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Particulate matter 2.5 triggers airway inflammation and bronchial hyperresponsiveness in mice by activating

《医学前沿（英文）》 2021年第15卷第5期页码 750-766 doi: 10.1007/s11684-021-0839-4

摘要： Exposure to particulate matter 2.5 (PM2.5) potentially triggers airway inflammation by activating nuclear factor-κB (NF-κB). Sirtuin 2 (SIRT2) is a key modulator in inflammation. However, the function and specific mechanisms of SIRT2 in PM2.5-induced airway inflammation are largely understudied. Therefore, this work investigated the mechanisms of SIRT2 in regulating the phosphorylation and acetylation of p65 influenced by PM2.5-induced airway inflammation and bronchial hyperresponsiveness. Results revealed that PM2.5 exposure lowered the expression and activity of SIRT2 in bronchial tissues. Subsequently, SIRT2 impairment promoted the phosphorylation and acetylation of p65 and activated the NF-κB signaling pathway. The activation of p65 triggered airway inflammation, increment of mucus secretion by goblet cells, and acceleration of tracheal stenosis. Meanwhile, p65 phosphorylation and acetylation, airway inflammation, and bronchial hyperresponsiveness were deteriorated in SIRT2 knockout mice exposed to PM2.5. Triptolide (a specific p65 inhibitor) reversed p65 activation and ameliorated PM2.5-induced airway inflammation and bronchial hyperresponsiveness. Our findings provide novel insights into the molecular mechanisms underlying the toxicity of PM2.5 exposure. Triptolide inhibition of p65 phosphorylation and acetylation could be an effective therapeutic approach in averting PM2.5-induced airway inflammation and bronchial hyperresponsiveness.

关键词： particulate matter 2.5 sirtuin 2 p65 airway inflammation bronchial hyperresponsiveness triptolide

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Abnormal expression of c-Myc in human bronchial epithelial cells malignantly transformed by anti-BPDE

FU Juan, JIANG Yiguo, CHEN Xuemin

《医学前沿（英文）》 2008年第2卷第4期页码 380-385 doi: 10.1007/s11684-008-0073-3

摘要： Anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (anti-BPDE) is a metabolite of benzo[a]pyrene (B[a]P) and acts as a potent mutagen in mammalian systems. However, molecular mechanisms related to anti-BPDE-induced carcinogenesis are poorly understood. Here, we investigated the expression of proto-oncogene c- in human bronchial epithelial cells (16HBE-T) transformed by exposure to anti-BPDE. The levels of mRNA and protein of c-Myc were examined in the 16HBE-T and vehicle-treated control cells (16HBE-N) by using different methods respectively, including reverse transcriptase-polymerase chain reaction (RT-PCR), quantitative real-time PCR (Q-PCR), western blot and immunocytochemical methods. The level of c- mRNA appeared to be significantly increased in 16HBE-T, as compared with those of the 16HBE-N. Likewise, the expression of c-Myc protein was significantly enhanced as compared with those of the control cells. Moreover, the localization of c-Myc protein shows mainly nuclear staining in 16HBE-T. In conclusion, the abnormal expression of c-Myc was present in anti-BPDE malignantly transformed 16HBE cells, which may be involved in the carcinogenesis molecular mechanism of anti-BPDE.

关键词： transcriptase-polymerase vehicle-treated understood molecular mechanism different