Nutr Res Pract.  2023 Dec;17(6):1113-1127. 10.4162/nrp.2023.17.6.1113.

Aqueous extract of Laurus nobilis leaf accelerates the alcohol metabolism and prevents liver damage in singleethanol binge rats

Affiliations
  • 1Industry coupled Cooperation Center for Bio Healthcare Materials, Hallym University, Chuncheon 24252, Korea
  • 2Department of Food and Nutrition, Sahmyook University, Seoul 01795, Korea
  • 3R&D Division, Daehan Chemtech Co. Ltd., Gwacheon 13840, Korea

Abstract

BACKGROUND/OBJECTIVES
Excessive alcohol consumption has harmful health effects, including alcohol hangovers and alcohol-related liver disease. Therefore, methods to accelerate the alcohol metabolism are needed. Laurus nobilis is a spice, flavoring agent, and traditional herbal medicine against various diseases. This study examined whether the standardized aqueous extract of L. nobilis leaves (LN) accelerates the alcohol metabolism and protects against liver damage in single-ethanol binge Sprague-Dawley (SD) rats.
MATERIALS/METHODS
LN was administered orally to SD rats 1 h before ethanol administration (3 g/kg body weight [BW]) at 100 and 300 mg/kg BW. Blood samples were collected 0.5, 1, 2, and 4 h after ethanol administration. The livers were excised 1 h after ethanol administration to determine the hepatic enzyme activity. The alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities in the liver tissue were measured.
RESULTS
LN decreased the serum ethanol and acetaldehyde levels in ethanol-administered rats. LN increased the hepatic ADH and ALDH activities but decreased the alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase activities in the ethanol-administered rats. In addition, LN inhibited lipid peroxidation and increased the activities of SOD and GPx.
CONCLUSIONS
LN modulates the mediators of various etiological effects of excessive alcohol consumption and enhances the alcohol metabolism and antioxidant activity, making it a potential candidate for hangover treatments.

Keyword

Laurus nobilis; alcohol dehydrogenase; aldehyde dehydrogenase; superoxide dismutase; glutathione peroxidase

Figure

  • Fig. 1 High-performance liquid chromatography analysis of isoquercetin in LN. (A) Standard, 0.06 mg/mL isoquercetin; (B) 5.07 mg/mL LN.LN, standardized aqueous extract of Laurus nobilis leaf.

  • Fig. 2 Effects of LN on the serum ethanol and acetaldehyde concentrations in single-ethanol binge SD rats. SD rats were administered LN orally. After 1 h, the rats were given ethanol at a dose of 3 g/kg body weight by oral gavage. Blood was collected at 0.5, 1, 2, and 4 h after ethanol administration, and serum was obtained from blood. The ethanol (A) and acetaldehyde (C) concentrations in serum were measured using the relevant assay kits. The AUC for serum ethanol (B) and acetaldehyde (D) were calculated. Each bar represents the mean ± SE of mean (n = 10).LN, standardized aqueous extract of Laurus nobilis leaf; AUC, area under the concentration-time curve; NC, normal control group; EC, ethanol control group; LN100, ethanol + 100 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group; LN300, ethanol + 300 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group; SD, Sprague-Dawley.***P < 0.001 indicates a significant difference from the NC group.Different letters indicate significant differences between the EC, LN100, and LN300 groups at P < 0.05.

  • Fig. 3 Effects of LN on hepatic ADH and ALDH activities in single-ethanol binge SD rats. SD rats were administered LN orally. After 1 h, the rats were given ethanol at a dose of 3 g/kg body weight by oral gavage. After 1 h of ethanol administration, the livers were excised from the rats. Hepatic ADH (A) and ALDH (B) activities were estimated using the relevant assay kits. Each bar represents the mean ± SE of mean (n = 10).LN, standardized aqueous extract of Laurus nobilis leaf; ADH, alcohol dehydrogenase; ALDH, aldehyde dehydrogenase; NC, normal control group; EC, ethanol control group; LN100, ethanol + 100 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group; LN300, ethanol + 300 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group; SD, Sprague-Dawley.**P < 0.01 indicate significant difference from the NC group.The different letters indicate significant differences between the EC, LN100, and LN300 groups at P < 0.05.

  • Fig. 4 Effects of LN on the serum AST, ALT, and γ-GT activities in single-ethanol binge Sprague-Dawley rats. The rats were administered LN orally. After 1 h, the rats were given ethanol at a dose of 3 g/kg body weight by oral gavage. After 1 h of ethanol administration, blood was collected, and serum was obtained. The AST (A), ALT (B), and γ-GT (C) activities in serum were measured using a blood chemistry autoanalyzer. Each bar represents the mean ± SE of mean (n = 10).LN, standardized aqueous extract of Laurus nobilis leaf; ALT, alanine aminotransferase; AST, aspartate aminotransferase; γ-GT, gamma-glutamyl transferase; NC, normal control group; EC, ethanol control group; LN100, ethanol + 100 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group; LN300, ethanol + 300 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group.**P < 0.01 indicates a significant difference from the NC group.The different letters indicate significant differences between the EC, LN100, and LN300 groups at P < 0.05.

  • Fig. 5 Effects of LN on hepatic MDA contents in single-ethanol binge Sprague-Dawley rats. The rats were administered LN and ethanol, and the livers were excised as described in Fig. 3. MDA content in livers was measured using a thiobarbituric acid reactive substances assay kit. Each bar represents the mean ± SE of mean (n = 10).LN, standardized aqueous extract of Laurus nobilis leaf; MDA, malondialdehyde; NC, normal control group; EC, ethanol control group; LN100, ethanol + 100 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group; LN300, ethanol + 300 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group.**P < 0.01 show significant difference from the NC group.The different letters indicate significant differences between the EC, LN100, and LN300 groups at P < 0.05.

  • Fig. 6 Effects of hepatic SOD, GPx, and catalase activities in single-ethanol binge Sprague-Dawley rats. The rats were administered with LN and ethanol, and the livers were excised as described in Fig. 3. SOD (A), GPx (B), and catalase (C) activities in the liver were measured using the relevant assay kits. Each bar represents the mean ± SE of mean (n = 10).LN, standardized aqueous extract of Laurus nobilis leaf; SOD, superoxide dismutase; GPx, glutathione peroxidase; NC, normal control group; EC, ethanol control group; LN100, ethanol + 100 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group; LN300, ethanol + 300 mg/kg body weight standardized aqueous extract of Laurus nobilis leaf-treated group; ns, not significant.*P < 0.05, **P < 0.01 indicates a significant difference from the NC group.The different letters indicate significant differences between the EC, LN100, and LN300 groups at P < 0.05.


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