Effect of water extract of bay laurel (Laurus nobilis L.) on non-alcoholic fatty liver disease (NAFLD)

  • Minhee Lee Department of Food Innovation and Health, Kyung Hee University, Yongin 17104, Korea
  • Jeongjin Park Division of Food and Nutrition and Human Ecology Research Institute, Chonnam National University, Gwangju 61186, Republic of Korea
  • Dakyung Kim Department of Medical Nutrition, Kyung Hee University, Yongin 17104, Korea
  • Seong-Hoo Park Department of Medical Nutrition, Kyung Hee University, Yongin 17104, Korea
  • Jaeeun Jung Department of Medical Nutrition, Kyung Hee University, Yongin 17104, Korea
  • Woojin Jun Division of Food and Nutrition and Human Ecology Research Institute, Chonnam National University, Gwangju 61186, Republic of Korea
  • Jinhak Kim R&D Division, Daehan Chemtech Co. Ltd., Gwacheon 13840, Korea
  • Kwang-Soo Baek R&D Division, Daehan Chemtech Co. Ltd., Gwacheon 13840, Korea
  • Ok-Kyung Kim Division of Food and Nutrition and Human Ecology Research Institute, Chonnam National University, Gwangju 61186, Republic of Korea
  • Jeongmin Lee Department of Food Innovation and Health, Kyung Hee University, Yongin 17104, Korea
Keywords: NAFLD, bay laurel leaves, lipid accumulation, inflammation, apoptosis

Abstract

Non-alcoholic fatty liver disease (NAFLD) involves lipid accumulation in liver without consumption of alcohol and affects many people worldwide. NAFLD is associated with metabolic syndrome disease such as obesity, insulin resistance, hyperlipidemia, and diabetes. However, there are no pharmacologic therapies for NAFLD. Recently, there are increasing reports that several natural plants can inhibit lipid accumulation in hepatocytes. Bay laurel (Laurus nobilis L.) leaves have been used in traditional medicine for rheumatism, stomach ache, emetic, skin rashes, and earaches. Our objective was to investigate the effect of bay laurel leaves water extract (BLW) on free fatty acid (FFA) treated hepatocyte and high fructose, high fat (HFHF) diet in a mouse model of NAFLD. In vitro, lipid accumulation increased only in the FFA treated group, while BLW reduced lipid accumulation to a level comparable to that only in the FFA treated group. Cellular antioxidants were increased in the BLW compared to the only FFA-treated group, but cellular MDA levels were decreased in the BLW compared to the only FFA treated group. Cellular lipid accumulation, inflammation, and apoptosis were reduced in the BLW compared to the only FFA treated group. In vivo, serum ALT, AST, and GGT levels in the BLW supplementation group were significantly decreased compared with the HFHF group. Hepatic TC, TG, and MDA levels were significantly decreased in the HFHF+100 and HFHF+200 groups compared to the HFHF group. The hepatic antioxidant activities in the BLW supplementation groups were significantly increased compared to the HFHF group. The expression of proteins related to hepatic inflammation and apoptosis was reduced in the BLW supplementation groups compared to the HFHF group. These results suggest that BLW could be potentially useful in the treatment of NAFLD due to its inhibitory effects on hepatic lipogenesis, hepatic inflammation, and hepatic apoptosis.

Downloads

Download data is not yet available.

References


1.
Mashek DG, Khan SA, Sathyanarayan A, Ploeger JM, Franklin MP. Hepatic lipid droplet biology: getting to the root of fatty liver. Hepatology 2015; 62: 964–7. doi: 10.1002/hep.27839


2.
Wong SW, Chan WK. Epidemiology of non-alcoholic fatty liver disease in Asia. Indian J Gastroenterol 2020; 39(1): 1–8. doi: 10.1007/s12664-020-01018-x


3.
Im HJ, Ahn YC, Wang J, Lee MM, Son CG. Systematic review on the prevalence of nonalcoholic fatty liver disease in South Korea. Clin Res Hepatol Gastroenterol 2020; 9: 101526. doi: 10.1016/j.clinre.2020.06.022


4.
Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005; 112: 2735–52. doi: 10.1161/CIRCULATIONAHA.105.169404


5.
Hadizadeh F, Faghihimani E, Adibi P. Nonalcoholic fatty liver disease: diagnostic biomarkers. World J Gastrointest Pathophysiol 2017; 8(2): 11–26. doi: 10.4291/wjgp.v8.i2.11


6.
Ito M, Suzuki J, Tsujioka S, Sasaki M, Gomori A, Shirakura T, et al. Longitudinal analysis of murine steatohepatitis model induced by chronic exposure to high-fat diet. Hepatol Res 2007; 37: 50–7. doi: 10.1111/j.1872-034X.2007.00008.x


