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Caffeic acid improves cell viability and protects against DNA damage: involvement of reactive oxygen species and extracellular signal-regulated kinase.

Li Y, Chen LJ, Jiang F, Yang Y, Wang XX, Zhang Z, Li Z, Li L - Braz. J. Med. Biol. Res. (2015)

Bottom Line: However, whether CaA-induced protection is a hormetic effect remains unknown, as is the molecular mechanism that is involved.We found that a low concentration (10 μM) of CaA increased human liver L-02 cell viability, attenuated hydrogen peroxide (H2O2)-mediated decreases in cell viability, and decreased the extent of H2O2-induced DNA double-strand breaks (DSBs).In L-02 cells exposed to H2O2, CaA treatment reduced ROS levels, which might have played a protective role.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, China.

ABSTRACT
Hormesis is an adaptive response to a variety of oxidative stresses that renders cells resistant to harmful doses of stressing agents. Caffeic acid (CaA) is an important antioxidant that has protective effects against DNA damage caused by reactive oxygen species (ROS). However, whether CaA-induced protection is a hormetic effect remains unknown, as is the molecular mechanism that is involved. We found that a low concentration (10 μM) of CaA increased human liver L-02 cell viability, attenuated hydrogen peroxide (H2O2)-mediated decreases in cell viability, and decreased the extent of H2O2-induced DNA double-strand breaks (DSBs). In L-02 cells exposed to H2O2, CaA treatment reduced ROS levels, which might have played a protective role. CaA also activated the extracellular signal-regulated kinase (ERK) signal pathway in a time-dependent manner. Inhibition of ERK by its inhibitor U0126 or by its specific small interfering RNA (siRNA) blocked the CaA-induced improvement in cell viability and the protective effects against H2O2-mediated DNA damage. This study adds to the understanding of the antioxidant effects of CaA by identifying a novel molecular mechanism of enhanced cell viability and protection against DNA damage.

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Related in: MedlinePlus

Caffeic acid (CaA) decreased H2O2-induceddouble-strand breads (DSBs) in L-02 cells. A,B, L-02 cells were exposed to 0, 10, 20, 40, or 80 μMH2O2 for 6 h. A, Western blotanalysis and B, relative γ-H2AX protein levels. **P<0.01compared with control cells. C, D, L-02 cellswere pretreated with 0 or 10 μM CaA for 24 h and then exposed to 40(lanes 2 and 3) or 80 (lanes4 and 5) μM H2O2 for 6 h.C, Western blot analysis and D, relativeγ-H2AX protein levels. *P<0.05 and **P<0.01 compared with L-02 cellstreated with H2O2 alone (Student'st-test). Bands were normalized to glyceraldehyde 3-phosphatedehydrogenase (GAPDH).
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f02: Caffeic acid (CaA) decreased H2O2-induceddouble-strand breads (DSBs) in L-02 cells. A,B, L-02 cells were exposed to 0, 10, 20, 40, or 80 μMH2O2 for 6 h. A, Western blotanalysis and B, relative γ-H2AX protein levels. **P<0.01compared with control cells. C, D, L-02 cellswere pretreated with 0 or 10 μM CaA for 24 h and then exposed to 40(lanes 2 and 3) or 80 (lanes4 and 5) μM H2O2 for 6 h.C, Western blot analysis and D, relativeγ-H2AX protein levels. *P<0.05 and **P<0.01 compared with L-02 cellstreated with H2O2 alone (Student'st-test). Bands were normalized to glyceraldehyde 3-phosphatedehydrogenase (GAPDH).

Mentions: Oxidative DNA damage is the leading cause of decreased cell viability (13,14). Weexposed L-02 cells to 0, 10, 20, 40, or 80 μM H2O2 for 6 h andfound dose-dependent increases in the expression of γ-H2AX, which is a biomarker ofDSBs (Figure 2A and B). We then evaluated theability of CaA to protect against the DNA damage that resulted fromH2O2 treatment. After pretreating L-02 cells with 0 or 10 μMCaA for 24 h, they were exposed to 40 or 80 μM of H2O2 for 6 h.As shown in Figure 2C and D, CaA attenuated theH2O2-induced increase in γ-H2AX expression. These resultsindicate that a low concentration of CaA decreased H2O2-inducedDSBs in L-02 cells.


