Ethanol extract of Cyclolepis genistoides D. Don (palo azul) induces formation of myotubes, which involves differentiation of C2C12 myoblast cells

Sato, Hiromi; Funaki, Asami; Kimura, Yuki; Sumitomo, Mai; Yoshida, Hiroya; Fukata, Hideki; Ueno, Koichi

doi:10.1016/j.nutres.2016.02.011

Cited by 8 publications

(10 citation statements)

References 27 publications

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“…S1a). The generation of skeletal muscle may be inhibited in myotubes with dysfunctional differentiation [2][3][4][5][6]. Collectively, these findings and the present results suggest that the cell death or dysfunction of myoblasts that gain excess glucose or fructose and generate high levels of intracellular TAGE may inhibit the differentiation of myoblasts.…”

Section: Discussionmentioning

confidence: 55%

“…condition that is characterized by decreases in skeletal muscle mass and function, resulting in the deterioration of activities of daily living and quality of life as well as increases in the risk of falls and mortality [2]. Skeletal muscle consists of myotubes that differentiate from myoblasts; therefore, one of the mechanisms contributing to the loss of skeletal muscle is the death of or dysfunctions in myoblasts [2][3][4][5][6]. Accumulating evidence has shown that lifestyle-related diseases (LSRD) such as type 2 diabetes mellitus (T2DM) and non-alcoholic steatohepatitis (NASH) has an increased risk of sarcopenia [2,7,8].…”

mentioning

confidence: 99%

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Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death

Takata

Sakasai-Sakai

Takeuchi

2020

Diabetol Metab Syndr

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Background: Sarcopenia is a progressive condition that is characterized by decreases in skeletal muscle mass and function. Although sarcopenia is associated with lifestyle-related diseases (LSRD), the mechanisms underlying cell death in myoblasts, which differentiate to myotubes, remain unclear. We previously designated glyceraldehyde (an intermediate of glucose/fructose metabolism)-derived advanced glycation end-products (AGEs) as toxic AGEs (TAGE) because of their cytotoxicity and involvement in LSRD, and hypothesized that TAGE contribute to cell death in myoblasts. Methods: C2C12 cells, which are murine myoblasts, were treated with 0, 0.5, 1, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE were then assessed using 5-[2,4,-bis(sodioxysulfonyl)phenyl]-3-(2-methoxy-4-nitrophenyl)-2-(4-nitrophenyl)-2H-tetrazole-3-ium (WST-8) and slot blot assays. Cells were pretreated with 8 mM aminoguanidine, an inhibitor of AGE production, for 2 h, followed by 0, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE levels were then assessed. Serum TAGE levels in STAM mice, in which there were four stages (no steatosis, simple steatosis, steatohepatitis, and fibrosis), were measured using a competitive enzyme-linked immunosorbent assay. Results were expressed as TAGE units (U) per milliliter of serum, with 1 U corresponding to 1.0 μg of glyceraldehyde-derived AGE-bovine serum albumin (BSA) (TAGE-BSA). The viability of cells treated with 20, 50, and 100 μg/mL non-glycated BSA and TAGE-BSA for 24 h was assessed using the WST-8 assay. Results: In C2C12 cells treated with 1.5 and 2 mM glyceraldehyde, cell viability decreased to 47.7% (p = 0.0021) and 5.0% (p = 0.0001) and intracellular TAGE levels increased to 6.0 and 15.9 μg/mg protein, respectively. Changes in cell viability and TAGE production were completely inhibited by 8 mM aminoguanidine. Serum TAGE levels at the steatohepatitis and fibrosis stages were 10.51 ± 1.16 and 10.44 ± 0.95 U/mL, respectively, and were higher than those at the no steatosis stage (7.27 ± 0.18 U/mL). Cell death was not induced by 20 or 50 μg/mL TAGE-BSA. The viabilities of C2C12 cells treated with 100 μg/mL non-glycated BSA and TAGE-BSA were 105.0% (p = 0.2890) and 85.3% (p = 0.0217), respectively. Conclusion: Intracellular TAGE strongly induced cell death in C2C12 cells and may also induce myoblast cell death in LSRD model mice.

show abstract

Section: Discussionmentioning

confidence: 55%

mentioning

confidence: 99%

Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death

Takata

Sakasai-Sakai

Takeuchi

2020

Diabetol Metab Syndr

View full text Add to dashboard Cite

show abstract

“…S1a). The generation of skeletal muscle may be inhibited in myotubes with dysfunctional differentiation [2][3][4][5][6]. Collectively, these ndings and the present results suggest that the cell death or dysfunction of myoblasts that gain excess glucose or fructose and generate high levels of intracellular TAGE may inhibit the differentiation of myoblasts.…”

Section: Discussionmentioning

confidence: 61%

“…Sarcopenia is a progressive condition that is characterized by decreases in skeletal muscle mass and function, resulting in the deterioration of activities of daily living and quality of life as well as increases in the risk of falls and mortality [2]. Skeletal muscle consists of myotubes that differentiate from myoblasts; therefore, one of the mechanisms contributing to the loss of skeletal muscle is the death of or dysfunctions in myoblasts [2][3][4][5][6]. Accumulating evidence has shown that lifestyle-related diseases (LSRD) such as type 2 diabetes mellitus (T2DM) and non-alcoholic steatohepatitis (NASH) has an increased risk of sarcopenia [2,7,8].…”