7.
Lowe ME. The triglyceride lipases of the pancreas. J Lipid Res 2002; 43: 2007–16. doi: 10.1194/jlr.R200012-JLR200


8.
Linden D, William-Olsson L, Rhedin M, Asztely AK, Clapham JC, Schreyer S. Overexpression of mitochondrial GPAT in rat hepatocytes leads to decreased fatty acid oxidation and increased glycerolipid biosynthesis. J Lipid Res 2004; 45: 1279–88. doi: 10.1194/jlr.M400010-JLR200


9.
Cohen DE, Fisher EA. Lipoprotein metabolism, dyslipidemia, and nonalcoholic fatty liver disease. Semin Liver Dis 2013; 33: 380–8. doi: 10.1055/s-0033-1358519


10.
Bradbury MW. Lipid metabolism and liver inflammation. I. Hepatic fatty acid uptake: possible role in steatosis. Am J Physiol Gastrointest Liver Physiol 2006; 290: G194–8. doi: 10.1152/ajpgi.00413.2005


11.
Papa S, Zazzeroni F, Pham CG, Bubici C, Franzoso G. Linking JNK signaling to NF-kappaB: a key to survival. J Cell Sci 2004; 117: 5197–208. doi: 10.1242/jcs.01483


12.
Tsuruta F, Sunayama J, Mori Y, Hattori S, Shimizu S, Tsujimoto Y, et al. JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins. EMBO J 2004; 23: 1889–99. doi: 10.1038/sj.emboj.7600194


13.
Vasarri M, Barletta E, Degl’Innocenti D. Posidonia oceanica (L.) delile extract reduces lipid accumulation through autophagy activation in HepG2 cells. Pharmaceuticals (Basel) 2021; 14(10): 969. doi: 10.3390/ph14100969


14.
Mohammed RR, Omer AK, Yener Z, Uyar A, Ahmed AK. Biomedical effects of Laurus nobilis L. leaf extract on vital organs in streptozotocin-induced diabetic rats: experimental research. Ann Med Surg 2020; 61: 188–97.


15.
Fotschki B, Juśkiewicz J, Jurgoński A, Sójka M. Fructo-oligosaccharides and pectins enhance beneficial effects of raspberry polyphenols in rats with nonalcoholic fatty liver. Nutrients 2021; 13(3): 833. doi: 10.3390/nu13030833


16.
Sellmann C, Priebs J, Landmann M, Degen C, Engstler AJ, Jin CJ, et al. Diets rich in fructose, fat or fructose and fat alter intestinal barrier function and lead to the development of nonalcoholic fatty liver disease over time. J Nutr Biochem 2015; 26: 183–92. doi: 10.1016/j.jnutbio.2015.05.011


17.
Choi EY, Choi JO, Park CY, Kim SH, Kim D. Water extract of Artemisia annua l. exhibits hepatoprotective effects through improvement of lipid accumulation and oxidative stress-induced cytotoxicity. J Med Food 2020; 23(12): 1312–22.


18.
Guo WL, Deng JC, Pan YY, Xu JX, Hong JL, Shi FF, et al. Hypoglycemic and hypolipidemic activities of Grifola frondosa polysaccharides and their relationships with the modulation of intestinal microflora in diabetic mice induced by high-fat diet and streptozotocin. Int J Biol Macromol 2020; 153: 1231–40. doi: 10.1016/j.ijbiomac.2019.10.253


19.
Kortgen A, Recknagel P, Bauer M. How to assess liver function? Curr Opin Crit Care 2016; 16(2): 136–41. doi: 10.1097/MCC.0b013e3283361813


20.
Gholam PM, Flancbaum L, Machan JT, Charney DA, Kotler DP. Nonalcoholic fatty liver disease in severely obese subjects. Am J Gastroenterol 2007; 102: 399–408. doi: 10.1111/j.1572-0241.2006.01041.x


21.
Schieber M, Chandel NS. ROS function in redox signaling and oxidative stress. Curr Biol 2014; 24(10): R453–62. doi: 10.1016/j.cub.2014.03.034


22.
Chance B, Sies H, Boveris A. Hydroperoxide metabolism in mammalian organs. Physiol Rev 1979; 59: 527–605. doi: 10.1152/physrev.1979.59.3.527


23.
Yoo D, Song Y, Cho E, Lee S, Park J, Yu J, et al. Alteration of APE1/ref-1 expression in non-small cell lung cancer: the implications of impaired extracellular superoxide dismutase and catalase antioxidant systems. Lung Cancer 2008; 60: 277–84. doi: 10.1016/j.lungcan.2007.10.015


24.
Sun SZ, Empie MW. Fructose metabolism in humans – what isotopic tracer studies tell us. Nutr Metab 2012; 9: 89. doi: 10.1186/1743-7075-9-89


25.
Leavens KF, Birnbaum MJ. Insulin signaling to hepatic lipid metabolism in health and disease. Crit Rev Biochem Mol Biol 2011; 46: 200–15. doi: 10.3109/10409238.2011.562481


