DocumentCode
527170
Title
Notice of Retraction
Effect of Asparagus saponins on HepG2 apoptosis and mitochondrial membrane potential and ROS level
Author
Chen feng Ji ; Lei Yue ; Yu Bin Ji ; Shi Yong Gao
Author_Institution
Eng. Res. Center on Natural Antineoplastic Drugs of Educ. Minist., Harbin Univ. of Commerce, Harbin, China
Volume
3
fYear
2010
fDate
17-18 July 2010
Firstpage
727
Lastpage
730
Abstract
Notice of Retraction
After careful and considered review of the content of this paper by a duly constituted expert committee, this paper has been found to be in violation of IEEE´s Publication Principles.
We hereby retract the content of this paper. Reasonable effort should be made to remove all past references to this paper.
The presenting author of this paper has the option to appeal this decision by contacting TPII@ieee.org.
To study the effect of Saponins of asparagus on HepG2 apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential (Δψm) levels. Saponins of asparagus with different concentration was treated with HepG2 at different time, MTT assay was used to detect inhibitory rate, fluorescence staining was used to observe apoptosis morphology, flow cytometry was used to detect apoptosis rate and cell cycle, also ROS and Δψm were measured by flow cytometry. The results showed Saponins of asparagus inhibited cell proliferation, the IC50 on HepG2 was 172.3 mg/L. Apoptosis morphology was observed by fluorescence microscope. The cell cycle of HepG2 was arrested at S phase, G2/M phase percent decreased. After 72h the treated group appeared apoptosis peak, and apoptosis rate with high dose group 30.94 ± 1.74%; After 48h the ROS in treated group increased with high dose group 77.7 ± 4.5%; and Δψm decreased with high dose group 77.8 ± 1.9%. Saponins of asparagus can induce HepG2 cell apoptosis, which is caused by increasing ROS and decreasing Δψm of HepG2.
After careful and considered review of the content of this paper by a duly constituted expert committee, this paper has been found to be in violation of IEEE´s Publication Principles.
We hereby retract the content of this paper. Reasonable effort should be made to remove all past references to this paper.
The presenting author of this paper has the option to appeal this decision by contacting TPII@ieee.org.
To study the effect of Saponins of asparagus on HepG2 apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential (Δψm) levels. Saponins of asparagus with different concentration was treated with HepG2 at different time, MTT assay was used to detect inhibitory rate, fluorescence staining was used to observe apoptosis morphology, flow cytometry was used to detect apoptosis rate and cell cycle, also ROS and Δψm were measured by flow cytometry. The results showed Saponins of asparagus inhibited cell proliferation, the IC50 on HepG2 was 172.3 mg/L. Apoptosis morphology was observed by fluorescence microscope. The cell cycle of HepG2 was arrested at S phase, G2/M phase percent decreased. After 72h the treated group appeared apoptosis peak, and apoptosis rate with high dose group 30.94 ± 1.74%; After 48h the ROS in treated group increased with high dose group 77.7 ± 4.5%; and Δψm decreased with high dose group 77.8 ± 1.9%. Saponins of asparagus can induce HepG2 cell apoptosis, which is caused by increasing ROS and decreasing Δψm of HepG2.
Keywords
bio-optics; biochemistry; bioelectric potentials; biomembranes; cancer; cellular biophysics; fluorescence; molecular biophysics; optical microscopy; oxygen; HepG2 cell apoptosis; ROS level; asparagus; cell proliferation; flow cytometry; fluorescence microscope; fluorescence staining; mitochondrial membrane potential level; reactive oxygen species; saponins; time 48 h; time 72 h; Biomembranes; Drugs; Fluid flow measurement; Fluorescence; Humans; Microscopy; Morphology; Asparagus officinalis; HepG2; Saponins; apoptosis;
fLanguage
English
Publisher
ieee
Conference_Titel
Environmental Science and Information Application Technology (ESIAT), 2010 International Conference on
Conference_Location
Wuhan
Print_ISBN
978-1-4244-7387-8
Type
conf
DOI
10.1109/ESIAT.2010.5568423
Filename
5568423
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