Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 -- 2721 2024-02-23 11:25:15 |
2 references update and layout + 5 word(s) 2726 2024-02-27 06:41:27 |

Video Upload Options

Do you have a full video?


Are you sure to Delete?
If you have any further questions, please contact Encyclopedia Editorial Office.
Bartel, I.; Mandryk, I.; Horbańczuk, J.O.; Wierzbicka, A.; Koszarska, M. Nutraceutical Properties of Syringic Acid in Civilization Diseases. Encyclopedia. Available online: (accessed on 16 April 2024).
Bartel I, Mandryk I, Horbańczuk JO, Wierzbicka A, Koszarska M. Nutraceutical Properties of Syringic Acid in Civilization Diseases. Encyclopedia. Available at: Accessed April 16, 2024.
Bartel, Iga, Izabela Mandryk, Jarosław O. Horbańczuk, Agnieszka Wierzbicka, Magdalena Koszarska. "Nutraceutical Properties of Syringic Acid in Civilization Diseases" Encyclopedia, (accessed April 16, 2024).
Bartel, I., Mandryk, I., Horbańczuk, J.O., Wierzbicka, A., & Koszarska, M. (2024, February 23). Nutraceutical Properties of Syringic Acid in Civilization Diseases. In Encyclopedia.
Bartel, Iga, et al. "Nutraceutical Properties of Syringic Acid in Civilization Diseases." Encyclopedia. Web. 23 February, 2024.
Nutraceutical Properties of Syringic Acid in Civilization Diseases

Civilization diseases account for a worldwide health issue. They result from daily behavioral, environmental, and genetic factors. One of the most significant opportunities to prevent and alleviate the occurrence of these diseases is a diet rich in antioxidants like polyphenols. Providing bioactive compounds may exert a favorable effect on preventing the risk of civilization diseases. The prominent groups of bioactive compounds are phenolic acids, which belong to polyphenols that are widely distributed in plants. Phenolic acids are found in fruits, vegetables, whole grain products, and beverages such as green and black tea and coffee. One crucial example of phenolic acids is syringic acid (SA).

syringic acid civilization diseases phenolic acid

1. Introduction

In past years, knowledge of nutrigenomics research has significantly advanced. Due to the development of this scientific field, it is more effortless to understand the nutritional influence on human health. On the other hand, this development provides a great chance to prevent and support the treatment of many diseases, especially diet-related diseases such as diabetes type 2, cardiovascular diseases (CVDs), and obesity [1]. These diseases, representing civilization diseases (also referred to as “lifestyle diseases” or “non-communicable diseases”), account for a global health problem. Many of them could be eliminated by maintaining proper daily behavior linked to a balanced diet. Providing bioactive compounds may exert a favorable effect on preventing the risk of civilization diseases. The prominent groups of bioactive compounds are phenolic acids, which belong to polyphenols that are widely distributed in plants. Phenolic acids are found in fruits, vegetables, whole grain products, and beverages such as green and black tea and coffee. One crucial example of phenolic acids is syringic acid (SA). 

2. Syringic Acid (SA)

SA belongs to the hydroxybenzoic acids subgroup. SA’s chemical structure comprises one benzene ring containing two methoxy (-OCH3) groups, one hydroxyl (-OH) group, and one carboxyl (-COOH) group. Furthermore, the presence of these methoxy groups at positions 3 and 5 on the benzene ring may contribute to its favorable biological properties. In turn, the hydroxyl group has influence on radical-scavenging activities [2]. Secondary metabolites, including SA, are formed via the shikimate pathway, which occurs in higher plants and microorganisms, but not in animals [3]. The main purpose of the shikimate pathway is to produce precursors essential for aromatic molecules, which are base substrates for both protein biosynthesis and the formation of polyphenolic compounds in plants [4]. In phenolic metabolism, many enzymes are involved, and the main metabolite is shikimic acid. This process is composed of seven stages, starting with an aldol-type condensation of phosphoenolpyruvic acid (PEP), derived from the glycolytic pathway, and D-erythrose-4-phosphate, sourced from the pentose phosphate cycle. The outcome is the formation of 3-deoxy-D-arabino-heptulosonic acid 7-phosphate (DAHP). Chorismic acid, the end product of this process, is a pivotal compound marking the culmination of the shikimate pathway. It serves as a crucial junction leading to post-chorismic acid pathways, facilitating the synthesis of L-phenylalanine, L-Tyrosine, and L-Tryptophan [5]. Phenylalanine plays a crucial role in the biosynthesis of SA, acting as a key compound for the conversion to hydroxycinnamic acids, including p-coumaric acid, CA, or FA. Further, the transformation into derivatives of hydroxybenzoic acids takes place via enzymatic β-oxidation reactions [6]. Many studies were conducted to demonstrate the various pharmacological impact of SA, but the safety and toxicity mechanism is still not confirmed in the literature [7]. A daily intake of 1–2 g of polyphenols is related to prevention of chronic illnesses [8], while phenolic acids should account for approximately 200 mg/d [9]. According to the available literature reports, the daily intake of phenolic acids is different in numerous countries, as follows: in Germany, the average is 222 mg [10]; in Finland, the average is 641 mg [11]; in France, the average is 599 mg [12]; and in Brazil, the average is 729.5 mg [13]. Similar differences are observed when it comes to the consumption of SA within Europe. The average expressed in mg/d is as follows: in the southern region, it is 3.427 ± 0.065; in the central region, it is 1.815 ± 0.062; and in the northern region, it is 2.118 ± 0.064 [14].
SA’s high content has been identified in many products such as olives (Olea Europea), pumpkins (Cucurbita), grapes (Vitis vinifera L.), blueberries (Vaccinium myrtilus), date palms (Phoenix dactylifera L.), walnuts (Corylus avellana L.), chard (Beta vulgaris var. vulgaris), acai palms (Euterpe oleracea), red wine, floral honey, and a number of other plants [6]
SA has multiple biomedical effects, including antioxidant, anti-inflammation, anticancer, anti-microbial, anti-diabetic, and hepatoprotective activities [15][16][17][18]. Moreover, it is a valuable compound in the industrial sector, due to being a part of the lignin, which is a plant cell wall component. SA seems to be a crucial substrate for the fungal laccase enzyme, demonstrating significant importance in bioremediation and in the pulp industry [19]. Due to its reducing properties, SA is useful as a dental-resin component in stomatology [20]. Natural derivatives of SA such as syringol, syringin, sinapine, canolol, and syringaldehyde are widespread in the plant kingdom. For example, syringaldehyde, a component of grapes and red wines stored in wooden barrels, is also found in wood smoke [21]. Baker et al., in their study, confirmed that acetosyringone, along with potentially other extracellular phenolics, may exhibit bioactive properties capable of impacting the interplay between plants and bacterial pathogenesis [22]. Another study, conducted by Zhou et al., revealed that SA contributed to the interaction between plants and soil microorganisms. SA hindered cucumber growth and modified rhizosphere microbial communities [23]. SA also demonstrated its photocatalytic ozonation activity under various operating conditions, with titanium dioxide as a photocatalyst [24]. SA is soluble in alcohols and ethers such as methanol, ethanol, and ethyl ether. In turn, solubility in water is relatively low. Although SA has strong antioxidant properties, in vivo studies have shown that its bioavailability is insufficient to achieve beneficial effects [25]. Hence, researchers are still seeking ways to increase its bioavailability, and among the promising carrier systems are liposomes, mainly nanoliposomes, which are modified using functional material [26]. Various techniques associated with nanoformulation have been researched, including cyclodextrin inclusion [27] and micelles [28].