26.
Hashimoto T, Cook WS, Qi C, Yeldandi AV, Reddy JK, Rao MS. Defect in peroxisome proliferator-activated receptor alpha-inducible fatty acid oxidation determines the severity of hepatic steatosis in response to fasting. J Biol Chem 2000; 275: 28918–28. doi: 10.1074/jbc.M910350199


27.
Havel RJ. Postprandial hyperlipidemia and remnant lipoproteins. Curr Opin Lipidol 1994; 5: 102–9. doi: 10.1097/00041433-199404000-00006


28.
Sanders FW, Grifn JL. De novo lipogenesis in the liver in health and disease: more than just a shunting yard for glucose. Biol Rev Camb Philos Soc 2016; 91: 452–68. doi: 10.1111/brv.12178


29.
Yamashita H, Takenoshita M, Sakurai M, Bruick RK, Henzel WJ, Shillinglaw W, et al. A glucose-responsive transcription factor that regulates carbohydrate metabolism in the liver. Proc Natl Acad Sci USA 2001; 98: 9116–21. doi: 10.1073/pnas.161284298


30.
Hellerstein MK. De novo lipogenesis in humans: metabolic and regulatory aspects. Eur J Clin Nutr 1999; 53: S53–65. doi: 10.1038/sj.ejcn.1600744


31.
Lambert JE, Ramos-Roman MA, Browning JD, Parks EJ. Increased de novo lipogenesis is a distinct characteristic of individuals with nonalcoholic fatty liver disease. Gastroenterology 2014; 146: 726–35. doi: 10.1053/j.gastro.2013.11.049


32.
Diraison F, Moulin P, Beylot M. Contribution of hepatic de novo lipogenesis and reesterification of plasma non esterified fatty acids to plasma triglyceride synthesis during non-alcoholic fatty liver disease. Diabetes Metab 2003; 29: 478–85. doi: 10.1016/S1262-3636(07)70061-7


33.
Oeckinghaus A, Ghosh S. The NF-kappaB family of transcription factors and its regulation. Cold Spring Harb Perspect Biol 2009; 1: a000034. doi: 10.1101/cshperspect.a000034


34.
Beinke S, Ley SC. Functions of NF-kappaB1 and NF-kappaB2 in immune cell biology. Biochem J 2004; 382: 393–409. doi: 10.1042/BJ20040544


35.
Tie F, Ding J, Hu N, Dong Q, Chen Z, Wang H. Kaempferol and kaempferide attenuate oleic acid-induced lipid accumulation and oxidative stress in HepG2 cells. Int J Mol Sci 2021; 22: 8847. doi: 10.3390/ijms22168847


36.
Shramko VS, Polonskaya YV, Kashtanova EV, Stakhneva EM, Ragino YI. The short overview on the relevance of fatty acids for human cardiovascular disorders. Biomolecules 2020; 10: 1127. doi: 10.3390/biom10081127


37.
Ameliushkina VA, Aripovskiĭ AV, Titov VN, Kaba SI, Kotkina TI, Parkhimovich RM. The fatty acids in blood plasma and erythrocytes in test of glucose tolerance. Klin Lab Diagn 2014; (4): 4–11.


38.
Qin G, Ma J, Huang Q, Yin H, Han J, Li M, et al. Isoquercetin im-proves hepatic lipid accumulation by activating AMPK pathway and suppressing TGF-beta signaling on an HFD-induced nonalcoholic fatty liver disease rat model. Int J Mol Sci 2018; 19: 4126. doi: 10.3390/ijms19124126


39.
Zhou J, Yoshitomi H, Liu T, Zhou B, Sun W, Qin L, et al. Isoquercitrin activates the AMP-activated protein kinase (AMPK) signal pathway in rat H4IIE cells. BMC Complement Altern Med 2014; 14: 42. doi: 10.1186/1472-6882-14-42


40.
Tig F, Ding J, Hu N, Dong Q, Chen Z, Wang H. Kaempferol and kampferide attenuated oleic acid-induced lipid accumulation and oxidative stress in HepG2 cells. Int J Mol Sci 2021; 22: 8847. doi: 10.3390/ijms22168847


41.
Weston CR, Davis RJ. The JNK signal transduction pathway. Curr Opin Cell Biol 2007; 19: 142–9. doi: 10.1016/j.ceb.2007.02.001


42.
Hua ZC, Sohn SJ, Kang C, Cado D, Winoto A. A function of Fas-associated death domain protein in cell cycle progression localized to a single amino acid at its C-terminal region. Immunity 2003; 18: 513–21. doi: 10.1016/S1074-7613(03)00083-9
Published
2025-04-24
How to Cite
Lee , M., Park , J., Kim , D., Park , S.-H., Jung , J., Jun , W., Kim , J., Baek , K.-S., Kim , O.-K., & Lee , J. (2025). Effect of water extract of bay laurel (<em>Laurus nobilis L.</em&gt;) on non-alcoholic fatty liver disease (NAFLD). Food & Nutrition Research, 69. https://doi.org/10.29219/fnr.v69.10668
Section
Original Articles