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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 protein kinase A inhibition on intracellular ROS formation of ethanol and Ecklonia cava polyphenol (ECP)-treated hepatocytes. Hepatocytes were incubated for 6 or 9 h with 100 mM ethanol, with or without ECP (6.25 μg/mL). Protein kinase A inhibitor, H-89 (10 μM) was added to the medium with ethanol and ECP simultaneously. ROS formation was detected as described in the Materials and Methods section. (a) Control, 6 h; (b) 100 mM ethanol, 6 h; (c) 100 mM ethanol and 6.25 μg/mL ECP, 6 h; (d) 100 mM ethanol, 6.25 μg/mL ECP and 10 μM H-89, 6 h; (e) Control, 9 h; (f) 100 mM ethanol, 9 h; (g) 100 mM ethanol and 6.25 μg/mL ECP, 9 h; (h) 100 mM ethanol plus 6.25 μg/mL ECP plus 10 μM H-89, 9 h.
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marinedrugs-13-03877-f007: Effects of protein kinase A inhibition on intracellular ROS formation of ethanol and Ecklonia cava polyphenol (ECP)-treated hepatocytes. Hepatocytes were incubated for 6 or 9 h with 100 mM ethanol, with or without ECP (6.25 μg/mL). Protein kinase A inhibitor, H-89 (10 μM) was added to the medium with ethanol and ECP simultaneously. ROS formation was detected as described in the Materials and Methods section. (a) Control, 6 h; (b) 100 mM ethanol, 6 h; (c) 100 mM ethanol and 6.25 μg/mL ECP, 6 h; (d) 100 mM ethanol, 6.25 μg/mL ECP and 10 μM H-89, 6 h; (e) Control, 9 h; (f) 100 mM ethanol, 9 h; (g) 100 mM ethanol and 6.25 μg/mL ECP, 9 h; (h) 100 mM ethanol plus 6.25 μg/mL ECP plus 10 μM H-89, 9 h.

Mentions: To examine whether ECP protects ethanol-induced liver injury via regulating alcohol metabolic enzymes in a cAMP-dependent manner, we tested the effects of H89 on the production of ROS in hepatocytes after ethanol and/or ECP incubation. As shown in Figure 1 and Figure 7, exposure to 100 mM ethanol and 6.25 μg/mL ECP caused a decrease in intracellular ROS levels. However, H89 treatment increased the intracellular ROS level to the levels in ethanol-alone-treated hepatocytes.


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 protein kinase A inhibition on intracellular ROS formation of ethanol and Ecklonia cava polyphenol (ECP)-treated hepatocytes. Hepatocytes were incubated for 6 or 9 h with 100 mM ethanol, with or without ECP (6.25 μg/mL). Protein kinase A inhibitor, H-89 (10 μM) was added to the medium with ethanol and ECP simultaneously. ROS formation was detected as described in the Materials and Methods section. (a) Control, 6 h; (b) 100 mM ethanol, 6 h; (c) 100 mM ethanol and 6.25 μg/mL ECP, 6 h; (d) 100 mM ethanol, 6.25 μg/mL ECP and 10 μM H-89, 6 h; (e) Control, 9 h; (f) 100 mM ethanol, 9 h; (g) 100 mM ethanol and 6.25 μg/mL ECP, 9 h; (h) 100 mM ethanol plus 6.25 μg/mL ECP plus 10 μM H-89, 9 h.
© Copyright Policy
Related In: Results  -  Collection

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

marinedrugs-13-03877-f007: Effects of protein kinase A inhibition on intracellular ROS formation of ethanol and Ecklonia cava polyphenol (ECP)-treated hepatocytes. Hepatocytes were incubated for 6 or 9 h with 100 mM ethanol, with or without ECP (6.25 μg/mL). Protein kinase A inhibitor, H-89 (10 μM) was added to the medium with ethanol and ECP simultaneously. ROS formation was detected as described in the Materials and Methods section. (a) Control, 6 h; (b) 100 mM ethanol, 6 h; (c) 100 mM ethanol and 6.25 μg/mL ECP, 6 h; (d) 100 mM ethanol, 6.25 μg/mL ECP and 10 μM H-89, 6 h; (e) Control, 9 h; (f) 100 mM ethanol, 9 h; (g) 100 mM ethanol and 6.25 μg/mL ECP, 9 h; (h) 100 mM ethanol plus 6.25 μg/mL ECP plus 10 μM H-89, 9 h.
Mentions: To examine whether ECP protects ethanol-induced liver injury via regulating alcohol metabolic enzymes in a cAMP-dependent manner, we tested the effects of H89 on the production of ROS in hepatocytes after ethanol and/or ECP incubation. As shown in Figure 1 and Figure 7, exposure to 100 mM ethanol and 6.25 μg/mL ECP caused a decrease in intracellular ROS levels. However, H89 treatment increased the intracellular ROS level to the levels in ethanol-alone-treated hepatocytes.

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