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Cited by 31Asthma and respiratory diseasesAllergic Rhinitis and SensitizationOccupational exposure and asthma

Picroside II Attenuates Airway Inflammation by Downregulating the Transcription Factor GATA3 and Th2-Related Cytokines in a Mouse Model of HDM-Induced Allergic Asthma

Open access
Choi, Jin, Choi, Bo Kyong, Kim, Jin seok, Lee, Jae-Won, Park, Hyun Ah, Ryu, Hyung Won, Lee, Su Ui, Hwang, Kwang Woo +5 more·2016·PLOS ONE
DOI 10.1371/journal.pone.0167098PMC PMC5117775
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Abstract

Picroside II isolated from Pseudolysimachion rotundum var. subintegrum has been used as traditional medicine to treat inflammatory diseases. In this study, we assessed whether picroside II has inhibitory effects on airway inflammation in a mouse model of house dust mite (HDM)-induced asthma. In the HDM-induced asthmatic model, picroside II significantly reduced inflammatory cell counts in the bronchoalveolar lavage fluid (BALF), the levels of total immunoglobulin (Ig) E and HDM-specific IgE and IgG1 in serum, airway inflammation, and mucus hypersecretion in the lung tissues. ELISA analysis showed that picroside II down-regulated the levels of Th2-related cytokines (including IL-4, IL-5, and IL-13) and asthma-related mediators, but it up-regulated Th1-related cytokine, IFNγ in BALF. Picroside II also inhibited the expression of Th2 type cytokine genes and the transcription factor GATA3 in the lung tissues of HDM-induced mice. Finally, we demonstrated that picroside II significantly decreased the expression of GATA3 and Th2 cytokines in developing Th2 cells, consistent with in vivo results. Taken together, these results indicate that picroside II has protective effects on allergic asthma by reducing GATA3 expression and Th2 cytokine bias.

AI snapshot

Written from the paper’s full text.

TL;DR

Picroside II reduced house dust mite (HDM)-induced allergic airway inflammation in mice, including inflammatory cell influx, IgE responses, mucus hypersecretion, and Th2 cytokine production. The effects were associated with downregulation of GATA3 and Th2-related cytokines, with no suppression of Th17/IL-17 or STAT6 phosphorylation.

Key findings

  • In HDM-challenged mice, oral picroside II (15 and 30 mg/kg) significantly reduced total BALF inflammatory cells, including macrophages (p<0.01), eosinophils (p<0.01), and lymphocytes (p<0.05) versus model; effects were better than YPL-001 and comparable to dexamethasone (1 mg/kg).
  • Picroside II significantly reduced serum total IgE, HDM-specific IgE, and HDM-specific IgG1, and attenuated BALF IL-4, IL-5, IL-13, and IL-33 while increasing IFNγ in a dose-dependent manner.
  • In lung tissue, picroside II suppressed mRNA for Il4, Il13, Il33, Mcp1, and Muc5ac, suppressed Il5 to a lesser extent, increased Ifng mRNA, and did not meaningfully decrease Il17 mRNA. It downregulated GATA3 mRNA/protein, upregulated Tbx21 mRNA, but did not change T-bet protein.
  • In developing Th2 cells, picroside II showed no cytotoxicity up to 20 μM, decreased IL-5 and IL-13 dose-dependently, suppressed GATA3 mRNA/protein, and did not affect STAT6 phosphorylation.

Methods

  • Female BALB/c mice were divided into 5 groups (n=6/group): normal control, HDM model, YPL-001 (15 and 30 mg/kg), picroside II (15 and 30 mg/kg), and dexamethasone (1 mg/kg). Mice were sensitized intranasally with HDM (10 μg protein) on days 0 and 3, challenged on days 10–12, and sacrificed on day 14; drugs were given orally 1 h before HDM challenges for 3 days.
  • Outcomes included BALF differential cell counts, serum IgE/IgG1 ELISA, BALF cytokine ELISA, lung H&E and PAS histology, quantitative RT-PCR for cytokines/transcription factors, and Western blot for T-bet/GATA3.
  • In vitro, splenic CD4+ T cells were stimulated with anti-CD3/anti-CD28 under Th2-polarizing conditions (IL-4 plus anti-IFNγ), treated with picroside II (5, 10, 20 μM), and analyzed by ELISA, RT-PCR, and Western blot. Statistics used ANOVA with Dunnett’s adjustment; p<0.05 was significant.

