Limits...
Ecklonia cava Polyphenol Has a Protective Effect against Ethanol-Induced Liver Injury in a Cyclic AMP-Dependent Manner.

Yamashita H, Goto M, Matsui-Yuasa I, Kojima-Yuasa A - Mar Drugs (2015)

Bottom Line: Here, we examined the effects of ECP on the activities of alcohol-metabolizing enzymes and their regulating mechanisms in ethanol-treated hepatocytes.These changes in activities of CYP2E1 and ADH were suppressed by treatment with H89, an inhibitor of protein kinase A.ECP treatment with ethanol enhanced cyclic AMP concentrations compared with those of control cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka 558-8585, Japan. yuzu_chiffon_o712@yahoo.co.jp.

ABSTRACT
Previously, we showed that Ecklonia cava polyphenol (ECP) treatment suppressed ethanol-induced increases in hepatocyte death by scavenging intracellular reactive oxygen species (ROS) and maintaining intracellular glutathione levels. Here, we examined the effects of ECP on the activities of alcohol-metabolizing enzymes and their regulating mechanisms in ethanol-treated hepatocytes. Isolated hepatocytes were incubated with or without 100 mM ethanol. ECP was dissolved in dimethylsulfoxide. ECP was added to cultured cells that had been incubated with or without ethanol. The cells were incubated for 0-24 h. In cultured hepatocytes, the ECP treatment with ethanol inhibited cytochrome P450 2E1 (CYP2E1) expression and activity, which is related to the production of ROS when large quantities of ethanol are oxidized. On the other hand, ECP treatment with ethanol increased the activity of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase. These changes in activities of CYP2E1 and ADH were suppressed by treatment with H89, an inhibitor of protein kinase A. ECP treatment with ethanol enhanced cyclic AMP concentrations compared with those of control cells. ECP may be a candidate for preventing ethanol-induced liver injury via regulating alcohol metabolic enzymes in a cyclic AMP-dependent manner.

No MeSH data available.


Related in: MedlinePlus

Effects of Ecklonia cava polyphenol (ECP) on the ethanol-induced increases in ADH activity in hepatocytes. Hepatocytes were incubated for 0–9 h with 100 mM, ethanol with or without ECP (6.25 μg/mL). ADH activity analysis was performed as described in the Materials and Methods section. Data are presented as the mean ± S.D. of three separate experiments. Values without a common letter are significantly different (p < 0.05 at 4 h, p < 0.01 at 9 h). ○: Control; ●: 100 mM ethanol; ▲: 100 mM ethanol plus 6.25 μg/mL ECP; △: 6.25 μg/mL ECP.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4483661&req=5

marinedrugs-13-03877-f003: Effects of Ecklonia cava polyphenol (ECP) on the ethanol-induced increases in ADH activity in hepatocytes. Hepatocytes were incubated for 0–9 h with 100 mM, ethanol with or without ECP (6.25 μg/mL). ADH activity analysis was performed as described in the Materials and Methods section. Data are presented as the mean ± S.D. of three separate experiments. Values without a common letter are significantly different (p < 0.05 at 4 h, p < 0.01 at 9 h). ○: Control; ●: 100 mM ethanol; ▲: 100 mM ethanol plus 6.25 μg/mL ECP; △: 6.25 μg/mL ECP.

Mentions: To determine their potential protective mechanisms against ethanol-induced hepatotoxicity, we examined the activities of the major alcohol metabolizing enzymes ADH and ALDH. ECP treatment significantly enhanced ADH activity in these cells over a period of 2, 4 and 9 h (Figure 3). Furthermore, ALDH activity was also significantly enhanced by 6.25 μg/mL ECP after a 4-h incubation with ECP (Figure 4).


Ecklonia cava Polyphenol Has a Protective Effect against Ethanol-Induced Liver Injury in a Cyclic AMP-Dependent Manner.

Yamashita H, Goto M, Matsui-Yuasa I, Kojima-Yuasa A - Mar Drugs (2015)

Effects of Ecklonia cava polyphenol (ECP) on the ethanol-induced increases in ADH activity in hepatocytes. Hepatocytes were incubated for 0–9 h with 100 mM, ethanol with or without ECP (6.25 μg/mL). ADH activity analysis was performed as described in the Materials and Methods section. Data are presented as the mean ± S.D. of three separate experiments. Values without a common letter are significantly different (p < 0.05 at 4 h, p < 0.01 at 9 h). ○: Control; ●: 100 mM ethanol; ▲: 100 mM ethanol plus 6.25 μg/mL ECP; △: 6.25 μg/mL ECP.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4483661&req=5

marinedrugs-13-03877-f003: Effects of Ecklonia cava polyphenol (ECP) on the ethanol-induced increases in ADH activity in hepatocytes. Hepatocytes were incubated for 0–9 h with 100 mM, ethanol with or without ECP (6.25 μg/mL). ADH activity analysis was performed as described in the Materials and Methods section. Data are presented as the mean ± S.D. of three separate experiments. Values without a common letter are significantly different (p < 0.05 at 4 h, p < 0.01 at 9 h). ○: Control; ●: 100 mM ethanol; ▲: 100 mM ethanol plus 6.25 μg/mL ECP; △: 6.25 μg/mL ECP.
Mentions: To determine their potential protective mechanisms against ethanol-induced hepatotoxicity, we examined the activities of the major alcohol metabolizing enzymes ADH and ALDH. ECP treatment significantly enhanced ADH activity in these cells over a period of 2, 4 and 9 h (Figure 3). Furthermore, ALDH activity was also significantly enhanced by 6.25 μg/mL ECP after a 4-h incubation with ECP (Figure 4).

Bottom Line: Here, we examined the effects of ECP on the activities of alcohol-metabolizing enzymes and their regulating mechanisms in ethanol-treated hepatocytes.These changes in activities of CYP2E1 and ADH were suppressed by treatment with H89, an inhibitor of protein kinase A.ECP treatment with ethanol enhanced cyclic AMP concentrations compared with those of control cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka 558-8585, Japan. yuzu_chiffon_o712@yahoo.co.jp.

ABSTRACT
Previously, we showed that Ecklonia cava polyphenol (ECP) treatment suppressed ethanol-induced increases in hepatocyte death by scavenging intracellular reactive oxygen species (ROS) and maintaining intracellular glutathione levels. Here, we examined the effects of ECP on the activities of alcohol-metabolizing enzymes and their regulating mechanisms in ethanol-treated hepatocytes. Isolated hepatocytes were incubated with or without 100 mM ethanol. ECP was dissolved in dimethylsulfoxide. ECP was added to cultured cells that had been incubated with or without ethanol. The cells were incubated for 0-24 h. In cultured hepatocytes, the ECP treatment with ethanol inhibited cytochrome P450 2E1 (CYP2E1) expression and activity, which is related to the production of ROS when large quantities of ethanol are oxidized. On the other hand, ECP treatment with ethanol increased the activity of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase. These changes in activities of CYP2E1 and ADH were suppressed by treatment with H89, an inhibitor of protein kinase A. ECP treatment with ethanol enhanced cyclic AMP concentrations compared with those of control cells. ECP may be a candidate for preventing ethanol-induced liver injury via regulating alcohol metabolic enzymes in a cyclic AMP-dependent manner.

No MeSH data available.


Related in: MedlinePlus