open access

Vol 73, No 4 (2022)
Original paper
Submitted: 2022-01-13
Accepted: 2022-01-18
Published online: 2022-06-10
Get Citation

Exploration of the main active components and pharmacological mechanism of Yerba Mate based on network pharmacology

Zhaodi Yue123, Hui Fu4, Huifen Ma, Huifen Ma, Li Li1, Ziyun Feng1, Yanyan Yin123, Fangqi Wang3, Bingyu Du123, Yibo Liu123, Renjie Zhao123, Mengfan Kan123, Helin Sun12, Zhongwen Zhang12, Shaohong Yu15
·
Pubmed: 36059165
·
Endokrynol Pol 2022;73(4):725-735.
Affiliations
  1. Department of Rehabilitation Medicine, Department of Endocrinology and Metabology, Shandong University of Traditional Chinese Medicine, The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, China
  2. Department of Endocrinology and Metabology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Key Laboratory of Rheumatic Disease and Translational medicine, Shandong Institute of Nephrology, Jinan, China
  3. College of Rehabilitation Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China
  4. Cheeloo College of Medicine, Shandong University, Jinan, China
  5. The Second Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, China

open access

Vol 73, No 4 (2022)
Original Paper
Submitted: 2022-01-13
Accepted: 2022-01-18
Published online: 2022-06-10

Abstract

Introduction: Yerba mate is widely consumed in South American countries and is gaining popularity around the world. Long-term consumption of yerba mate has been proven to have health-care functions and therapeutic effects on many diseases; however, its underlying mechanism has not been clearly elucidated. In this research, we explored the pharmacological mechanism of yerba mate through a network pharmacological approach.

Material and methods: The bioactive components of yerba mate were screened from published literature and the Traditional Chinese Medicine System Pharmacology Database (TCMSP), and the targets and related diseases were retrieved by TCMSP. Furthermore, the component-target-disease network an protein-protein interaction (PPI) network were constructed, and combined with gene ontology (GO) functional analysis and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment analysis to explore the pharmacological mechanism of yerba mate.

Results: As a result, 16 bioactive components of yerba mate were identified, which acted on 229 targets in total. Yerba mate can be used to treat 305 diseases, such as breast cancer, asthma, Alzheimer’s disease, osteoarthritis, diabetes mellitus, atherosclerosis, and obesity. Protein kinase B (AKT1), signal transducer and activator of transcription 3 (STAT3), mitogen-activated protein kinase 1 (MAPK1), transcription factor AP-1 (JUN), cellular tumour antigen (p53) TP53, tumour necrosis factor (TNF), transcription factor p65 (RELA), interleukin-6 (IL6), amyloid-beta precursor protein (APP), and vascular endothelial growth factor A (VEGFA) were identified as the key targets of yerba mate playing pharmacological roles. The signalling pathways identified by KEGG pathway enrichment analysis that were most closely related to the effects of yerba mate included pathways in cancer, fluid shear stress and atherosclerosis, and human cytomegalovirus infection.

Conclusion: the results of our study preliminarily verify the basic pharmacological action and possible mechanism of yerba mate and provide a reference for the further development of its medicinal value.

Abstract

Introduction: Yerba mate is widely consumed in South American countries and is gaining popularity around the world. Long-term consumption of yerba mate has been proven to have health-care functions and therapeutic effects on many diseases; however, its underlying mechanism has not been clearly elucidated. In this research, we explored the pharmacological mechanism of yerba mate through a network pharmacological approach.

Material and methods: The bioactive components of yerba mate were screened from published literature and the Traditional Chinese Medicine System Pharmacology Database (TCMSP), and the targets and related diseases were retrieved by TCMSP. Furthermore, the component-target-disease network an protein-protein interaction (PPI) network were constructed, and combined with gene ontology (GO) functional analysis and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment analysis to explore the pharmacological mechanism of yerba mate.