Limitations

  • The paper states that further studies are necessary to elucidate the molecular mechanism by which picroside II inhibits GATA3, since it did not detect an effect on STAT6 phosphorylation.
  • The paper has no dedicated limitations section; evident constraints are that efficacy is shown only in female BALB/c mice and in vitro CD4+ T cells, with no human clinical data.
  • Airway hyper-responsiveness is mentioned as an asthma feature in the introduction but was not measured in the reported experiments.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1371/journal.pone.0167098

Cites

42 of 42 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

10 of 37 cited sources checked · 5 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    Excessive cytokines IL-4, IL-5, and IL-13 produced by Th2 cells are significant risk factors in asthma pathogenesis.

    “Therefore, excessive cytokines IL-4, IL-5, and IL-13 produced by Th2 cells are significant risk factors in asthma pathogenesis [19].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [19] K Boniface, 2008, From interleukin-23 to T-helper 17 cells: human T-helper cell differentiation revisited, Immunol Rev source

      The section on IL-23/Th17 and IL-12/Th1-mediated autoimmune diseases reports that Th2 cells were identified in inflamed tissue from patients with severe asthma. It does not say that excessive Th2-derived IL-4, IL-5, and IL-13 are significant risk factors in asthma pathogenesis. The Characterization of IL-23 bioactivity section mentions IL-4 and IL-13 in relation to IgE production, not asthma risk. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
  • Premisecitation

    Asthma is controlled by Th2 immune response, which leads to high levels of IgE, airway eosinophilia, and mucus production.

    “Asthma is controlled by Th2 immune response, which leads to the high levels of IgE, airway eosinophilia, and mucus production [18].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [18] JA Elias, 2003, New insights into the pathogenesis of asthma, J Clin Invest source

      The Th1/Th2 paradigm section says Th2 responses predominate in asthmatic airways and elicit eosinophilia. The section on chronic effector functions of Th2 cytokines links IL-13 to mucus metaplasia. The copy does not state that Th2 responses cause high IgE levels, and describing asthma as wholly controlled by Th2 responses overstates its account. Page numbers are unavailable in our copy. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
  • Premisecitation

    Verproside is predominantly metabolized to picroside II in vivo.

    “However, verproside is predominantly metabolized to picroside II in vivo [35].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [35] MG Kim, 2012, In vitro and in vivo metabolism of verproside in rats, Molecules source

      The Results and Discussion report that picroside II was recovered in rat bile and urine and that O-methylation was a major metabolic pathway after intravenous verproside administration. The Conclusions describe that pathway as producing both picroside II and isovanilloylcatalpol, followed by further metabolism; they do not establish picroside II alone as the predominant in vivo product generally. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
  • Findingown data

    Picroside II down-regulated IL-4 levels in BALF.

    “down-regulated the levels of Th2-related cytokines (including IL-4, IL-5, and IL-13)”
    • Also stated in: § Effects of picroside II on cytokine secretion in the BALF · plain
      “Administration of picroside II significantly attenuated the Th2 related cytokines (including IL-4, IL-5 and IL-13)”
    Quote in the paperSubstantial claim
  • Findingown data

    Dexamethasone did not significantly change Ifng mRNA level.

    “On the contrary, the level of Ifng mRNA was not significantly changed by dexamethasone.”
    Quote in the paperNot a substantial claim
  • Classified as probably not a substantial claim. 17
  • May combine two claims. 14

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Appropriate differentiation of CD4+ T-cell subsets requires activation of transcription factors, including STATs.

