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  • Wiley  (5)
  • 2020-2024  (5)
  • Pharmacy  (5)
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  • Wiley  (5)
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  • 2020-2024  (5)
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  • Pharmacy  (5)
  • 1
    Online Resource
    Online Resource
    Streptococcus pneumoniae aminopeptidase N regulates dendritic cells that attenuates type‐2 airway inflammation in murine allergic asthma
    Wiley ; 2020
    In:  British Journal of Pharmacology Vol. 177, No. 22 ( 2020-11), p. 5063-5077
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 177, No. 22 ( 2020-11), p. 5063-5077
    Abstract: Epidemiological and experimental studies suggest that microbial exposure in early childhood is linked with reduced risk to suffer asthma. Thus microbial components with immunoregulatory capabilities might serve as a preventive strategy for allergic asthma. Recently, it was identified that Streptococcus pneumoniae aminopeptidase N (PepN) could suppress T cell effector function. We sought to investigate the effect of PepN on murine allergic asthma and elucidate the underlying mechanism. Experimental Approach The effects of intranasal administration of PepN during or before sensitization were examined in ovalbumin (OVA)‐induced murine allergic asthma. The roles of CD11b + dendritic cells in PepN treated OVA‐induced allergic asthma were evaluated by flow cytometry, cytokines detection and adoptive transfer. Moreover, the numbers of lung type 2 innate lymphoid cells (ILC2s) were also detected. Key Results Administration of PepN during or before sensitization attenuated type‐2 airway inflammation (eosinophilia, mucus hypersecretion, Th2 cytokines production and IgE production) in allergic asthma mice. PepN reduced lung accumulation of CD11b + dendritic cells, which was accompanied by diminished dendritic cell‐attracting chemokine CCL20 production as well as CCL17 and CCL22, which are Th2‐cell chemokines predominantly produced by CD11b + dendritic cells. Adoptive transfer of BM‐derived CD11b + dendritic cells abolished the inhibitory effect of PepN on OVA‐induced type‐2 airway inflammation. The numbers of lung ILC2s were decreased in asthmatic mice receiving PepN. Conclusion and Implications PepN alleviated type‐2 inflammation in OVA‐induced allergic asthma mice, which was mediated by regulation of lung CD11b + dendritic cells. Our study provides a novel strategy for the prevention of allergic asthma.
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.v177.22
    DOI: 10.1111/bph.15216
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2029728-2
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Combined 5‐hydroxymethylcytosine content of human leucocyte antigen‐B and human leucocyte antigen‐DQB1 as novel biomarker for anti‐tuberculosis drug‐induced liver injury
    Wiley ; 2020
    In:  Basic & Clinical Pharmacology & Toxicology Vol. 127, No. 3 ( 2020-09), p. 234-240
    Details
    In: Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 127, No. 3 ( 2020-09), p. 234-240
    Abstract: This study investigated the diagnostic value of 5‐methylcytosine (5‐mC) and 5‐hydroxymethylcytosine (5‐hmC) contents of human leucocyte antigen (HLA)‐B and HLA‐DQB1 in anti‐tuberculosis drug‐induced liver injury (ADLI). In total, 110 ADLI patients and 120 patients without ADLI controls were enrolled. Enzyme‐linked immunosorbent assay (ELISA) was used to detect the 5‐mC and 5‐hmC content in DNA from peripheral blood leucocytes. The univariate analysis showed that smoking, drinking, and 5‐mC and 5‐hmC content of HLA‐B and HLA‐DQB1 were significantly associated with ADLI. After adjusting for drinking and smoking, we found that 5‐mC content of HLA‐B and HLA‐DQB1 were associated with ADLI (odds ratio [OR] = 0.251 and 0.347, respectively) and 5‐hmC contents of HLA‐B and HLA‐DQB1 were also associated with ADLI (OR = 1.848 and 4.705, respectively). Receiver operating characteristic (ROC) analysis indicated that the 5‐hmC contents of both HLA‐B and HLA‐DQB1 were more clinically significant than the 5‐mC contents were. The combined 5‐hmC level of HLA‐B and HLA‐DQB1 was the best diagnostic biomarker for ADLI, with the highest areas under the curve (AUC) for 0.953, sensitivity for 0.900 and specificity for 0.875. Therefore, combined 5‐hmC levels of HLA‐B and HLA‐DQB1 could be significant evidence for diagnosis of ADLI.
