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  1. Article ; Online: Vasicine alleviates 2,4-dinitrochlorobenzene-induced atopic dermatitis and passive cutaneous anaphylaxis in BALB/c mice.

    Zhang, Yi / Du, Wenxia / Zhu, Defen / Li, Meiling / Qu, Lu / Rao, Gaoxiong / Lin, Yuping / Tong, Xiaoyun / Sun, Yun / Huang, Feng

    Clinical immunology (Orlando, Fla.)

    2022  Volume 244, Page(s) 109102

    Abstract: Atopic dermatitis (AD), a type of skin inflammation, is associated with immune response mediated by T-helper 2 (Th2) cells, and mast cells. Vasicine is an alkaloid isolated from Adhatoda vasica, a popular Ayurvedic herbal medicine used for treating ... ...

    Abstract Atopic dermatitis (AD), a type of skin inflammation, is associated with immune response mediated by T-helper 2 (Th2) cells, and mast cells. Vasicine is an alkaloid isolated from Adhatoda vasica, a popular Ayurvedic herbal medicine used for treating inflammatory conditions. In the present study, the anti-AD effects of vasicine were evaluated on 2,4-dinitrochlorobenzene-induced AD-like skin lesions in BALB/c mice. The potential anti-allergic effects of vasicine were also assessed using the passive cutaneous anaphylaxis (PCA) test. The results showed that the oral administration of vasicine improved the severity of AD-like lesional skin by decreasing histopathological changes and restoring epidermal thickness. Vasicine also inhibited the infiltration of mast cells in the skin and reduced the levels of pro-Th2 and Th2 cytokines as well as immunoglobulin E in the serum. Finally, vasicine inhibited the expression of pro-Th2 and Th2 cytokines in skin tissues, indicating the therapeutic potential of vasicine for AD.
    MeSH term(s) Alkaloids/metabolism ; Alkaloids/pharmacology ; Alkaloids/therapeutic use ; Animals ; Anti-Allergic Agents/adverse effects ; Cytokines ; Dermatitis, Atopic/chemically induced ; Dermatitis, Atopic/drug therapy ; Dinitrochlorobenzene/metabolism ; Dinitrochlorobenzene/pharmacology ; Dinitrochlorobenzene/therapeutic use ; Immunoglobulin E ; Mice ; Mice, Inbred BALB C ; Passive Cutaneous Anaphylaxis ; Quinazolines ; Skin ; Skin Diseases/pathology
    Chemical Substances Alkaloids ; Anti-Allergic Agents ; Cytokines ; Dinitrochlorobenzene ; Quinazolines ; Immunoglobulin E (37341-29-0) ; vasicine (6C2ZBI733P)
    Language English
    Publishing date 2022-08-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2022.109102
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Inhibitory effects of catalpol on DNCB-induced atopic dermatitis and IgE-mediated mast cells reaction.

    Sun, Yun / Zhu, Defen / Qu, Lu / Li, Manping / Du, Wenxia / Wang, Mingming / Zhang, Yi / Chen, Guifang / Rao, Gaoxiong / Yu, Xiaoling / Wu, Xiangnong / Huang, Feng / Tong, Xiaoyun

    International immunopharmacology

    2023  Volume 126, Page(s) 111274

    Abstract: Atopic dermatitis (AD) is a chronic, inflammatory cutaneous disease driven by immune dysregulation. Catalpol is an iridoids, possessing anti-inflammatory, antioxidant, and neuroprotective activities. It can be added to food as a dietary supplement. To ... ...

    Abstract Atopic dermatitis (AD) is a chronic, inflammatory cutaneous disease driven by immune dysregulation. Catalpol is an iridoids, possessing anti-inflammatory, antioxidant, and neuroprotective activities. It can be added to food as a dietary supplement. To evaluate the effects and mechanisms of catalpol on AD, both in vitro and in vivo studies were conducted. It was found that catalpol downregulated the phosphorylation of Lyn and Syk to inhibit various downstream pathways, including intracellular Ca
    MeSH term(s) Mice ; Animals ; Dermatitis, Atopic/chemically induced ; Dermatitis, Atopic/drug therapy ; Mast Cells ; Dinitrochlorobenzene ; Immunoglobulin E/metabolism ; Skin ; Cytokines/metabolism ; Mice, Inbred BALB C
    Chemical Substances catalpol (2415-24-9) ; Dinitrochlorobenzene ; Immunoglobulin E (37341-29-0) ; Cytokines
    Language English
    Publishing date 2023-12-04
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2023.111274
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Isoproterenol induces actin depolymerization in human airway smooth muscle cells via activation of an Src kinase and GS.

    Hirshman, Carol A / Zhu, Defen / Pertel, Thomas / Panettieri, Reynold A / Emala, Charles W

    American journal of physiology. Lung cellular and molecular physiology

    2005  Volume 288, Issue 5, Page(s) L924–31

    Abstract: In a previous study, we showed that isoproterenol induced actin depolymerization in human airway smooth muscle cells by both protein kinase A (PKA)-dependent and -independent signaling pathways. We now investigate the signaling pathway of PKA-independent ...

