These results suggest that, among the four compounds examined, homogentisic acid showed the regulatory effect on the steps of gene expression, production and secretion of mucin, by directly acting on airway epithelial cells.

Effects of Nodakenin, Columbianadin, and Umbelliferone Isolated from the Roots of Angelica decursiva on the Gene Expression and Production of MUC5AC Mucin from Human Airway Epithelial NCI-H292 Cells

Effects of Nodakenin, Columbianadin, and Umbelliferone Isolated from the Roots of <i>Angelica decursiva</i> on the Gene Expression and Production of MUC5AC Mucin from Human Airway Epithelial NCI-H292 Cells

Effects of Anomalin, Hyuganin C and Pteryxin on Phorbol Ester- or Tumor Necrosis Factor-induced Gene Expression, Production and Secretion of MUC5AC Mucin from airway Epithelial Cells

We investigated whether anomalin, hyuganin C or pteryxin affects airway MUC5AC mucin gene expression, production and secretion induced by phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-α (TNF-α) from NCIH292 cells. Cells were pretreated with each agent for 30 min and then stimulated with PMA or TNF-α for 24h. The three compounds inhibited the gene expression, production and secretion of MUC5AC mucin from NCI-H292 cells. This result suggests that anomalin, hyuganin C and pteryxin can inhibit the secretion, production and gene expression of mucin induced by PMA or TNF-α, through directly acting on airway epithelial cells.

Pharmacological Activities and Applications of Spicatoside A.

Liriopogons (Liriope and Opiopogon) species are used as a main medicinal ingredient in several Asian countries. The Liriopes Radix (tuber, root of Liriope platyphylla) has to be a promising candidate due to their source of phytochemicals. Steroidal saponins and their glycosides, phenolic compounds, secondary metabolites are considered of active constituents in Liriopes Radix. Spicatoside A, a steroidal saponin, could be more efficacious drug candidate in future. In this review, we summarized the available knowledge on phytochemical and pharmacological activities for spicatoside A. It significantly suppressed the level of NF-κB, NO, iNOS, Cox-2, IL-1β, IL-6 and MAPKs in LPS-stimulated inflammation. The production of MUC5AC mucin was increased. MMP-13 expression was down-regulated in IL-1β-treated cells and reduced glycosaminoglycan release from IL-1α-treated cells. The neurite outgrowth activity, PI3K, Akt, ERK1/2, TrkA and CREB phosphorylation and neurotropic factors such as NGF and BDNF were upregulated with increased latency time. It also showed cell growth inhibitory activity on various carcinoma cells. From this, spicatoside A exerts anti-inflammation, anti-asthma, anti-osteoclastogenesis, neurite outgrowth, memory consolidation and anticancer activities. Further studies are needed on spicatoside A in order to understand mechanisms of action to treat various human diseases.

자음강화탕(滋陰降火湯)이 호흡기 점액의 생성 및 분비에 미치는 영향

Objectives In this study, the effects of Ja-eum-gang-hwa-tang (JGT) on the increase in airway epithelial mucosubstances of rats and ATP- or PMA- or EGF- or TNF-<TEX>${\alpha}$</TEX>-induced MUC5AC mucin production and gene expression from human airway epithelial cells were investigated. Materials and Methods Hypersecretion of airway mucus was produced by exposure of <TEX>$SO_2$</TEX> to rats for 3 weeks. The effect of orally-administered JGT for 2 weeks on increased epithelial mucosubstances from tracheal goblet cells of rats was assessed by using histopathological analysis after staining the epithelial tissue with Hematoxylin-eosin and PAS-alcian blue. Possible cytotoxicity of JGT was assessed by investigating the potential damage on kidneys and liver functions by measuring serum GOT/GPT activities and serum BUN concentration of rats and the body weight gain during experiment. Also, the effect of JGT on ATP- or PMA- or EGF- or TNF-<TEX>${\alpha}$</TEX>-induced MUC5AC mucin production and gene expression from human airway epithelial cells (NCI-H292) were investigated. Confluent NCI-H292 cells were pretreated for 30 min in the presence of JGT and treated with ATP (<TEX>$200{\mu}M$</TEX>) or PMA (<TEX>$10ng/ml$</TEX>) or EGF (<TEX>$25ng/ml$</TEX>) or TNF-<TEX>${\alpha}$</TEX> (0.2 nM) for 24 hrs to assess the effect of JGT both on ATP- or PMA- or EGF- or TNF-<TEX>${\alpha}$</TEX>-induced MUC5AC mucin production by using enzyme-linked immunosorbent assay (ELISA) and on gene expression by the same inducers using reverse transcription-polymerase chain reaction (RT-PCR). Results (1) JGT decreased the amount of intraepithelial mucosubstances of trachea of rats. (2) JGT did not show any renal and hepatic toxicities, and did not affect body weights either. (3) JGT significantly inhibited ATP-, PMA-, EGF-, and TNF-<TEX>${\alpha}$</TEX>-induced MUC5AC mucin productions from NCI-H292 cells. (4) JGT inhibited EGF-, and PMA-induced expression levels of MUC5AC gene in NCI-H292 cells. However, ATP- and TNF-<TEX>${\alpha}$</TEX>-induced MUC5AC gene expression levels were not affected in NCI-H292 cells. Conclusions The result from the present study suggests that JGT might control the production and gene expression of airway mucin observed in various respiratory diseases which accompanied by mucus hypersecretion. Also, JGT did not show liver toxicity or impact on kidney functions. The effect of JGT should be further studied by using animal experimental models which can show proper pathophysiology of airway diseases.

Verticine, ebeiedine and suchengbeisine isolated from the bulbs of Fritillaria thunbergii Miq. inhibited the gene expression and production of MUC5AC mucin from human airway epithelial cells

BackgroundThe bulb of Fritillaria thunbergii has been utilised as mucoregulators and expectorants for controlling the airway inflammatory diseases in folk medicine. Hypothesis/PurposeWe investigated whether verticine, ebeiedine and suchengbeisine isolated from the bulbs of Fritillaria thunbergii inhibit the gene expression and production of MUC5AC mucin from human airway epithelial cells. Study designConfluent NCI-H292 cells were pretreated with verticine, ebeiedine or suchengbeisine for 30min and then stimulated with EGF, PMA or TNF-α for 24h. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. Results(1) Verticine, ebeiedine or suchengbeisine inhibited the expression of MUC5AC mucin gene induced by EGF, PMA or TNF-α; (2) The production of MUC5AC mucin protein induced by EGF, PMA or TNF-α were also inhibited by treatment of verticine, ebeiedine or suchengbeisine. ConclusionThese results suggest that verticine, ebeiedine and suchengbeisine isolated from the bulbs of Fritillaria thunbergii inhibit the gene expression and production of MUC5AC mucin, by directly acting on airway epithelial cells, and the results are consistent with the traditional use of Fritillaria thunbergii as remedy for diverse inflammatory pulmonary diseases.

Effects of Caffeic Acid, Myristicin and Rosemarinic Acid on the Gene Expression and Production of Airway MUC5AC Mucin

Effects of Caffeic Acid, Myristicin and Rosemarinic Acid on the Gene Expression and Production of Airway MUC5AC Mucin