کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2587104 | 1130917 | 2008 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Molecular mechanism of apoptosis induced by schizandrae-derived lignans in human leukemia HL-60 cells
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کلمات کلیدی
Apaf-1, Apoptotic protease-activating factor-1DiOC6(3), 3,3′-dihexyloxacarbocyanine iodideIC50, 50% inhibitory concentration - IC50، 50٪ غلظت مهاریNAC, N-acetyl cysteine - NAC، N-acetyl-cysteinePI, propidium iodide - PI، پروتئین یدیدROS, Reactive Oxygen Species - ROS، انواع اکسیژن واکنشیΔΨm, mitochondrial membrane potential - ΔΨm، پتانسیل غشای میتوکندریApoptosis - خزان یاختهایHL-60 cells - سلول های HL-60Lignan - لیگنانMitochondria - میتوکندریاcaspase - کسپاز یا کاسپاز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
دانش تغذیه
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Molecular mechanism of apoptosis induced by schizandrae-derived lignans in human leukemia HL-60 cells Molecular mechanism of apoptosis induced by schizandrae-derived lignans in human leukemia HL-60 cells](/preview/png/2587104.png)
چکیده انگلیسی
Schizandrae chinensis, a traditional Chinese medicine herb, has been used to treat hepatitis B disease in Chinese hospital clinic. We have isolated two bioactive compounds, deoxyschizandrin and γ-schizandrin, from S. chinensis. In the present, we reported that deoxyschizandrin and γ-schizandrin could induce apoptosis in human promyelocytic leukemia cells (HL-60), as characterized by DNA fragmentation and poly (ADP) ribose polymerase (PARP) cleavage. Further molecular analysis showed that deoxyschizandrin and γ-schizandrin caused the loss of mitochondrial membrane potential (ÎΨm), cytochrome c release from mitochondrion to cytosol, truncation of Bid protein, and activation of caspase-3 and -9. However, they did not increase the intracellular level of reactive oxygen species (ROS). Antioxidants such as N-acetyl cysteine (NAC) and catalase did not block the apoptosis induced by deoxyschizandrin or γ-schizandrin. These findings suggest that deoxyschizandrin and γ-schizandrin-induced apoptosis in HL-60 cells involved ROS-independent mitochondrial dysfunction pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Food and Chemical Toxicology - Volume 46, Issue 2, February 2008, Pages 590-597
Journal: Food and Chemical Toxicology - Volume 46, Issue 2, February 2008, Pages 590-597
نویسندگان
Shigang Lin, Makoto Fujii, De-Xing Hou,