    Abstract In a previous study, we showed that isoproterenol induced actin depolymerization in human airway smooth muscle cells by both protein kinase A (PKA)-dependent and -independent signaling pathways. We now investigate the signaling pathway of PKA-independent actin depolymerization induced by isoproterenol in these cells. Cells were briefly exposed to isoproterenol or PGE(1) in the presence and absence of specific inhibitors of Src-family tyrosine kinases, phosphatidylinositol-3-kinase (PI3 kinase), or MAP kinase, and actin depolymerization was measured by concomitant staining of filamentous actin with FITC-phalloidin and globular actin with Texas red DNase I. Isoproterenol, cholera toxin, and PGE(1) induced actin depolymerization, indicated by a decrease in the intensity of filamentous/globular fluorescent staining. Pretreatment with the Src kinase inhibitors 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyriimidine (PP2) or geldanamycin or the PKA inhibitor Rp-cAMPS only partly inhibited isoproterenol- or PGE(1)-induced actin depolymerization. In contrast, PP2 and geldanamycin did not inhibit forskolin-induced actin depolymerization, and AG-213 (an EGF receptor tyrosine kinase inhibitor) did not inhibit isoproterenol- or PGE(1)-induced actin depolymerization. PI3 kinase or MAP kinase inhibition did not inhibit isoproterenol-induced actin depolymerization. Moreover, isoproterenol but not forskolin induced tyrosine phosphorylation of an Src family member at position 416. These results further confirm that both PKA-dependent and PKA-independent pathways mediate actin depolymerization in human airway smooth muscle cells and that the PKA-independent pathway by which isoproterenol induces actin depolymerization in human airway smooth muscle cells involves Src protein tyrosine kinases and the G(s) protein.
    MeSH term(s) Adjuvants, Immunologic/pharmacology ; Adrenergic beta-Agonists/pharmacology ; Benzoquinones ; Cells, Cultured ; Cholera Toxin/pharmacology ; Enzyme Inhibitors/pharmacology ; GTP-Binding Protein alpha Subunits, Gs/metabolism ; Humans ; Isoproterenol/pharmacology ; Lactams, Macrocyclic ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Phosphorylation ; Quinones/pharmacology ; Trachea/cytology ; Tyrosine/metabolism ; src-Family Kinases/antagonists & inhibitors ; src-Family Kinases/metabolism
    Chemical Substances Adjuvants, Immunologic ; Adrenergic beta-Agonists ; Benzoquinones ; Enzyme Inhibitors ; Lactams, Macrocyclic ; Quinones ; Tyrosine (42HK56048U) ; Cholera Toxin (9012-63-9) ; src-Family Kinases (EC 2.7.10.2) ; GTP-Binding Protein alpha Subunits, Gs (EC 3.6.5.1) ; Isoproterenol (L628TT009W) ; geldanamycin (Z3K3VJ16KU)
    Language English
    Publishing date 2005-03-09
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00463.2004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Expression and muscarinic receptor coupling of Lyn kinase in cultured human airway smooth muscle cells.

    Pertel, Thomas / Zhu, Defen / Panettieri, Reynold A / Yamaguchi, Naoto / Emala, Charles W / Hirshman, Carol A

    American journal of physiology. Lung cellular and molecular physiology

    2005  Volume 290, Issue 3, Page(s) L492–500

    Abstract: Src family tyrosine kinases are signaling intermediates in a diverse array of cellular events including cell differentiation, motility, proliferation, and survival. In nonairway smooth muscle cells, muscarinic receptors directly interact with Src family ... ...

    Abstract Src family tyrosine kinases are signaling intermediates in a diverse array of cellular events including cell differentiation, motility, proliferation, and survival. In nonairway smooth muscle cells, muscarinic receptors directly interact with Src family tyrosine kinases. As little is known about the expression and signaling of these Src family tyrosine kinases in human airway smooth muscle cells, we determined the expression of Src family members and characterized the muscarinic receptor-mediated activation of Lyn kinase in these cells. RT-PCR revealed mRNA transcripts for FYN, c-SRC, YES, FRK, and LYN. Fyn, c-Src, Yes, and Lyn were identified in cultured airway smooth muscle cells by immunoblot analysis. In both nontransformed human cultured airway smooth muscle cells and cells transduced with wild-type human Lyn kinase, carbachol increased Lyn kinase activity. Pertussis toxin pretreatment failed to block carbachol activation of Lyn kinase but did attenuate the carbachol-induced increase in ERK/MAPK phosphorylation. Moreover, carbachol inhibited adenylyl cyclase but failed to increase total inositol phosphate synthesis in these cells. The present study shows that Lyn kinase is expressed in human cultured airway smooth muscle cells at both the mRNA and protein levels and that carbachol, an M2 muscarinic receptor agonist in these cells, activates Lyn kinase by a pertussis toxin-insensitive signaling pathway.
    MeSH term(s) Adenylyl Cyclase Inhibitors ; Carbachol/pharmacology ; Cells, Cultured ; Cholinergic Agonists/pharmacology ; Gene Expression ; Humans ; Inositol Phosphates/metabolism ; Muscarinic Agonists ; Muscle, Smooth/drug effects ; Muscle, Smooth/metabolism ; Pertussis Toxin/pharmacology ; Phosphorylation ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptor, Muscarinic M2/genetics ; Receptor, Muscarinic M2/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/drug effects ; Trachea/cytology ; src-Family Kinases/antagonists & inhibitors ; src-Family Kinases/genetics ; src-Family Kinases/metabolism
    Chemical Substances Adenylyl Cyclase Inhibitors ; Cholinergic Agonists ; Inositol Phosphates ; Muscarinic Agonists ; RNA, Messenger ; Receptor, Muscarinic M2 ; Carbachol (8Y164V895Y) ; Pertussis Toxin (EC 2.4.2.31) ; lyn protein-tyrosine kinase (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2)
    Language English
    Publishing date 2005-10-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00344.2005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Expression and coupling of neurokinin receptor subtypes to inositol phosphate and calcium signaling pathways in human airway smooth muscle cells.