    Type of Medium: Online Resource
    ISSN: 1742-7835 , 1742-7843
    URL: Issue
    URL: Article
    DOI: 10.1111/bcpt.v127.3
    DOI: 10.1111/bcpt.13401
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2151592-X
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    Baicalin inhibits Salmonella typhimurium ‐induced inflammation and mediates autophagy through TLR4/MAPK/NF‐κB signalling pathway
    Wiley ; 2021
    In:  Basic & Clinical Pharmacology & Toxicology Vol. 128, No. 2 ( 2021-02), p. 241-255
    Details
    In: Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 128, No. 2 ( 2021-02), p. 241-255
    Abstract: Baicalin has been reported to protect mice against Salmonella typhimurium ( S. typhimurium ) infection, while its molecular mechanisms are unclear. In this study, multiplicity of infection (MOI) and observation time were measured. Cell viability and LDH levels were examined in RAW264.7 cells and H9 cells. RAW264.7 cells were stimulated with S typhimurium in the presence or absence of Baicalin, and the levels of pro‐inflammatory cytokines were detected by enzyme‐linked immunosorbent assay (ELISA). The changes in reactive oxygen species (ROS) production were determined by fluorescence microscopy and ELISA. The autophagy and TLR4/MAPK/NF‐κB signalling pathway were examined by immunofluorescence microscopy, quantitative reverse transcription‐polymerase chain reaction and Western blotting. The results indicated that MOI of 30 and duration of autophagy evident at 5 h were applicable to this study. Baicalin prevented death of macrophages, promoted bactericidal activity, decreased the levels of pro‐inflammatory cytokines and ROS and reduced the changes of key biomarkers in autophagy and TLR4/MAPK/NF‐κB signalling pathway infected by S typhimurium . TLR4‐overexpressed cells, autophagy and TLR4/MAPK/NF‐κB signalling pathway were activated by S typhimurium, which was suppressed by Baicalin. Our findings indicated that Baicalin exerts anti‐inflammatory and cell‐protective effects, and it mediates autophagy by down‐regulating the activity of TLR4 infected by S typhimurium .
    Type of Medium: Online Resource
    ISSN: 1742-7835 , 1742-7843
    URL: Issue
    URL: Article
    DOI: 10.1111/bcpt.v128.2
    DOI: 10.1111/bcpt.13497
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2151592-X
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    Licochalcone A restrains microphthalmia‐associated transcription factor expression and growth by activating autophagy in melanoma cells via miR‐142‐3p/Rheb/mTOR pathway
    Wiley ; 2020
    In:  Phytotherapy Research Vol. 34, No. 2 ( 2020-02), p. 349-358
    Details
    In: Phytotherapy Research, Wiley, Vol. 34, No. 2 ( 2020-02), p. 349-358
    Abstract: Licochalcone A (LCA) was found to possess anticancer effects. This study aimed to investigate the anticancer effects and mechanisms of LCA in melanoma. A375 and B16 melanoma cells were stimulated with LCA, MTT assay was used to assess cell proliferation. Expression of miR‐142‐3p, microphthalmia‐associated transcription factor (MITF, which regulates melanin production) and autophagy‐related genes was determined by Real‐time PCR or western blot. The apoptosis was analyzed by flow cytometry and caspase‐3 activity. The roles of miR‐142‐3p and Ras homolog enriched in brain (Rheb) in LCA‐affected cells were investigated by gain‐ and loss‐of functions. LCA inhibited proliferation and MITF expression, but increased apoptosis and autophagy of melanoma cells. Moreover, LCA elevated miR‐142‐3p expression, but decreased its target gene Rheb expression. The effects of LCA on melanoma cells were abrogated by miR‐142‐3p inhibitor or Rheb overexpression. LCA suppressed mTOR signaling activation via Rheb. Additionally, rapamycin (a mTOR antagonist) notably attenuated the effects of Rheb on the autophagy, proliferation, apoptosis, and MITF expression in LCA‐treated melanoma cells. In conclusion, LCA restrained MITF expression and growth by activating autophagy in melanoma cells via miR‐142‐3p/Rheb/mTOR pathway. This study suggested that LCA might be a potential therapeutic candidate for prevention and treatment of melanoma.
    Type of Medium: Online Resource
    ISSN: 0951-418X , 1099-1573
    URL: Issue
    URL: Article
    DOI: 10.1002/ptr.v34.2
    DOI: 10.1002/ptr.6525
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 1493490-5
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    Knockdown of ALK7 inhibits high glucose‐induced oxidative stress and apoptosis in retinal pigment epithelial cells
    Wiley ; 2020
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 47, No. 2 ( 2020-02), p. 313-321
    Details
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 47, No. 2 ( 2020-02), p. 313-321
    Abstract: Diabetic retinopathy (DR) is one of the diabetic complications associated with hyperglycaemia‐mediated oxidative stress. Activin receptor‐like kinase 7 (ALK7) has been proven to be a potential therapeutic approach for diabetic cardiomyopathy, which is another diabetic complication. However, the role of ALK7 in DR remains unclear. In the current study, ALK7 was found to be up‐regulated in clinical samples from DR patients and high glucose (HG)‐induced human retinal pigment epithelial cells (ARPE‐19). In vitro studies demonstrated that knockdown of ALK7 in ARPE‐19 cells through transfection with siRNA‐ALK7 (si‐ALK7) improved cell viability in HG‐induced ARPE‐19 cells. Knockdown of ALK7 suppressed HG‐induced reactive oxygen species (ROS) production, as well elevating the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) in ARPE‐19 cells. The number of apoptotic cells was significantly decreased after transfection with si‐ALK7. ALK7 knockdown also caused a significant decrease in bax expression and an increase in bcl‐2 expression in HG‐induced ARPE‐19 cells. In addition, ALK7 knockdown resulted in remarkable increase in the expressions of nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2) and heme oxygenase‐1 (HO‐1) in ARPE‐19 cells in response to HG induction. Taken together, knockdown of ALK7 protected ARPE‐19 cells from HG‐induced oxidative injury, which might be mediated by the activation of the Nrf2/HO‐1 signalling pathway.
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    URL: Article
    DOI: 10.1111/cep.v47.2
    DOI: 10.1111/1440-1681.13189
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2020033-X
    SSG: 15,3
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