Caffeic acid improves cell viability and protects against DNA damage: involvement of reactive oxygen species and extracellular signal-regulated kinase.

Li Y, Chen LJ, Jiang F, Yang Y, Wang XX, Zhang Z, Li Z, Li L - Braz. J. Med. Biol. Res. (2015)

Caffeic acid (CaA) decreased H2O2-induceddouble-strand breads (DSBs) in L-02 cells. A,B, L-02 cells were exposed to 0, 10, 20, 40, or 80 μMH2O2 for 6 h. A, Western blotanalysis and B, relative γ-H2AX protein levels. **P<0.01compared with control cells. C, D, L-02 cellswere pretreated with 0 or 10 μM CaA for 24 h and then exposed to 40(lanes 2 and 3) or 80 (lanes4 and 5) μM H2O2 for 6 h.C, Western blot analysis and D, relativeγ-H2AX protein levels. *P<0.05 and **P<0.01 compared with L-02 cellstreated with H2O2 alone (Student'st-test). Bands were normalized to glyceraldehyde 3-phosphatedehydrogenase (GAPDH).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4470308&req=5

f02: Caffeic acid (CaA) decreased H2O2-induceddouble-strand breads (DSBs) in L-02 cells. A,B, L-02 cells were exposed to 0, 10, 20, 40, or 80 μMH2O2 for 6 h. A, Western blotanalysis and B, relative γ-H2AX protein levels. **P<0.01compared with control cells. C, D, L-02 cellswere pretreated with 0 or 10 μM CaA for 24 h and then exposed to 40(lanes 2 and 3) or 80 (lanes4 and 5) μM H2O2 for 6 h.C, Western blot analysis and D, relativeγ-H2AX protein levels. *P<0.05 and **P<0.01 compared with L-02 cellstreated with H2O2 alone (Student'st-test). Bands were normalized to glyceraldehyde 3-phosphatedehydrogenase (GAPDH).
Mentions: Oxidative DNA damage is the leading cause of decreased cell viability (13,14). Weexposed L-02 cells to 0, 10, 20, 40, or 80 μM H2O2 for 6 h andfound dose-dependent increases in the expression of γ-H2AX, which is a biomarker ofDSBs (Figure 2A and B). We then evaluated theability of CaA to protect against the DNA damage that resulted fromH2O2 treatment. After pretreating L-02 cells with 0 or 10 μMCaA for 24 h, they were exposed to 40 or 80 μM of H2O2 for 6 h.As shown in Figure 2C and D, CaA attenuated theH2O2-induced increase in γ-H2AX expression. These resultsindicate that a low concentration of CaA decreased H2O2-inducedDSBs in L-02 cells.

Bottom Line: However, whether CaA-induced protection is a hormetic effect remains unknown, as is the molecular mechanism that is involved.We found that a low concentration (10 μM) of CaA increased human liver L-02 cell viability, attenuated hydrogen peroxide (H2O2)-mediated decreases in cell viability, and decreased the extent of H2O2-induced DNA double-strand breaks (DSBs).In L-02 cells exposed to H2O2, CaA treatment reduced ROS levels, which might have played a protective role.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, China.

ABSTRACT
Hormesis is an adaptive response to a variety of oxidative stresses that renders cells resistant to harmful doses of stressing agents. Caffeic acid (CaA) is an important antioxidant that has protective effects against DNA damage caused by reactive oxygen species (ROS). However, whether CaA-induced protection is a hormetic effect remains unknown, as is the molecular mechanism that is involved. We found that a low concentration (10 μM) of CaA increased human liver L-02 cell viability, attenuated hydrogen peroxide (H2O2)-mediated decreases in cell viability, and decreased the extent of H2O2-induced DNA double-strand breaks (DSBs). In L-02 cells exposed to H2O2, CaA treatment reduced ROS levels, which might have played a protective role. CaA also activated the extracellular signal-regulated kinase (ERK) signal pathway in a time-dependent manner. Inhibition of ERK by its inhibitor U0126 or by its specific small interfering RNA (siRNA) blocked the CaA-induced improvement in cell viability and the protective effects against H2O2-mediated DNA damage. This study adds to the understanding of the antioxidant effects of CaA by identifying a novel molecular mechanism of enhanced cell viability and protection against DNA damage.

Show MeSH
Related in: MedlinePlus