    “The appropriate differentiation of these CD4+ T-cell subsets requires activation of transcription factors, including signal transducers and activators of transcription (STATs) [11].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [11] JJ O'Shea, 2011, Genomic views of STAT function in CD4+ T helper cell differentiation, Nat Rev Immunol source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Picroside II has been shown to possess a broad range of pharmacological effects, including an anti-oxidant and anti-inflammation property.

    “Picroside II has been shown to possess a broad range of pharmacological effects, including an anti-oxidant and anti-inflammation property [21–23].”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [21] Y Cao, 2007, Synergistic protective effect of picroside II and NGF on PC12 cells against oxidative stress induced by H2O2, Pharmacol Rep
    • cites [22] HF Smit, 2000, Immunomodulatory and anti-inflammatory activity of Picrorhiza scrophulariiflora, J Ethnopharmacol source
    • cites [23] LJ He, 2009, Ethanol extraction of Picrorhiza scrophulariiflora prevents renal injury in experimental diabetes via anti-inflammation action, J Endocrinol source

      The Introduction and Discussion state that picroside II has antioxidant activity. The Discussion attributes anti-inflammatory activity to the ethanol extract and says picrosides I and II only “appear to play a major role”; it also says the component responsible remains to be studied. That does not establish an anti-inflammatory property of picroside II itself. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    IL-4 dependent STAT6 phosphorylation plays a critical role during Th2 differentiation.

    “IL-4 dependent STAT6 phosphorylation has been reported to play a critical role during Th2 differentiation [31].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [31] J Zhu, 2001, Stat6 is necessary and sufficient for IL-4&apos;s role in Th2 differentiation and cell expansion, J Immunol source

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    The STAT6 signaling pathway is mainly induced by IL-4, which induces the expression of GATA3.

    “The STAT6 signaling pathway is mainly induced by IL-4, which induces the expression of GATA3 [31, 40].”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [31] J Zhu, 2001, Stat6 is necessary and sufficient for IL-4&apos;s role in Th2 differentiation and cell expansion, J Immunol source
    • cites [40] KA Mowen, 2004, Signaling pathways in Th2 development, Immunol Rev source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    GATA3 expression can also be induced by T cell receptor (TCR) signaling and other pathways, such as Notch and WNT signaling.

    “In fact, GATA3 expression can also be induced by T cell receptor (TCR) signaling [41] and other pathways, such as Notch [42] and WNT signaling [43].”
    Quote in the paperNot a substantial claim2 of 3 sources checked
    • cites [41] H Yamane, 2005, Independent roles for IL-2 and GATA-3 in stimulating naive CD4+ T cells to generate a Th2-inducing cytokine environment, J Exp Med source
    • cites [42] D Amsen, 2007, Direct regulation of Gata3 expression determines the T helper differentiation potential of Notch, Immunity source
    • cites [43] Q Yu, 2009, T cell factor 1 initiates the T helper type 2 fate by inducing the transcription factor GATA-3 and repressing interferon-gamma, Nat Immunol source

      The Results section reports that TCF-1 and β-catenin induce Gata3-1b expression in activated CD4+ T cells, supporting a role for components of the Wnt pathway. But the Discussion says it remains unclear whether β-catenin is stabilized by TCR signals directly or by autocrine Wnt signaling; the paper does not establish that Wnt signaling itself induces GATA3. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Allergic asthma is primarily mediated by Th2 cells and is associated with imbalance of Th1/Th2 cells.

    “It is generally believed that allergic asthma is primarily mediated by Th2 cells, and associated with imbalance of Th1/Th2 cells [36].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [36] PJ Barnes, 2008, The cytokine network in asthma and chronic obstructive pulmonary disease, J Clin Invest source

  • May combine two claims.

    Findingown data

    Picroside II inhibited inflammatory cell infiltration and mucus hypersecretion in lung tissues of HDM-induced asthmatic mice.

