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RISS 인기검색어
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- 저자 : Zhang Jianshuang (검색결과 2 건)
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Wang Haizhen,Zhang Jianshuang 한국응용곤충학회 2023 Journal of Asia-Pacific Entomology Vol.26 No.4
Gynaephora qinghaiensis is an important pest that damages alpine meadow vegetation in Qinghai-Tibet Plateau (QTP) alpine pastoral areas. Pteromalus sanjiangyuanicus Yang is a parasitic natural enemy of pupal G. qinghaiensis. For biological control of G. qinghaiensis, local materials and G. qinghaiensis were used for P. sanjiangyuanicus propagation. Under natural field conditions, P. sanjiangyuanicus were propagated in artificial nests. Propagated P. sanjiangyuanicus were then released into the experimental area, where the G. qinghaiensis density was high, and the biological control effect was evaluated. In the propagation test plot (D), the average P. sanjiangyuanicus parasitism rate was 70.3% (46.3–87.0%). The P. sanjiangyuanicus parasitism rate in the experimental area was significantly higher than that in the control area, and the propagation effect was good. The P. sanjiangyuanicus parasitism rates in the biological control plots (A, B, and C) increased yearly from 2016 to 2019, indicating that the P. sanjiangyuanicus population size in the biological control area increased yearly and that the parasitoid population size effectively increased. From 2016 to 2019, the G. qinghaiensis population decline rates in the biological control plots (A, B and C) were 71.1%, 59.3% and 76.4%, respectively (average 68.9%). The control effects on G. qinghaiensis were 80.9%, 69.9% and 80.3%, respectively (average 77.0%). The results showed that P. sanjiangyuanicus was effective in controlling G. qinghaiensis. This study provides a reference for the large-scale propagation of P. sanjiangyuanicus and the further promotion and application of G. qinghaiensis biological control.
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Fu Qiang,Shen Na,Fang Tao,Zhang Hewei,Di Yanbo,Liu Xuan,Du Chao,Guo Jianshuang 한국유전학회 2024 Genes & Genomics Vol.46 No.3
Background ACT001 is an anti-inflammatory agent that has been widely investigated for its role in tumors, intracranial diseases, and fibrotic diseases, but its effect on acute lung injury is less known. Objective The purpose of this study was to investigate the effect and mechanism of ACT001 on regulating inflammation and pyroptosis in lipopolysaccharide (LPS)-induced alveolar macrophages. Methods NR8383 alveolar macrophages treated with LPS were used to replicate the proinflammatory macrophage phenotype observed during acute lung injury. After ACT001 treatment, we measured the secretion and expression levels of critical inflammatory cytokines, the rate of pyroptosis, and the expression of NLRP3 inflammasome-associated proteins and pyroptosis-associated proteins. In addition, we assessed the role of the PPAR-γ/NF-κB signaling pathways and further validated the results with a PPAR-γ inhibitor. Results Our findings confirmed that ACT001 reduced the expression and release of inflammatory factors, attenuated cell pyroptosis, and downregulated the expression of NLRP3, ASC, caspase-1 p20, and GSDMD-N. These effects may be achieved by activating PPAR-γ expression and then inhibiting the NF-κB signaling pathway. When macrophages were treated with the PPAR-γ inhibitor, the protective effects of ACT001 were reversed. Conclusion ACT001 significantly ameliorated inflammation and pyroptosis via the PPAR-γ/NF-κB signaling pathways in LPS-induced NR8383 alveolar macrophages. Background ACT001 is an anti-inflammatory agent that has been widely investigated for its role in tumors, intracranial diseases, and fibrotic diseases, but its effect on acute lung injury is less known. Objective The purpose of this study was to investigate the effect and mechanism of ACT001 on regulating inflammation and pyroptosis in lipopolysaccharide (LPS)-induced alveolar macrophages. Methods NR8383 alveolar macrophages treated with LPS were used to replicate the proinflammatory macrophage phenotype observed during acute lung injury. After ACT001 treatment, we measured the secretion and expression levels of critical inflammatory cytokines, the rate of pyroptosis, and the expression of NLRP3 inflammasome-associated proteins and pyroptosis-associated proteins. In addition, we assessed the role of the PPAR-γ/NF-κB signaling pathways and further validated the results with a PPAR-γ inhibitor. Results Our findings confirmed that ACT001 reduced the expression and release of inflammatory factors, attenuated cell pyroptosis, and downregulated the expression of NLRP3, ASC, caspase-1 p20, and GSDMD-N. These effects may be achieved by activating PPAR-γ expression and then inhibiting the NF-κB signaling pathway. When macrophages were treated with the PPAR-γ inhibitor, the protective effects of ACT001 were reversed. Conclusion ACT001 significantly ameliorated inflammation and pyroptosis via the PPAR-γ/NF-κB signaling pathways in LPS-induced NR8383 alveolar macrophages.
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