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Search Results (14)
  • Open Access

    ARTICLE

    Puerarin inactivates NLRP3-mediated pyroptotic cell death to alleviate cerebral ischemia/reperfusion (I/R) injury through modulating the LncRNA DUXAP8/miR-223-3p axis

    ZHENGUO SHI#,*, QIAOYUN WU#, HAIYAN SHI, SONGTIE YING, LIANG TAO

    BIOCELL, Vol.46, No.4, pp. 979-988, 2022, DOI:10.32604/biocell.2022.015345 - 15 December 2021

    Abstract NLRP3 inflammasome-mediated cell pyroptosis aggravates the development of cerebral ischemia/reperfusion (I/R) injury, and the aim of this study is to investigate the potential utilization of the Chinese medicine, Puerarin, in treating this disease. Through conducting in vitro and in vivo experiments, the present study illustrated that Puerarin regulated LncRNA double homeobox A pseudogene 8 (DUXAP8)/miR-223-3p axis to inactivate NLRP3-mediated pyroptotic cell death, resulting in the attenuation of I/R injury. Specifically, the cerebral I/R injury in rat models and hypoxia/reoxygenation (H/R) in primary hippocampus neuron (PHN) cells were inducted, which were subsequently exposed to Puerarin treatment. As expected,… More >

  • Open Access

    ARTICLE

    E2-Induced Activation of the NLRP3 Inflammasome Triggers Pyroptosis and Inhibits Autophagy in HCC Cells

    Qing Wei1, Rui Zhu1, Junying Zhu, Rongping Zhao, Min Li

    Oncology Research, Vol.27, No.7, pp. 827-834, 2019, DOI:10.3727/096504018X15462920753012

    Abstract Emerging evidence suggests that 17β-estradiol (E2) and estrogen receptor (ER) signaling are protective against hepatocellular carcinoma (HCC). In our previous study, we showed that E2 suppressed the carcinogenesis and progression of HCC by targeting NLRP3 inflammasome activation, whereas the molecular mechanism by which the NLRP3 inflammasome initiated cancer cell death was not elucidated. The present study aimed to investigate the effect of NLRP3 inflammasome activation on cell death pathways and autophagy of HCC cells. First, we observed an increasing mortality in E2-treated HCC cells, and then apoptotic and pyroptotic cell death were both detected. The… More >

  • Open Access

    ARTICLE

    NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1b/NF-kB p65 Signals

    Liping Xue*1, Bin Lu†1, Bibo Gao, Yangyang Shi, Jingqi Xu, Rui Yang, Bo Xu, Peng Ding

    Oncology Research, Vol.27, No.5, pp. 557-564, 2019, DOI:10.3727/096504018X15264647024196

    Abstract Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is a crucial component of the NLRP3 inflammasome, a multiprotein complex that can trigger caspase 1/interleukin-1 (IL-1)-mediated inflammatory response once activated and participates in the pathogeny of diverse inflammatory diseases as well as cancers. We examined the function of NLRP3 in the development of glioma. Glioma cells were treated with NLRP3 interference or overexpression vectors, recombinant IL-1 , IL-1 antibody, and NF- B inhibitor.… More >

  • Open Access

    ABSTRACT

    Role of NFAT5 in Hypertonic Stress-Induced Atherosclerosis in Endothelium

    Pingping Ma1, Wanqian Liu1,*, Li Yang1,*

    Molecular & Cellular Biomechanics, Vol.16, Suppl.2, pp. 95-95, 2019, DOI:10.32604/mcb.2019.07363

    Abstract Globally, consumption of sodium (5.8 g per day) was far above the optimal levels (2.3 g per day). High intake of sodium was the leading dietary risk factor for deaths, which caused by cardiovascular disease [1]. Nevertheless, how high-salt intake leads to the occurrence of many cardiovascular diseases such as atherosclerosis is still not very clear. Dmitrieva has reported that elevated sodium concentration promoted thrombogenesis by activating the signal pathway of NFAT5 (nuclear factor of activated T cells 5), a transcription factor which orchestrates cellular defense against osmotic stress [2]. Inflammatory is accompanied with the… More >

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