Results: As a result, 16 bioactive components of yerba mate were identified, which acted on 229 targets in total. Yerba mate can be used to treat 305 diseases, such as breast cancer, asthma, Alzheimer’s disease, osteoarthritis, diabetes mellitus, atherosclerosis, and obesity. Protein kinase B (AKT1), signal transducer and activator of transcription 3 (STAT3), mitogen-activated protein kinase 1 (MAPK1), transcription factor AP-1 (JUN), cellular tumour antigen (p53) TP53, tumour necrosis factor (TNF), transcription factor p65 (RELA), interleukin-6 (IL6), amyloid-beta precursor protein (APP), and vascular endothelial growth factor A (VEGFA) were identified as the key targets of yerba mate playing pharmacological roles. The signalling pathways identified by KEGG pathway enrichment analysis that were most closely related to the effects of yerba mate included pathways in cancer, fluid shear stress and atherosclerosis, and human cytomegalovirus infection.

Conclusion: the results of our study preliminarily verify the basic pharmacological action and possible mechanism of yerba mate and provide a reference for the further development of its medicinal value.

Get Citation

Keywords

yerba mate; pharmacological mechanism; biotargets; network pharmacology

Supp./Additional Files (1)
Supplementary File (List of abbreviations)
Download
130KB
About this article
Title

Exploration of the main active components and pharmacological mechanism of Yerba Mate based on network pharmacology

Journal

Endokrynologia Polska

Issue

Vol 73, No 4 (2022)

Article type

Original paper

Pages

725-735

Published online

2022-06-10

Page views

4930

Article views/downloads

1045

DOI

10.5603/EP.a2022.0026

Pubmed

36059165

Bibliographic record

Endokrynol Pol 2022;73(4):725-735.

Keywords

yerba mate
pharmacological mechanism
biotargets
network pharmacology

Authors

Zhaodi Yue
Hui Fu
Huifen Ma
Huifen Ma
Li Li
Ziyun Feng
Yanyan Yin
Fangqi Wang
Bingyu Du
Yibo Liu
Renjie Zhao
Mengfan Kan
Helin Sun
Zhongwen Zhang
Shaohong Yu

