• 제목/요약/키워드: Wang Chongyang

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Writing Miracles and Denominational Establishment: On the Belief Narratives of Quanzhen Daoism

  • ZHANG Shuqing
    • 대순사상과 동아시아종교
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    • 제3권2호
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    • pp.35-54
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    • 2024
  • This article focuses on the image of the ancestor of Quanzhen Daoism from a narrative perspective and also evaluates the influence of this image on the development of Quanzhen Daoism in terms of belief, genealogy, and the compilation of sacred history. Quanzhen Daoism has a rich tradition of narrating andwriting its history. In fact, narrating history is actually a form of constructing history. From the recounting of events such as the birth of the founder of the religion, Wang Chongyang (王重陽, 1112-1170), his conversion to Daoism, his practice and preaching, and his 'ascent to immortality' in Quanzhen historical hagiographies, readers can observe the recording of miracles as a narrative feature. The narratives of religious texts differ from ordinary historical narratives in that the former maintain the core concern of simultaneously promoting belief in miracles and strengthening the religious lineage of the respective tradition. Therefore, exploring the relationship between the narrative of the image of the ancestor and the development of the Quanzhen Sect, along with the establishment of beliefs, is the starting point of this article.

Fabrication of Ag/In2O3/TiO2/HNTs hybrid-structured and plasma effect photocatalysts for enhanced charges transfer and photocatalytic activity

  • Wang, Huiqin;Wu, Dongyao;Liu, Chongyang;Guan, Jingru;Li, Jinze;Huo, Pengwei;Liu, Xinlin;Wang, Qian;Yan, Yongsheng
    • Journal of Industrial and Engineering Chemistry
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    • 제67권
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    • pp.164-174
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    • 2018
  • The purpose of this work designed hybrid-structured and plasma effect photocatalyst of $Ag/In_2O_3/TiO_2/HNTs$ via sol-gel and photo-reduction methods. The structures, morphologies, optical and photoelectric performances of as-prepared photocatalysts were characterized via XRD, TEM, XPS, BET, UV-vis DRS, PL and photocurrents. The photocatalytic activity was evaluated by degradation of TC. The results showed that the hybrid-structure and plasma effect can effectively cause the multi-transfer of electrons and increase the separation rate of electron and hole pairs which obtained high photocatalytic activity. The photocatalytic degradation processes reveal that $^{\bullet}O_2{^-}$ and $h^+$ are major active species.

Metformin alleviates chronic obstructive pulmonary disease and cigarette smoke extract-induced glucocorticoid resistance by activating the nuclear factor E2-related factor 2/heme oxygenase-1 signaling pathway

  • Tao, Fulin;Zhou, Yuanyuan;Wang, Mengwen;Wang, Chongyang;Zhu, Wentao;Han, Zhili;Sun, Nianxia;Wang, Dianlei
    • The Korean Journal of Physiology and Pharmacology
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    • 제26권2호
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    • pp.95-111
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    • 2022
  • Chronic obstructive pulmonary disease (COPD) is an important healthcare problem worldwide. Often, glucocorticoid (GC) resistance develops during COPD treatment. As a classic hypoglycemic drug, metformin (MET) can be used as a treatment strategy for COPD due to its anti-inflammatory and antioxidant effects, but its specific mechanism of action is not known. We aimed to clarify the role of MET on COPD and cigarette smoke extract (CSE)-induced GC resistance. Through establishment of a COPD model in rats, we found that MET could improve lung function, reduce pathological injury, as well as reduce the level of inflammation and oxidative stress in COPD, and upregulate expression of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), multidrug resistance protein 1 (MRP1), and histone deacetylase 2 (HDAC2). By establishing a model of GC resistance in human bronchial epithelial cells stimulated by CSE, we found that MET reduced secretion of interleukin-8, and could upregulate expression of Nrf2, HO-1, MRP1, and HDAC2. MET could also increase the inhibition of MRP1 efflux by MK571 significantly, and increase expression of HDAC2 mRNA and protein. In conclusion, MET may upregulate MRP1 expression by activating the Nrf2/HO-1 signaling pathway, and then regulate expression of HDAC2 protein to reduce GC resistance.

Effects of G-Rh2 on mast cell-mediated anaphylaxis via AKT-Nrf2/NF-κB and MAPK-Nrf2/NF-κB pathways

  • Xu, Chang;Li, Liangchang;Wang, Chongyang;Jiang, Jingzhi;Li, Li;Zhu, Lianhua;Jin, Shan;Jin, Zhehu;Lee, Jung Joon;Li, Guanhao;Yan, Guanghai
    • Journal of Ginseng Research
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    • 제46권4호
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    • pp.550-560
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    • 2022
  • Background: The effect of ginsenoside Rh2 (G-Rh2) on mast cell-mediated anaphylaxis remains unclear. Herein, we investigated the effects of G-Rh2 on OVA-induced asthmatic mice and on mast cell-mediated anaphylaxis. Methods: Asthma model was established for evaluating airway changes and ear allergy. RPMCs and RBL-2H3 were used for in vitro experiments. Calcium uptake, histamine release and degranulation were detected. ELISA and Western blot measured cytokine and protein levels, respectively. Results: G-Rh2 inhibited OVA-induced airway remodeling, the production of TNF-α, IL-4, IL-8, IL-1β and the degranulation of mast cells of asthmatic mice. G-Rh2 inhibited the activation of Syk and Lyn in lung tissue of OVA-induced asthmatic mice. G-Rh2 inhibited serum IgE production in OVA induced asthmatic mice. Furthermore, G-Rh2 reduced the ear allergy in IgE-sensitized mice. G-Rh2 decreased the ear thickness. In vitro experiments G-Rh2 significantly reduced calcium uptake and inhibited histamine release and degranulation in RPMCs. In addition, G-Rh2 reduced the production of IL-1β, TNF-α, IL-8, and IL-4 in IgE-sensitized RBL-2H3 cells. Interestingly, G-Rh2 was involved in the FcεRI pathway activation of mast cells and the transduction of the Lyn/Syk signaling pathway. G-Rh2 inhibited PI3K activity in a dose-dependent manner. By blocking the antigen-induced phosphorylation of Lyn, Syk, LAT, PLCγ2, PI3K ERK1/2 and Raf-1 expression, G-Rh2 inhibited the NF-κB, AKT-Nrf2, and p38MAPK-Nrf2 pathways. However, G-Rh2 up-regulated Keap-1 expression. Meanwhile, G-Rh2 reduced the levels of p-AKT, p38MAPK and Nrf2 in RBL-2H3 sensitized IgE cells and inhibited NF-κB signaling pathway activation by activating the AKT-Nrf2 and p38MAPK-Nrf2 pathways. Conclusion: G-Rh2 inhibits mast cell-induced allergic inflammation, which might be mediated by the AKT-Nrf2/NF-kB and p38MAPK-Nrf2/NF-κB signaling pathways.