Study on the inhibition of PLD on IAV-induced pulmonary macrophage based on autophagy and apoptosis
Study on the inhibition of PLD on IAV-induced pulmonary macrophage based on autophagy and apoptosis
复制标题
基于自噬和凋亡的PLD抑制IAV诱导的肺巨噬细胞的研究
DOI:
10.4103/pm.pm_207_19
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发表时间:
2020-01
影响因子:
0.7
通讯作者:
He Qing-Hu
中科院分区:
文献类型:
--
作者:
Li Ling;Ning Yi;Wei Ke;Hu Jue;Wu Tao;Zhao Cheng;Lu Fang-Guo;He Qing-Hu
Background: Platycodin D (PLD) comes from the main triterpenoid saponins in the dry roots of Platycodon grandiflorum, which has been used in traditional Chinese medicine in the treatment of respiratory disease. This study aimed to evaluate the therapeutic effects of PLD on mouse alveolar macrophages induced by influenza A virus (IAV) in vitro and to investigate the PLD of its action. Materials and Methods: Raw264.7 mouse alveolar macrophages were grown in culture and the Cell Counting Kit-8 assay determined cell viability. Cells were treated for 24 h with increasing doses of PLD (0, 5, 10, 20, 40, 60, 80, 100 μM). The apoptosis was detected by Annexin V-FITC/PI and Tunel assay. Levels of interleukin (IL)-1 β, IL-6 and tumor necrosis factor (TNF)-α of supernatants were assessed using enzyme-linked immunosorbent assay. The numbers of phagophores, autophagosomes, and autolysosomes and the ultrastructure of cells were assessed using transmission electron microscope assay. The relative protein expression of microtubule-associated protein light chain (LC) 3I, LC3II, Beclin-1, and B cell lymphoma (Bcl2) was evaluated by Western blotting. The localizations of Beclin-1 and Bcl2 were viewed with a fluorescence microscope. Results: PLD treatment resulted in significant dose-dependent inhibition of the growth of Raw264.7 cells with the half-maximal inhibitory concentration of 115.74 μM at 24 h. After Raw264.7 cells infected by influenza virus, PLD (2.5, 5, and 10 μM) can improve the activity of cells, reducing apoptosis of cells, decreasing the concentrations of IL-1 β, IL-6, and TNF-α in the supernatant of cells, reducing autophagic injury of cells and regulating the protein expression of Beclin-1 and Bcl2. Conclusion: PLD could inhibit excessive apoptosis and autophagy of macrophage cells induced by IAV in a dose-dependent manner and then inhibits the secretion of inflammatory factors caused by influenza virus infection caused by apoptosis and autophagy and then ultimately regulate the pathogenesis of influenza virus.
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影响因子:
--
作者:
Zhang R;Chi X;Wang S;Qi B;Yu X;Chen JL
通讯作者:
Chen JL
影响因子:
10
作者:
Bhuiyan MU;Snelling TL;West R;Lang J;Rahman T;Granland C;de Gier C;Borland ML;Thornton RB;Kirkham LS;Sikazwe C;Martin AC;Richmond PC;Smith DW;Jaffe A;Blyth CC
通讯作者:
Blyth CC
DOI:
10.3390/v10110657
发表时间:
2018-11-21
期刊:
Viruses
影响因子:
--
作者:
Zhang M;Du T;Long F;Yang X;Sun Y;Duan M;Zhang G;Liu Y;Zhou EM;Chen W;Chen J
通讯作者:
Chen J
DOI:
10.3390/molecules23102631
发表时间:
2018-10-13
期刊:
Molecules (Basel, Switzerland)
影响因子:
--
作者:
Wang Z;Cai J;Fu Q;Cheng L;Wu L;Zhang W;Zhang Y;Jin Y;Zhang C
通讯作者:
Zhang C
影响因子:
30.3
作者:
Beale R;Wise H;Stuart A;Ravenhill BJ;Digard P;Randow F
通讯作者:
Randow F