References (60)
  1. Zieliński A, Alberti A, Bina E, et al. A multivariate approach to differentiate yerba mate (Ilex paraguariensis) commercialized in the southern Brazil on the basis of phenolics, methylxanthines and in vitro antioxidant activity. Food Sci Technol. 2020; 40(3): 645–652.
  2. Lutomski P, Goździewska M, Florek-Łuszczki M. Health properties of Yerba Mate. Ann Agric Environ Med. 2020; 27(2): 310–313.
  3. Zapata F, Rebollo-Hernanz M, Novakofski J, et al. Caffeine, but not other phytochemicals, in mate tea (Ilex paraguariensis St. Hilaire) attenuates high-fat-high-sucrose-diet-driven lipogenesis and body fat accumulation. J Functional Foods. 2020; 64: 103646.
  4. Sarria B, Martinez-Lopez S, García-Cordero J, et al. Yerba mate may prevent diabetes according to a crossover, randomized, controlled study in humans. Proceed Nutrition Soc. 2020; 79(OCE2).
  5. Sarria B, Martinez-Lopez S, Garcia-Cordero J, et al. Yerba mate improves cardiovascular health in normocholesterolemic and hypercholesterolemic subjects. Proceed Nutrition Soc. 2020; 79(OCE2).
  6. Tate P, Marazita M, Marquioni-Ramella M, et al. Ilex paraguariensis extracts and its polyphenols prevent oxidative damage and senescence of human retinal pigment epithelium cells. Journal of Functional Foods. 2020; 67: 103833.
  7. Garcia-Lazaro RS, Lamdan H, Caligiuri LG, et al. In vitro and in vivo antitumor activity of Yerba Mate extract in colon cancer models. J Food Sci. 2020; 85(7): 2186–2197.
  8. Hopkins AL, Hopkins AL. Network pharmacology. Nat Biotechnol. 2007; 25(10): 1110–1111.
  9. Li R, Ma X, Song Y, et al. Anti-colorectal cancer targets of resveratrol and biological molecular mechanism: Analyses of network pharmacology, human and experimental data. J Cell Biochem. 2019 [Epub ahead of print].
  10. da Silveira TF, Meinhart AD, de Souza TC, et al. Phenolic compounds from yerba mate based beverages--A multivariate optimisation. Food Chem. 2016; 190: 1159–1167.
  11. Baeza G, Sarriá B, Bravo L, et al. Polyphenol content, in vitro bioaccessibility and antioxidant capacity of widely consumed beverages. J Sci Food Agric. 2018; 98(4): 1397–1406.
  12. Salvador JAR, Leal AS, Valdeira AS, et al. Oleanane-, ursane-, and quinone methide friedelane-type triterpenoid derivatives: Recent advances in cancer treatment. Eur J Med Chem. 2017; 142: 95–130.
  13. Guo JL, Han T, Bao Le, et al. Ursolic acid promotes the apoptosis of cervical cancer cells by regulating endoplasmic reticulum stress. J Obstet Gynaecol Res. 2019; 45(4): 877–881.
  14. Spivak A, Khalitova R, Nedopekina D, et al. Synthesis and Evaluation of Anticancer Activities of Novel C-28 Guanidine-Functionalized Triterpene Acid Derivatives. Molecules. 2018; 23(11).
  15. Naowaboot J, Chung CH, Choi R. Rutin Stimulates Adipocyte Differentiation and Adiponectin Secretion in 3T3-L1 Adipocytes. J Med Assoc Thai. 2015; 98 Suppl 3: S1–S6.
  16. Patel R, Mistry B, Shinde S, et al. Therapeutic potential of quercetin as a cardiovascular agent. Eur J Med Chem. 2018; 155: 889–904.
  17. Wang H, Chen L, Zhang X, et al. Kaempferol protects mice from d-GalN/LPS-induced acute liver failure by regulating the ER stress-Grp78-CHOP signaling pathway. Biomed Pharmacother. 2019; 111: 468–475.
  18. Han X, Liu CF, Gao Na, et al. Kaempferol suppresses proliferation but increases apoptosis and autophagy by up-regulating microRNA-340 in human lung cancer cells. Biomed Pharmacother. 2018; 108: 809–816.
  19. Ronco AL, Stefani EDe, Mendoza B, et al. Mate and Tea Intake, Dietary Antioxidants and Risk of Breast Cancer: a Case-Control Study. Asian Pac J Cancer Prev. 2016; 17(6): 2923–2933.
  20. DeChristopher LR, Tucker KL, DeChristopher LR, et al. Intakes of apple juice, fruit drinks and soda are associated with prevalent asthma in US children aged 2-9 years. Public Health Nutr. 2016; 19(1): 123–130.
