کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5849887 | 1561769 | 2015 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Furazolidone induces apoptosis through activating reactive oxygen species-dependent mitochondrial signaling pathway and suppressing PI3K/Akt signaling pathway in HepG2 cells
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کلمات کلیدی
MMPAMLFZDPARPIGF-1PMSFDCFH-DAqRT-PCRNACDCMPBSHepG2FBSBSA - BSADMSO - DMSOMTT - MTTbovine serum albumin - آلبومین سرم گاوinsulin-like growth factor-1 - انسولین مانند عامل رشد 1minimum essential medium - حداقل حداقل مورد نیازDimethyl sulfoxide - دیمتیل سولفواکسیدfetal bovine serum - سرم جنین گاوphenylmethyl sulfonylfluoride - فنیل متیل سولفونیلفلوریدFurazolidone - فورازولیدونacute myeloid leukemia - لوسمی حاد میلوئیدی یا به اختصار AMLMEM - مامانphosphate buffered solution - محلول بافر فسفاتNitrocellulose - نیترو سلولزN-acetyl cysteine - نیتستیل سیستئینMitochondrial membrane potential - پتانسیل غشای میتوکندریpoly (ADP-ribose) polymerase - پلی (ADP-ribose) پلیمرازDilated cardiomyopathy - کاردیومیوپاتی دیلاته، کاردیومیوپاتی کامل
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
دانش تغذیه
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Furazolidone (FZD), a synthetic nitrofuran with a broad spectrum of antimicrobial activities, has been shown to be genotoxic and potentially carcinogenic in several types of cells. However, the proper molecular mechanisms of FZD toxicity remain unclear. This study was aimed to explore the effect of FZD on apoptosis in HepG2 cells and uncover signaling pathway underlying the cytotoxicity of FZD. The results showed that FZD induced apoptosis in HepG2 cells in a dose-dependent manner characterized by nuclei morphology changes, cell membrane phosphatidylserine translocation, poly (ADP-ribose) polymerase (PARP) cleavage and a cascade activation of caspase-9 and -3. FZD could enhance reactive oxygen species (ROS) generation, up-regulate Bax/Bcl-2 ratio, disrupt mitochondrial membrane potential (MMP) and subsequently cause cytochrome c release. Both ROS scavenger (N-acetyl cysteine, NAC) and caspase inhibitors suppressed FZD-induced apoptosis. Furthermore, NAC attenuated FZD-induced ROS generation and mitochondrial dysfunction. Meanwhile, FZD treatment inhibited both the activation and expression of Akt, and PI3K/Akt inhibitor LY294002 promoted FZD-induced apoptosis. On the contrary, PI3K/Akt activator insulin-like growth factor-1 (IGF-1) attenuated lethality of FZD in HepG2 cells. In conclusion, it is first demonstrated that FZD-induced apoptosis in HepG2 cells might be mediated through ROS-dependent mitochondrial signaling pathway and involves PI3K/Akt signaling.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Food and Chemical Toxicology - Volume 75, January 2015, Pages 173-186
Journal: Food and Chemical Toxicology - Volume 75, January 2015, Pages 173-186
نویسندگان
Sijun Deng, Shusheng Tang, Shen Zhang, Chaoming Zhang, Congcong Wang, Yan Zhou, Chongshan Dai, Xilong Xiao,