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首页> 外文期刊>Cellular Physiology and Biochemistry >Curcumin Inhibits Heat-Induced Apoptosis by Suppressing NADPH Oxidase 2 and Activating the Akt/mTOR Signaling Pathway in Bronchial Epithelial Cells
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Curcumin Inhibits Heat-Induced Apoptosis by Suppressing NADPH Oxidase 2 and Activating the Akt/mTOR Signaling Pathway in Bronchial Epithelial Cells

机译：姜黄素通过抑制NADPH氧化酶2并激活支气管上皮细胞中的Akt / mTOR信号通路来抑制热诱导的细胞凋亡。

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>Background: Heat causes bronchial epithelial cell apoptosis, which is a known factor contributing to airway damage during inhalation injury. Accumulating evidence has shown the effect of curcumin on inhibiting apoptosis. In this study, we investigated whether curcumin suppresses heat-induced apoptosis in bronchial epithelial cells and the underlying mechanism. Methods: Bronchial epithelial cell line 16HBE140 cells were incubated at either 42???°C, 47???°C, 52???°C, or 57???°C for 5 min in a cell incubator and then returned back to normal culture conditions (37???°C). An in vivo thermal inhalation injury rat model was established with a heat gun blowing hot air into the airway of rats. 16HBE140 cells and lung tissue were obtained for further study with or without curcumin treatment. Cell viability was determined by measuring the absorbance of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). 2',7'-dichlorofluorescein diacetate fluorescence was used as a measure of reactive oxygen species (ROS) production. Levels of Bcl2, Bax, ?±-ATP, cleaved Poly (ADP-ribose) polymerase (PARP), cleaved caspase-3, gp91phox, p47phox, p67phox, p22phox, p40phox, and Rac were determined by Western blotting. TUNEL staining was used to determine apoptosis. Results: Heat treatment triggered the apoptosis of 16HBE140 cells as shown by the increase in apoptosis molecular markers, including Bcl-2, Bax, cleaved PARP, and cleaved caspase-3. Administration of curcumin significantly inhibited apoptosis of 16HBE140 cells and suppressed the membrane translocation of NADPH oxidase 2 cytosolic components, as well as ROS production. Downregulation of Akt and mTOR phosphorylation induced by heat was also reversed by curcumin. Furthermore, we demonstrated that NADPH oxidase 2 is upstream of Akt/mTOR in heat-induced apoptosis. The protective role of curcumin on bronchial epithelia apoptosis was also confirmed in vivo by a rat inhalation injury model. Conclusion: This study demonstrates that one of the critical mechanisms underlying curcumin inhibiting heat-induced apoptosis is through suppressing NADPH Oxidase 2 and activating the Akt/mTOR signaling pathway in bronchial epithelial cells.
机译：> 背景： 热量导致支气管上皮细胞凋亡，这是导致吸入性损伤中气道受损的已知因素。越来越多的证据表明姜黄素可以抑制细胞凋亡。在这项研究中，我们调查姜黄素是否抑制热诱导的支气管上皮细胞凋亡及其潜在机制。 方法： 支气管上皮细胞系16HBE140细胞在42°C，47°C，52°C或57°C下孵育。在细胞培养箱中于25℃保持5分钟，然后恢复到正常的培养条件（37℃）。用热枪将热空气吹入大鼠气道，建立体内热吸入损伤大鼠模型。获得16HBE140细胞和肺组织用于有或没有姜黄素治疗的进一步研究。通过测量3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化物（MTT）的吸光度来确定细胞活力。 2'，7'-二氯荧光素二乙酸酯荧光用作活性氧（ROS）产生的量度。 Bcl2，Bax，α±ATP，裂解的聚ADP-核糖聚合酶（PARP），裂解的caspase-3，gp91 phox ，p47 phox ，p67 <用蛋白质印迹法测定了sup> phox ，p22 phox ，p40 phox 和Rac。 TUNEL染色用于确定细胞凋亡。 结果： 热处理触发了16HBE140细胞的凋亡，其凋亡分子标记包括Bcl-2，Bax，PARP裂解和caspase-3裂解的增加表明了这一点。给予姜黄素可显着抑制16HBE140细胞凋亡，并抑制NADPH氧化酶2胞质组分的膜移位以及ROS的产生。姜黄素也可以逆转由热引起的Akt下调和mTOR磷酸化。此外，我们证明了NADPH氧化酶2在热诱导的细胞凋亡中位于Akt / mTOR的上游。还通过大鼠吸入损伤模型在体内证实了姜黄素对支气管上皮细胞凋亡的保护作用。 结论： 该研究表明姜黄素抑制热诱导凋亡的关键机制之一是通过抑制NADPH氧化酶2并激活支气管上皮细胞中的Akt / mTOR信号通路。 。

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