  21. DeChristopher LR, Uribarri J, Tucker KL. Intake of high-fructose corn syrup sweetened soft drinks, fruit drinks and apple juice is associated with prevalent arthritis in US adults, aged 20-30 years. Nutr Diabetes. 2016; 6: e199.
  22. Zhang Z, Wu H, Huang S, et al. AMD3465 (hexahydrobromide) rescues the MG63 osteoblasts against the apoptosis induced by high glucose. Biomed Pharmacother. 2021; 138: 111476.
  23. Bains Y, Gugliucci A. Ilex paraguariensis and its main component chlorogenic acid inhibit fructose formation of advanced glycation endproducts with amino acids at conditions compatible with those in the digestive system. Fitoterapia. 2017; 117: 6–10.
  24. Rocha DS, Casagrande L, Model JF, et al. Effect of yerba mate (Ilex paraguariensis) extract on the metabolism of diabetic rats. Biomed Pharmacother. 2018; 105: 370–376.
  25. Choi MS, Park HJ, Kim SR, et al. Long-Term Dietary Supplementation with Yerba Mate Ameliorates Diet-Induced Obesity and Metabolic Disorders in Mice by Regulating Energy Expenditure and Lipid Metabolism. J Med Food. 2017; 20(12): 1168–1175.
  26. Wang S, Sarriá B, Mateos R, et al. TNF-α-induced oxidative stress and endothelial dysfunction in EA.hy926 cells is prevented by mate and green coffee extracts, 5-caffeoylquinic acid and its microbial metabolite, dihydrocaffeic acid. Int J Food Sci Nutr. 2019; 70(3): 267–284.
  27. Yue Z, Li Li, Fu H, et al. Effect of dapagliflozin on diabetic patients with cardiovascular disease via MAPK signalling pathway. J Cell Mol Med. 2021; 25(15): 7500–7512.
  28. Balsan G, Pellanda LC, Sausen G, et al. Effect of yerba mate and green tea on paraoxonase and leptin levels in patients affected by overweight or obesity and dyslipidemia: a randomized clinical trial. Nutr J. 2019; 18(1): 5.
  29. Balasuriya N, McKenna M, Liu X, et al. Phosphorylation-Dependent Inhibition of Akt1. Genes (Basel). 2018; 9(9).
  30. Riggio M, Perrone MC, Polo ML, et al. AKT1 and AKT2 isoforms play distinct roles during breast cancer progression through the regulation of specific downstream proteins. Sci Rep. 2017; 7: 44244.
  31. Zhou J, Sun M, Jin S, et al. Combined using of paclitaxel and salinomycin active targeting nanostructured lipid carriers against non-small cell lung cancer and cancer stem cells. Drug Deliv. 2019; 26(1): 281–289.
  32. Huan LeC, Phuong CV, Truc LeC, et al. (E)-N'-Arylidene-2-(4-oxoquinazolin-4(3H)-yl) acetohydrazides: Synthesis and evaluation of antitumor cytotoxicity and caspase activation activity. J Enzyme Inhib Med Chem. 2019; 34(1): 465–478.
  33. Vakili Saatloo M, Aghbali AA, Koohsoltani M, et al. Akt1 and Jak1 siRNA based silencing effects on the proliferation and apoptosis in head and neck squamous cell carcinoma. Gene. 2019; 714: 143997.
  34. Guanizo AC, Fernando CD, Garama DJ, et al. STAT3: a multifaceted oncoprotein. Growth Factors. 2018; 36(1-2): 1–14.
  35. Qin J, Shen X, Zhang J, et al. Allosteric inhibitors of the STAT3 signaling pathway. Eur J Med Chem. 2020; 190: 112122.
  36. Sun F, Zhang Y, Li Q. Therapeutic mechanisms of ibuprofen, prednisone and betamethasone in osteoarthritis. Mol Med Rep. 2017; 15(2): 981–987.
  37. Almeida-Oliveira AR, Aquino-Junior J, Abbasi A, et al. Effects of aerobic exercise on molecular aspects of asthma: involvement of SOCS-JAK-STAT. Exerc Immunol Rev. 2019; 25: 50–62.
  38. Saukkonen T, Mutt SJ, Jokelainen J, et al. Adipokines and inflammatory markers in elderly subjects with high risk of type 2 diabetes and cardiovascular disease. Sci Rep. 2018; 8(1): 12816.
  39. Sun X, Zhang H, Liu J, et al. Serum vascular endothelial growth factor level is elevated in patients with impaired glucose tolerance and type 2 diabetes mellitus. J Int Med Res. 2019; 47(11): 5584–5592.
