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The Role of Fas-FasL Signaling Pathway in Induction of Apoptosis in Patients with Sulfur Mustard-Induced Chronic Bronchiolitis

机译:Fas-FasL信号通路在硫芥子气诱发的慢性细支气管炎患者凋亡诱导中的作用

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摘要

Sulfur mustard (SM) is an alkylating agent that induces apoptosis and necrosis in cells. Fas-Fas ligand (FasL) interaction could induce apoptosis as well. In this study, it was hypothesized that apoptosis might play an important role in the pathogenesis of SM-induced lung injury via Fas-FasL signaling pathway. In a case-control study, Fas and FasL levels, caspase-3 activity and percent of apoptotic cells were measured in bronchoalveolar lavage (BAL) fluid of patients 20 years after exposure to sulfur mustard and compared with the control group. Results show that Fas and FasL levels were significantly higher in BAL fluid cells in patients group compared with the control (P = .001). No significant differences were observed between mild and moderate-severe groups. BAL fluid cells caspase-3 activity was not significantly different among the mild, moderate-severe, and control groups. The data suggest that Fas-FasL-induced apoptosis was impaired in BAL fluid cells of SM-exposed patients which might be one of the initiators of pathogenesis in SM-induced lung injury in these patients.
机译:芥菜硫(SM)是一种烷化剂,可诱导细胞凋亡和坏死。 Fas-Fas配体(FasL)相互作用也可以诱导细胞凋亡。在这项研究中,假设凋亡可能通过Fas-FasL信号通路在SM诱导的肺损伤的发病机理中发挥重要作用。在一项病例对照研究中,在接触硫芥子气20年后,测量患者支气管肺泡灌洗液(BAL)中Fas和FasL水平,caspase-3活性和凋亡细胞百分比,并与对照组进行比较。结果显示,与对照组相比,患者组中BAL液细胞的Fas和FasL水平显着升高(P = .001)。在轻度和中度重度组之间未观察到显着差异。在轻,中,重度和对照组之间,BAL液细胞caspase-3活性无明显差异。数据表明,Fs-FasL诱导的SM暴露患者的BAL液细胞中的细胞凋亡受到损害,这可能是这些患者SM诱导的肺损伤的发病机制的发起者之一。

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