    “In line with cytokine profiles, picroside II inhibited total IgE, HDM-specific IgE and HDM-specific IgG1 in serum, and inflammatory cell infiltration and mucus hypersecretion in lung tissues.”
    • Also stated in: § Discussion · plain
      “Indeed, lung histological analysis revealed reduced inflammatory cells and attenuated mucus hypersecretion.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingreasoning

    Picroside II inhibited total IgE, HDM-specific IgE and HDM-specific IgG1 in serum of HDM-induced asthmatic mice.

    “In line with cytokine profiles, picroside II inhibited total IgE, HDM-specific IgE and HDM-specific IgG1 in serum, and inflammatory cell infiltration and mucus hypersecretion in lung tissues.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Premisecitation

    Exposure to allergens causes differentiation of CD4+ T cells into effector T cells, Th1, Th2 and Th17 cells, which produce lineage-specific cytokines IFNγ, IL-4 and IL-17, respectively.

    “Exposure to allergens causes differentiation of CD4+ T cells into effector T cells, Th1, Th2 and Th17 cells, which produce lineage-specific cytokines IFNγ, IL-4 and IL-17, respectively [9, 10].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [9] J Rengarajan, 2000, Transcriptional regulation of Th1/Th2 polarization, Immunol Today source
    • cites [10] CT Weaver, 2007, IL-17 family cytokines and the expanding diversity of effector T cell lineages, Annu Rev Immunol source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    Picroside II purity was more than 99.5% as determined by UPLC.

    “Picroside II purity was more than 99.5% as determined by ultra-performance liquid chromatography (S1 and S2 Figs).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Picroside II is also known as major constituent in the rhizome of Picrorhiza scrophulariiflora, and often used in Asian traditional medicine for the treatment of a number of diseases.

    “In addition, picroside II is also known as major constituent in the rhizome of Picrorhiza scrophulariiflora, and often used in Asian traditional medicine for the treatment of a number of diseases [24].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [24] JX Li, 1998, Three phenylethanoid glycosides and an iridoid glycoside from Picrorhiza scrophulariiflora, Phytochemistry source

  • May combine two claims.

    Premisecitation

    GATA3 induces Th2 cell development by promoting Th2 cytokine expression, but simultaneously inhibits Th1 differentiation by inhibiting T-bet and thus plays a critical role in asthma.

    “GATA3 induces Th2 cell development by promoting Th2 cytokine expression, but simultaneously inhibits Th1 differentiation by inhibiting T-bet and thus plays a critical role in asthma [14, 16, 17].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [14] W Zheng, 1997, The transcription factor GATA-3 is necessary and sufficient for Th2 cytokine gene expression in CD4 T cells, Cell source
    • cites [16] CC Lee, 2008, Lentiviral-mediated GATA-3 RNAi decreases allergic airway inflammation and hyperresponsiveness, Mol Ther source
    • cites [17] K Hirahara, 2008, Repressor of GATA regulates TH2-driven allergic airway inflammation and airway hyperresponsiveness, J Allergy Clin Immunol source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Picroside II, isolated from Pseudolysimachion rotundum var. subintegrum, has been used as traditional medicine to treat inflammatory diseases.

    “Picroside II isolated from Pseudolysimachion rotundum var. subintegrum has been used as traditional medicine to treat inflammatory diseases.”
    • Also stated in: § Introduction · plain
      “Picroside II (PIC II), a catalpol derivative, is isolated from Pseudolysimachion rotundum var. subintegrum that has been used as traditional medicine to treat inflammatory diseases [20].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [20] Kim JK. Illustrated Natural Drugs Encyclopedia. Namsandang, Seoul, Korea. 1984:141.

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductnone given

    All data are representative of three independent experiments and represented as the mean ± SEM (n = 6 mice/group).

    “All data are representative of three independent experiments and represented as the mean ± SEM (n = 6mice/group).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    Data are representative of three independent experiments.