  40. Mazidi M, Rezaie P, Kengne AP, et al. VEGF, the underlying factor for metabolic syndrome; fact or fiction? Diabetes Metab Syndr. 2017; 11 Suppl 1: S61–S64.
  41. Escobedo N, Oliver G. The Lymphatic Vasculature: Its Role in Adipose Metabolism and Obesity. Cell Metab. 2017; 26(4): 598–609.
  42. Kaess BM, Preis SR, Beiser A, et al. Circulating vascular endothelial growth factor and the risk of cardiovascular events. Heart. 2016; 102(23): 1898–1901.
  43. Yang H, Zhang X, Cai XY, et al. From big data to diagnosis and prognosis: gene expression signatures in liver hepatocellular carcinoma. PeerJ. 2017; 5: e3089.
  44. Wang Q, Lin F, He Qi, et al. Assessment of the Effects of Bisphenol A on Dopamine Synthesis and Blood Vessels in the Goldfish Brain. Int J Mol Sci. 2019; 20(24).
  45. Nauclér CS, Geisler J, Vetvik K. The emerging role of human cytomegalovirus infection in human carcinogenesis: a review of current evidence and potential therapeutic implications. Oncotarget. 2019; 10(42): 4333–4347.
  46. Bai B, Wang X, Chen E, et al. Human cytomegalovirus infection and colorectal cancer risk: a meta-analysis. Oncotarget. 2016; 7(47): 76735–76742.
  47. Du Yu, Zhang G, Liu Z. Human cytomegalovirus infection and coronary heart disease: a systematic review. Virol J. 2018; 15(1): 31.
  48. Li D, Li Bo, Yang L, et al. Human cytomegalovirus infection is correlated with atherosclerotic plaque vulnerability in carotid artery. J Gene Med. 2020; 22(10): e3236.
  49. Lebedeva AM, Shpektor AV, Vasilieva EYu, et al. Cytomegalovirus Infection in Cardiovascular Diseases. Biochemistry (Mosc). 2018; 83(12): 1437–1447.
  50. Ru J, Li P, Wang J, et al. TCMSP: a database of systems pharmacology for drug discovery from herbal medicines. J Cheminform. 2014; 6: 13.
  51. Feng W, Ao H, Yue S, et al. Systems pharmacology reveals the unique mechanism features of Shenzhu Capsule for treatment of ulcerative colitis in comparison with synthetic drugs. Sci Rep. 2018; 8(1): 16160.
  52. Bao H, Guo H, Feng Z, et al. Deciphering the underlying mechanism of Xianlinggubao capsule against osteoporosis by network pharmacology. BMC Complement Med Ther. 2020; 20(1): 208.
  53. Chen J, Chen Y, Shu A, et al. Radix Rehmanniae and Corni Fructus against Diabetic Nephropathy via AGE-RAGE Signaling Pathway. J Diabetes Res. 2020; 2020: 8358102.
  54. UniProt Consortium. UniProt: a worldwide hub of protein knowledge. Nucleic Acids Res. 2019; 47(D1): D506–D515.
  55. Wishart D, Feunang Y, Guo A, et al. DrugBank 5.0: a major update to the DrugBank database for 2018. Nucleic Acids Res. 2017; 46(D1): D1074–D1082.
  56. Szklarczyk D, Gable AL, Lyon D, et al. STRING v11: protein-protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets. Nucleic Acids Res. 2019; 47(D1): D607–D613.
  57. Zhou Y, Zhou B, Pache L, et al. Metascape provides a biologist-oriented resource for the analysis of systems-level datasets. Nat Commun. 2019; 10(1): 1523.
  58. Shannon P, Markiel A, Ozier O, et al. Cytoscape: a software environment for integrated models of biomolecular interaction networks. Genome Res. 2003; 13(11): 2498–2504.
  59. Missiuro PV, Liu K, Zou L, et al. Information flow analysis of interactome networks. PLoS Comput Biol. 2009; 5(4): e1000350.
  60. Zhang Y, Li X, Guo C, et al. Mechanisms of Spica Prunellae against thyroid-associated Ophthalmopathy based on network pharmacology and molecular docking. BMC Complement Med Ther. 2020; 20(1): 229.

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

Via MedicaWydawcą jest  VM Media Group sp. z o.o., Grupa Via Medica, ul. Świętokrzyska 73, 80–180 Gdańsk

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl