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  • Zhang, Chunhui  (4)
  • Pharmacy  (4)
  • 1
    In: Bioorganic & Medicinal Chemistry Letters, Elsevier BV, Vol. 26, No. 9 ( 2016-05), p. 2284-2288
    Type of Medium: Online Resource
    ISSN: 0960-894X
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2016
    detail.hit.zdb_id: 1501505-1
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Journal of Cardiovascular Pharmacology Vol. 78, No. 5 ( 2021-11), p. e761-e772
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 78, No. 5 ( 2021-11), p. e761-e772
    Abstract: Circular RNAs (circRNAs) are reported to play pivotal regulatory roles in atherosclerosis progression. In the present study, we explored the biological role of circRNA ubiquitin-specific peptidase 36 (circ_USP36; hsa_circ_0003204) in oxidized low-density lipoprotein (ox-LDL)-induced dysfunction of endothelial cells (ECs). RNA and protein levels were determined by reverse transcription-quantitative polymerase chain reaction and Western blot assay, respectively. Cell proliferation was analyzed by 5-ethynyl-2′-deoxyuridine assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Flow cytometry was conducted to analyze cell cycle progression and cell apoptosis. The release of tumor necrosis factor α in the supernatant was measured by enzyme linked immunosorbent assay. Cell death was evaluated by lactate dehydrogenase assay. Intermolecular interaction was verified by dual-luciferase reporter assay. Circ_USP36 expression was significantly up-regulated in the serum of atherosclerosis patients and ox-LDL-stimulated HUVECs than that in their corresponding controls. ox-LDL exposure inhibited the proliferation ability and cell cycle progression and triggered the apoptosis and inflammation of HUVECs, and these effects were largely overturned by the knockdown of circ_USP36. microRNA-197-3p (miR-197-3p) was a target of circ_USP36, and circ_USP36 knockdown-mediated protective role in ox-LDL-induced HUVECs was largely counteracted by the silence of miR-197-3p. miR-197-3p interacted with the 3′ untranslated region of roundabout guidance receptor 1 (ROBO1). Circ_USP36 knockdown reduced ROBO1 expression partly by up-regulating miR-197-3p in HUVECs. ROBO1 overexpression reversed miR-197-3p accumulation-mediated effects in ox-LDL-induced HUVECs. In conclusion, circ_USP36 interference alleviated ox-LDL-induced dysfunction in HUVECs by targeting miR-197-3p/ROBO1 axis.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    SAGE Publications ; 2020
    In:  Natural Product Communications Vol. 15, No. 11 ( 2020-11), p. 1934578X2097351-
    In: Natural Product Communications, SAGE Publications, Vol. 15, No. 11 ( 2020-11), p. 1934578X2097351-
    Abstract: To evaluate the relationship between tree peony cultivars and the quality consistency of Cortex Moutan, a sensitive, reliable, and validated method based on high-performance liquid chromatography-electrospray ionization/mass spectrometry was developed for the quantitative analysis of paeonol and chemical fingerprinting of Cortex Moutan. Results from quantitative analysis showed that the content of paeonol in Paeonia ostii “Feng Dan” was the highest (24.51 ± 0.83 mg/g), followed by Paeonia suffruticosa “Luoyang Hong” (14.29 ± 0.76 mg/g), P. suffruticosa “Taiping Hong” (13.99±1.13 mg/g), and P. suffruticosa “Zhaofen” (13.08±0.85 mg/g). Paeonia ostii “Luoyang Feng Dan” was found to have the lowest content (8.76±0.46 mg/g) of paeonol. In qualitative analysis, 5 tree peony cultivars collected from different plantations in China were used to establish the fingerprint. For the fingerprint analysis, 17 characteristic peaks were used to evaluate similarities among tree peony cultivars, and they were found to show similarities. In short, the results of quantitative and qualitative analyses suggested that there was no significant difference in the chemical composition of Cortex Moutan from different tree peony varieties; however, there were significant differences in the levels of chemical components. The method developed in this study provides an important reference to establish a quality control method for other related traditional Chinese medicinal preparations.
    Type of Medium: Online Resource
    ISSN: 1934-578X , 1555-9475
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2020
    detail.hit.zdb_id: 2430442-6
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 42, No. 6 ( 2017), p. 2182-2193
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 42, No. 6 ( 2017), p. 2182-2193
    Abstract: Background/Aims: Cardiotoxicity is a predominant side-effect of nilotinib during chronic myeloid leukemia treatment. The underlying molecular mechanism remains unclear. The role of autophagy and mitochondrial signaling was investigated in nilotinib-treated cardiac H9C2 cells. Methods: Cytotoxicity was assessed using Cell Death Detection kit. Immunoblot and immunofluorescence staining was performed, and cathepsin B and caspase3 activity was assessed in nilotinib-treated H9C2 cells with or without distinct pathway inhibitor or specific siRNA. Results: Nilotinib time- and dose-dependently induced H9C2 apoptosis, which was not completely prevented by the pan caspase inhibitor z-VAD-fmk. Following nilotinib treatment, mitochondrial membrane potential decreased significantly accompanied with remarkable morphological changes. Nuclear translocation of mitochondrial apoptosis inducing factor (AIF) and increased p53 was detected in nilotinib-treated cells. AIF knockdown prevented nilotinib-induced increase of p53 and apoptosis. Additionally, increased cathepsin B activity was detected, and inhibition of cathepsin B by CA-074Me prevented nilotinib-induced apoptosis and nuclear translocation of AIF. Moreover, increased Atg5 and transition of LC3-I to LC3-II was revealed following nilotinib treatment. Increased cathepsin B activity and apoptosis by nilotinib was significantly prohibited by specific autophagy inhibitor bafilomycin A and Atg5 knockdown. Conclusion: Our findings demonstrate that nilotinib increases autophagy and cathepsin B activity, leading to mitochondrial AIF release and nuclear translocation, which is responsible for p53 and apoptosis induction in H9C2 cells.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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