    “All data are representative of three independent experiments and represented as the mean ± SEM (n = 6 mice/group).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    House dust mite (HDM) is the most prevalent cause of allergic sensitization and a risk factor for persistent asthma in human subjects.

    “Among many factors, house dust mite (HDM) is the most prevalent cause of allergic sensitization [4, 6], and a risk factor for persistent asthma in human subjects [7, 8].”
    Quote in the paperNot a substantial claim0 of 4 sources checked
    • cites [4] A Jacquet, 2011, The role of innate immunity activation in house dust mite allergy, Trends Mol Med source
    • cites [6] WR Thomas, 2010, House dust mite allergens in asthma and allergy, Trends Mol Med source
    • cites [7] JR Johnson, 2004, Continuous exposure to house dust mite elicits chronic airway inflammation and structural remodeling, Am J Respir Crit Care Med source
    • cites [8] MR Sears, 2003, A longitudinal, population-based, cohort study of childhood asthma followed to adulthood, N Engl J Med source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Mice were randomly divided into 5 groups.

    “Mice were randomly divided into 5 groups and each consisted of 6 mice”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Study design and conductnone given

    The data were normalized to Gapdh gene expression.

    “The data were normalized to Gapdh gene expression.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    STAT signals are involved in induction of subset-specific transcription factors: T-bet for Th1; GATA3 for Th2; RORγt for Th17.

    “STAT signals have been shown to be involved in the induction of subset-specific transcription factors: T-box expressed in T-cells (T-bet) for Th1; GATA-binding protein-3 (GATA3) for Th2; and retinoic acid receptor-related orphan receptor γt (RORγt) for Th17 cells [12–15].”
    Quote in the paperNot a substantial claim0 of 4 sources checked
    • cites [12] II Ivanov, 2006, The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells, Cell source
    • cites [13] SJ Szabo, 2002, Distinct effects of T-bet in TH1 lineage commitment and IFN-gamma production in CD4 and CD8 T cells, Science source
    • cites [14] W Zheng, 1997, The transcription factor GATA-3 is necessary and sufficient for Th2 cytokine gene expression in CD4 T cells, Cell source
    • cites [15] SJ Szabo, 2000, A novel transcription factor, T-bet, directs Th1 lineage commitment, Cell source

  • May combine two claims.

    Interpretationown data

    Picroside II inhibited Th2 cytokines via inhibiting the transcription factor GATA3 in HDM-induced asthmatic mice as well as developing Th2 cells.

    “We further demonstrated that picroside II inhibited the Th2 cytokines via inhibiting the transcription factor GATA3 in HDM-induced asthmatic mice as well as developing Th2 cells.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    MCP1 and MUC5AC are responsible for inflammatory cell infiltration and hypersecretion of mucus.

    “Actually, MCP1 and MUC5AC are responsible for inflammatory cells infiltration[37] and hypersecretion of mucus [38].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [37] A Mantovani, 2006, Tuning inflammation and immunity by chemokine sequestration: decoys and more, Nat Rev Immunol source
    • cites [38] YF Tan, 2011, The effect of formoterol on airway goblet cell hyperplasia and protein Muc5ac expression in asthmatic mice, Eur Rev Med Pharmacol Sci

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation

    Verproside is a major biologically active compound of this plant, showing potent anti-inflammatory, antioxidant, and anti-asthmatic activities.

    “Recently, we reported that verproside is a major biologically active compound of this plant, showing potent anti-inflammatory, antioxidant, and anti-asthmatic activities [33, 34].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [33] SR Oh, 2006, Suppressive effect of verproside isolated from Pseudolysimachion longifolium on airway inflammation in a mouse model of allergic asthma, Int Immunopharmacol source
    • cites [34] SU Lee, 2016, Verproside inhibits TNF-alpha-induced MUC5AC expression through suppression of the TNF-alpha/NF-kappaB pathway in human airway epithelial cells, Cytokine source

  • May combine two claims.

    Premisecitation

    Dexamethasone is used for acute exacerbations of asthma and has multiple adverse effects including adrenal and growth suppression.

