THE VIABILITY TEST OF SAPPAN WOOD (CAESALPINIA SAPPAN L.) ETHANOL EXTRACT IN THE H9C2 CELL LINE

2020 ◽  
pp. 76-78
Author(s):  
IFA SULISTIYORINI ◽  
RATU SAFITRI ◽  
RONNY LESMANA ◽  
MAS RIZKY A. A. SYAMSUNARNO
Keyword(s):  
Cell Viability ◽  
Cell Line ◽  
Control Cell ◽  
Ethanol Extract ◽  
Optimal Dose ◽  
H9c2 Cell ◽  
Caesalpinia Sappan ◽  
Viable Cells ◽  
Dose Concentration ◽  
H9c2 Cell Line

Objective: In this study, the embryonic rat cardiomyocyte cell line H9C2 was used to investigate the cardiotoxicity effect of sappan wood ethanol extract (SWEE). Methods: Sappan wood was extracted in 96% ethanol and divided into dose concentrations of 2.5, 5, 10, 50, 100, and 150 μg/ml, with deferiprone used as a control. Cell viability was assessed using the PrestoBlue Cell Viability Reagent, according to manufacturer protocols. Results: Microscopic examination showed that the cell viability of H9C2 was preserved by SWEE treatments at a dose of 10 μg/ml and suggested dose concentrations of 50 μg/ml of SWEE. The percentage of viable cells was greater than 95% with a dose concentration of 10 μg/ml of SWEE, but it was significantly reduced with a dose concentration of 50 μg/ml of SWEE (p<0.05). Conclusion: The optimal dose concentration of SWEE to reach 95% cell viability was 10 μg/ml.

scholarly journals Over‐expression of FXRG and miR‐1 increases formation of RISC complexes in H9C2 cell line

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Lisa Walker ◽  
Karen Dockstader ◽  
Dobromir Slavov ◽  
Carmen Sucharov
Keyword(s):  
Cell Line ◽  
H9c2 Cell ◽  
Over Expression ◽  
H9c2 Cell Line

scholarly journals Cytoprotective potential of anti-ischemic drugs against chemotherapy-induced cardiotoxicity in H9c2 myoblast cell line

2013 ◽  
Vol 63 (4) ◽  
pp. 493-503 ◽  
Author(s):  
Tiam Feridooni ◽  
Chris Mac Donald ◽  
Di Shao ◽  
Pollen Yeung ◽  
Remigius U. Agu
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Cancer Drug ◽  
H9c2 Cell ◽  
Drug Induced ◽  
Cardiac Model ◽  
Myoblast Cell Line ◽  
Myoblast Cell ◽  
H9c2 Cell Line

Abstract To investigate potential prevention or attenuation of anti- cancer drug induced cardiotoxicity using anti-ischemic drugs, a rat myoblast (H9c2) cell line was used as our in vitro cardiac model. Irinotecan and doxorubicin were found to be cytotoxic for the H9c2 cell line with IC50 of 30.69 ± 6.20 and 20.94 ± 6.05 mmol L-1, respectively. 5-Flurouracil and cladribine were not cytotoxic and thus IC50 could not be calculated. When 100 mmol L-1 doxorubicin was incubated for 72 hours with 50 mmol L-1 diltiazem, 100 mmol L-1 dexrazoxane and 100 mmol L-1 losartan, respectively, there was a 58.7 ± 10.2, 52.2 ± 11.7 and 44.7 ± 5.4 % reduction in cell death. When 200 mmol L-1 irinotecan was incubated for 72 hours with 100 mmol L-1 dexrazoxane, losartan and diltiazem, respectively, a 27.7 ± 6.9, 25.6 ± 5.1, and 19.1 ± 2.3 % reduction in cell death was observed. Our data suggests that losartan and diltiazem were as effective as dexrazoxane in protecting the cells against irinotecan- and doxorubicin-induced cell toxicity. These findings offer potential uses of anti- -ischemic drugs for ablation of cytotoxicity in response to mitochondrial injury, thereby improving patient outcomes and reducing health-care costs.

scholarly journals Erratum to: Isoproterenol Cytotoxicity is Dependent on the Differentiation State of the Cardiomyoblast H9c2 Cell Line

2011 ◽  
Vol 11 (3) ◽  
pp. 284-284
Author(s):  
Ana F. Branco ◽  
Sandro L. Pereira ◽  
Ana C. Moreira ◽  
Jon Holy ◽  
Vilma A. Sardão ◽  
...  
Keyword(s):  
Cell Line ◽  
H9c2 Cell ◽  
H9c2 Cell Line

scholarly journals Effect of the Conditioned Medium from H9C2 Cell Line Treated with Dehydroepiandrosterone and Exposed to Damage on the Motility of Mesenchymal Stem Cells

2017 ◽  
Author(s):  
◽  
G. X. Castro-Santos
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Cell Line ◽  
Conditioned Medium ◽  
Therapeutic Strategy ◽  
H9c2 Cell ◽  
Wound Healing Assay ◽  
Heart Damage ◽  
Stimulation Of ◽  
H9c2 Cell Line

Cardiovascular diseases (CVD) are the leading cause of death worldwide. Mesenchymal Stem Cell (MSC) therapy is an alternative for patients who cannot recover with current treatments. Ensure movilization of MSC to the affected organs would represent an advantage for therapeutic management of CVD. Dehydroepiandrosterone (DHEA) is a hormone precursor whose levels decrease throughout life, which has been associated with the onset of CVD. Several studies have shown that DHEA consumption, prevents and improves heart condition, although it is not known if this is because an effect on cardiomyocytes is exercised on these cells and this, in turn, to CTM. The aim of this study was to determine the effect of conditioned medium from H9C2 cell line pretreated with DHEA and subjected to damage, on the motility of CTM, performing a wound healing assay. Pretreatment with DHEA and damage to H9C2 cell line, promotes motility of CTM. Stimulation of CTM motility by an indirect effect of DHEA could be a therapeutic strategy for heart damage.

Bax translocates from cytosol to mitochondria in cardiac cells during apoptosis: development of a GFP-Bax-stable H9c2 cell line for apoptosis analysis

2005 ◽  
Vol 289 (1) ◽  
pp. H477-H487 ◽  
Author(s):  
Qi Hou ◽  
Yi-Te Hsu
Keyword(s):  
Cell Death ◽  
Membrane Potential ◽  
Cell Line ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
H9c2 Cell ◽  
Serum Withdrawal ◽  
Induction Of Apoptosis ◽  
H9c2 Cell Line ◽  
Hypoxia Reoxygenation

The proapoptotic protein Bax plays an important role in cardiomyocytic cell death. Ablation of this protein has been shown to diminish cardiac damage in Bax-knockout mice during ischemia-reperfusion. Presently, studies of Bax-mediated cardiac cell death examined primarily the expression levels of Bax and its prosurvival factor Bcl-2 rather than the localization of this protein, which dictates its function. Using immunofluorescence labeling, we have shown that in neonatal rat cardiomyocytes and in H9c2 cardiomyoblasts, Bax translocates from cytosol to mitochondria upon the induction of apoptosis by hypoxia-reoxygenation-serum withdrawal and by the presence of the free-radical inducer menadione. Also, we found that Bax translocation to mitochondria was associated with the exposure of an NH2-terminal epitope, and that this translocation could be partially blocked by the prosurvival factors Bcl-2 and Bcl-XL. To visualize the translocation of Bax in living cells, we have developed an H9c2 cell line that stably expresses green fluorescent protein (GFP)-tagged Bax. This cell line has GFP-Bax localized primarily in the cytosol in the absence of apoptotic inducers. Upon induction of apoptosis by a number of stimuli, including menadione, staurosporine, sodium nitroprusside, and hypoxia-reoxygenation-serum withdrawal, we could observe the translocation of Bax from cytosol to mitochondria. This translocation was not affected by retinoic acid-induced differentiation of H9c2 cells. Additionally, this translocation was associated with loss of mitochondrial membrane potential, release of cytochrome c, and fragmentation of nuclei. Finally, using a tetramethylrhodamine-based dye, we have shown that a rapid screening process based on the loss of mitochondrial membrane potential could be developed to monitor GFP-Bax translocation to mitochondria. Overall, the GFP-Bax-stable H9c2 cell line that we have developed represents a unique tool for examining Bax-mediated apoptosis, and it could be of great importance in screening therapeutic compounds that could block Bax translocation to mitochondria to attenuate apoptosis.

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