    Mizuta, Kentaro / Gallos, George / Zhu, Defen / Mizuta, Fumiko / Goubaeva, Farida / Xu, Dingbang / Panettieri, Reynold A / Yang, Jay / Emala, Charles W

    American journal of physiology. Lung cellular and molecular physiology

    2008  Volume 294, Issue 3, Page(s) L523–34

    Abstract: Neuropeptide tachykinins (substance P, neurokinin A, and neurokinin B) are present in peripheral terminals of sensory nerve fibers within the respiratory tract and cause airway contractile responses and hyperresponsiveness in humans and most mammalian ... ...

    Abstract Neuropeptide tachykinins (substance P, neurokinin A, and neurokinin B) are present in peripheral terminals of sensory nerve fibers within the respiratory tract and cause airway contractile responses and hyperresponsiveness in humans and most mammalian species. Three subtypes of neurokinin receptors (NK1R, NK2R, and NK3R) classically couple to Gq protein-mediated inositol 1,4,5-trisphosphate (IP3) synthesis and liberation of intracellular Ca2+, which initiates contraction, but their expression and calcium signaling mechanisms are incompletely understood in airway smooth muscle. All three subtypes were identified in native and cultured human airway smooth muscle (HASM) and were subsequently overexpressed in HASM cells using a human immunodeficiency virus-1-based lentivirus transduction system. Specific NKR agonists {NK1R, [Sar9,Met(O2)11]-substance P; NK2R, [beta-Ala8]-neurokinin A(4-10); NK3R, senktide} stimulated inositol phosphate synthesis and increased intracellular Ca2+ concentration ([Ca2+]i) in native HASM cells and in HASM cells transfected with each NKR subtype. These effects were blocked by NKR-selective antagonists (NK1R, L-732138; NK2R, GR-159897; NK3R, SB-222200). The initial transient and sustained phases of increased [Ca2+]i were predominantly inhibited by the IP3 receptor antagonist 2-aminoethoxydiphenyl borate (2-APB) or the store-operated Ca2+ channel antagonist SKF-96365, respectively. These results show that all three subtypes of NKRs are expressed in native HASM cells and that IP3 levels are the primary mediators of NKR-stimulated initial [Ca2+]i increases, whereas store-operated Ca2+ channels mediate the sustained phase of the [Ca2+]i increase.
    MeSH term(s) Boron Compounds/pharmacology ; Calcium Signaling/physiology ; Humans ; Imidazoles/pharmacology ; Inositol 1,4,5-Trisphosphate/biosynthesis ; Muscle, Smooth/cytology ; Muscle, Smooth/drug effects ; Muscle, Smooth/physiology ; Neurokinin A/analogs & derivatives ; Neurokinin A/pharmacology ; Peptide Fragments/pharmacology ; RNA, Messenger/metabolism ; Receptors, Neurokinin-1/agonists ; Receptors, Neurokinin-1/biosynthesis ; Receptors, Neurokinin-1/physiology ; Receptors, Neurokinin-2/agonists ; Receptors, Neurokinin-2/biosynthesis ; Receptors, Neurokinin-2/physiology ; Receptors, Neurokinin-3/agonists ; Receptors, Neurokinin-3/biosynthesis ; Receptors, Neurokinin-3/physiology ; Substance P/analogs & derivatives ; Substance P/pharmacology ; Trachea/cytology ; Trachea/drug effects ; Trachea/physiology
    Chemical Substances Boron Compounds ; Imidazoles ; Peptide Fragments ; RNA, Messenger ; Receptors, Neurokinin-1 ; Receptors, Neurokinin-2 ; Receptors, Neurokinin-3 ; senktide (106128-89-6) ; substance P, Sar(9)-Met(O2)(11)- (110880-55-2) ; neurokinin A (4-10), beta-Ala(8)- (122063-01-8) ; Substance P (33507-63-0) ; Inositol 1,4,5-Trisphosphate (85166-31-0) ; Neurokinin A (86933-74-6) ; 2-aminoethoxydiphenyl borate (E4ES684O93) ; 1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole (I61V87164A)
    Language English
    Publishing date 2008-01-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00328.2007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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