    “Although dexamethasone, a type of corticosteroids, is used for acute exacerbations of asthma, there are multiple adverse effects of this drug including adrenal and growth suppression [32].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [32] T Gulliver, 2007, Inhaled corticosteroids in children with asthma: pharmacologic determinants of safety and efficacy and other clinical considerations, Paediatr Drugs source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    IL-33 is implicated in various forms of allergic asthma.

    “Accumulating evidence also indicate that IL-33 is implicated in various form of allergic asthma [39].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [39] D Prefontaine, 2009, Increased expression of IL-33 in severe asthma: evidence of expression by airway smooth muscle cells, J Immunol source
24 of 24

  • The paper relies on this without support.

    Picroside II-mediated anti-inflammatory effect in a mouse model of asthma has not been investigated.

    “However, picroside II-mediated anti-inflammatory effect in a mouse model of asthma has not been investigated.”

  • The paper relies on this without support.

    The HDM-induced mouse model reproduces key features of human allergic asthma.

    “We induced asthma as previously described with some modification [26].”

  • The paper relies on this without support.

    Picroside II is a constituent of YPL-001, which is being developed as a botanical drug of COPD treatment.

    “Picroside II is one of constituents of YPL-001, which is being developed as a botanical drug of COPD treatment.”
3 of 3

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Developing-Th2 results cite the wrong figure

    Minor

    The text cites Fig 6D and 6E for GATA3 measurements in developing Th2 cells, but the corresponding panels are identified in the Fig 7 caption. The same section also cites Fig 6C and 6F for results assigned to Fig 7C and 7F.

  • Five stated mouse groups, but seven groups are listed

    Minor

    The methods say the mice were divided into five groups, but the two YPL-001 doses and two picroside II doses are listed separately alongside the normal, model, and dexamethasone groups, making seven groups.

2 of 2

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Authors
Choi, J., Choi, B. K., Kim, J. S., Lee, J.-W., Park, H. A., Ryu, H. W., Lee, S. U., Hwang, K. W., Yun, W.-K., Kim, H.-C., Ahn, K.-S., Oh, S.-R., & Lee, H.-J.
Affiliations
  • Korea Research Institute of Bioscience and Biotechnology (KR)
  • Chung-Ang University (KR)
Corresponding author
Lee, Hyun-Jun
ORCID
Venue
PLOS ONE
Publisher
Public Library of Science (PLoS)
Published
2016-11-21
Volume
11
Issue
11
Pages
e0167098
ISSN
1932-6203 (ISSN-L)
DOI
10.1371/journal.pone.0167098
PMC
PMC5117775
OpenAlex
W2554190925
Semantic Scholar
4ca33e6e629d210db9ea6e55b65617e670c5f909
Cited by
30
References
42
Citations by year
2025: 1 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 5 · 2020: 5 · 2019: 3 · 2018: 3 · 2017: 5
FWCI
2.52
Type
journal article
Language
en
Update notices
correction (2017-01-20)
Open access
Licence
Locations
  • PLoS ONE (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (submittedVersion, cc-by)
  • PubMed Central (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Figshare (submittedVersion, cc-by)
  • KRIBB Repository (submittedVersion)
Funders
  • KRIBB Research Initiative Program (KGM1221622)
  • Center for Women In Science Engineering and Technology (WISET) (2016-167)
Topics
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Occupational exposure and asthma
Keywords
picroside II, allergic asthma, house dust mites, airway inflammation, GATA3, Th2 cytokines, Th1/Th2 balance, mucus hypersecretion, IgE, IL-4, IL-5, IL-13, interferon-gamma, traditional Chinese medicine
MeSH terms
Animals, Asthma, Cinnamates, Disease Models, Animal, Female, Gene Expression Regulation, Lung, Mice, Inbred BALB C, Cytokines, Th1 Cells, Th2 Cells, Pyroglyphidae, GATA3 Transcription Factor, Mice, Iridoid Glucosides

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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