Section: Introductionmentioning

confidence: 99%

Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death:A non-clinical study

Takata¹,

Sakasai-Sakai²,

Takeuchi³

2020

Preprint

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Background: Sarcopenia is a progressive condition that is characterized by decreases in skeletal muscle mass and function. Although sarcopenia is associated with lifestyle-related diseases (LSRD), the mechanisms underlying cell death in myoblasts, which differentiate to myotubes, remain unclear. We previously designated glyceraldehyde (an intermediate of glucose/fructose metabolism)-derived advanced glycation end-products (AGEs) as toxic AGEs (TAGE) because of their cytotoxicity and involvement in LSRD, and hypothesized that TAGE contribute to cell death in myoblasts. Methods: C2C12 cells, which are murine myoblasts, were treated with 0, 0.5, 1, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE were then assessed using 5-[2,4,-bis(sodioxysulfonyl)phenyl]-3-(2-methoxy-4-nitrophenyl)-2-(4-nitrophenyl)-2H-tetrazole-3-ium (WST-8) and slot blot assays. Cells were pretreated with 8 mM aminoguanidine , an inhibitor of AGE production, for 2 h, followed by 0, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE levels were then assessed. Serum TAGE levels in STAM mice, in which there were four stages (no steatosis, simple steatosis, steatohepatitis, and fibrosis), were measured using a competitive enzyme-linked immunosorbent assay. Results were expressed as TAGE units (U) per milliliter of serum, with 1 U corresponding to 1.0 μg of glyceraldehyde-derived AGE-bovine serum albumin (BSA) (TAGE-BSA). The viability of cells treated with 20, 50, and 100 μg/mL non-glycated BSA and TAGE-BSA for 24 h was assessed using the WST-8 assay. Results: In C2C12 cells treated with 1.5 and 2 mM glyceraldehyde, cell viability decreased to 47.7% ( p =0.0021) and 5.0% ( p =0.0001) and intracellular TAGE levels increased to 6.0 and 15.9 μg/mg protein, respectively. Changes in cell viability and TAGE production were completely inhibited by 8 mM aminoguanidine. Serum TAGE levels at the steatohepatitis and fibrosis stages were 10.51 ±1.16 and 10.44±0.95 U/mL, respectively, and were higher than those at the no steatosis stage ( 7.27 ±0.18 U/mL). Cell death was not induced by 20 or 50 μg/mL TAGE-BSA. The viabilities of C2C12 cells treated with 100 μg/mL non-glycated BSA and TAGE-BSA were 105.0% ( p =0.2890) and 85.3% ( p =0.0217), respectively. Conclusion: Intracellular TAGE strongly induced cell death in C2C12 cells and may also induce myoblast cell death in LSRD model mice.

show abstract

Section: Introductionmentioning

confidence: 99%

Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death: A non-clinical study

Takata¹,

Sakasai-Sakai²,

Takeuchi³

2020

Preprint

View full text Add to dashboard Cite

Background: Sarcopenia is a progressive condition that is characterized by decreases in skeletal muscle mass and function. Although previous studies reported that sarcopenia is associated with non-alcoholic steatohepatitis (NASH), the underlying mechanisms remain unclear. We herein focused on glyceraldehyde, an intermediate of glucose/fructose metabolism. We previously designated glyceraldehyde-derived advanced glycation end-products (AGEs) as toxic AGEs (TAGE) because of their cytotoxicity and involvement in lifestyle-related diseases, such as NASH. We hypothesized that TAGE is associated with sarcopenia. Methods: C2C12 cells, which are murine myoblasts, were treated with 0, 0.5, 1, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE were then assessed using 5-[2,4,-Bis(sodioxysulfonyl)phenyl]-3-(2-methoxy-4-nitrophenyl)-2-(4-nitrophenyl)-2H-tetrazole-3-ium (WST-8) and slot blot assays. Cells were pretreated with 8 mM aminoguanidine , an inhibitor of AGE production, for 2 h followed by 0, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE were then assessed. Serum TAGE levels in STAM mice, in which there were four stages (no steatosis, simple steatosis, steatohepatitis, and fibrosis), were measured using an enzyme-linked immunosorbent assay. Results were expressed as TAGE units (U) per milliliter of serum, with 1 U corresponding to 1.0 μg of glyceraldehyde-derived AGE-bovine serum albumin (BSA) (TAGE-BSA). The viability of cells treated with 20, 50, and 100 μg/mL non-glycated BSA and TAGE-BSA for 24 h was assessed using the WST-8 assay. Results: In C2C12 cells treated with 1.5 and 2 mM glyceraldehyde, cell viability decreased to 47.7% ( p =0.0021) and 5.0% ( p =0.0001) and intracellular TAGE levels increased to 6.0 and 15.9 μg/mg protein, respectively. Changes in cell viability and TAGE production were completely inhibited by 8 mM aminoguanidine. Serum TAGE levels at the steatohepatitis and fibrosis stages were 10.51 ±1.16 and 10.44±0.95 U/mL, respectively, and were higher than that at the no steatosis stage (7.27±0.18 U/mL). Cell death was not induced by 20 or 50 μg/mL TAGE-BSA. The viabilities of C2C12 cells treated with 100 μg/mL non-glycated BSA and TAGE-BSA were 105.0% ( p =0.2890) and 85.3% ( p =0.0217), respectively. Conclusion: Intracellular TAGE strongly induce myoblast cell death and may cause sarcopenia. Therefore, TAGE may play a crucial role in sarcopenia associated with NASH .

show abstract

Ethanol extract of Cyclolepis genistoides D. Don (palo azul) induces formation of myotubes, which involves differentiation of C2C12 myoblast cells

Cited by 8 publications

References 27 publications

Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death

Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death

Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death:A non-clinical study

Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death: A non-clinical study

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