3. Cardioprotective Effects of Syringic Acid

Diabetic cardiomyopathy (DC) has emerged as a significant complication in individuals with diabetes. Sabahi et al. investigated the protective impact of SA on diabetes-induced cardiac injury in a rat model. Treatment with SA exhibited protective effects against diabetic cardiomyopathy by diminishing lipid peroxidation and protein carbonylation. These effects may be attributed to the antioxidant properties of this phenolic acid [29]. SA also demonstrated anti-hypertensive effects induced by N-nitro-L-arginine methyl ester (L-NAME) [30]. There is clear evidence that SA treatment may lower blood pressure and decrease lipid peroxides, while increasing NO availability and antioxidant levels in blood samples from rats [30]. Previous research evaluated the mechanism through which dietary quercetin (Q) might mitigate cardiac hypertrophy in the context of a fixed aortic constriction. A Q diet (including SA as a phenolic compound) reduced blood pressure and protected against damage in hypertensive rats [31]. SA was shown to reduce heart weight, fibrosis, and pathological cardiac remodeling in isoproterenol-treated mice. The same study demonstrated that SA downregulated Fn1 and collagen accumulation, but reduced the upregulation of Ereg, Myc and Ngfr. In isoproterenol-treated cells, SA lowers the upregulation of Fn1 and Nppb and also lowers cell size. This study confirmed the potential of SA as a beneficial agent in the treatment of cardiac hypertrophy and fibrosis [32]. Another study proved the cardio-protective effect of SA and resveratrol (RV) combined together, in rats, with isoproterenol (ISO)-induced cardio-toxicity. SA–RV pre-treatment significantly decreased serum CK-MB, LDH, and alkaline phosphatase, in contrast to cardiac tissue CK-MB, LDH, and SOD, CAT, the levels of which were increased by SA–RV pre-treatment. SA–RV together decreased levels of total cholesterol, triglycerides, low density lipoprotein cholesterol, very low-density lipoprotein cholesterol, and thiobarbutyric acid reactive substances and raised the level of density lipoprotein cholesterol in serum and in the heart. As well, the levels of NF-κB and TNF-α were significantly lowered by SA–RV [33].
All the above-described studies confirmed the cardioprotective properties of SA and showed the possibility of using it as a valuable agent in the fight against CVDs.

4. Anti-Cancer Properties of Syringic Acid

Phytochemicals found in plants present innovative possibilities as potent drug agents in cancer therapy, owing to their lower toxicity and enhanced tolerance rates. Mihanfar et al. evaluated the effects of SA in vitro on human colorectal cancer cells (SW-480) and in vivo on colorectal cancer-induced rats. The in vitro study showed that SA treatment resulted in the inhibition of cellular proliferation, the induction of apoptosis through increasing cellular ROS and DNA damage levels, and the downregulation of major proliferative genes. In vivo observations, on the other hand, revealed a statistically significant decrease in both tumor volume and incidence when compared to the control group [18]. Velu et al. presented the mechanism of SA, extracted from Alpinia calcarata Roscoe, which mediated chemoprevention on 7,12-dimethylbenz(a)anthracene (DMBA)-induced hamster buccal pouch carcinogenesis (HBPC). The result of the study was the inhibition of the adverse changes in biochemical parameters of plasma and buccal mucosal tissues and also the downregulation of molecular markers expression (PCNA, Cyclin D1, and mutant p53) [34]. SA was also investigated in terms of cytotoxicity, oxidative stress, mitochondrial membrane potential, apoptosis, and inflammatory responses in gastric cancer cell culture (AGS). In that study, SA demonstrated anti-cancer activities by losing MMP, cell viability, and enhancing intracellular ROS. SA induced apoptosis in a selective, dose-dependent fashion by upregulating caspase-3, caspase-9, and poly ADP-ribose polymerase (PARP), while simultaneously downregulating the expression levels of p53 and BCL-2, lowering SOD, CAT, and GPx activities, suppressing gastric cancer cell proliferation and inflammation, and inducing apoptosis by upregulating mTOR via the AKT signaling pathway [35]. Lavanya et al. investigated the therapeutic benefits of SA on Wistar rats with induced hepatocellular carcinoma. Serum samples were employed to assess the levels of liver markers, while liver tissue samples were utilized for histopathological analysis and the evaluation of apoptotic and anti-apoptotic protein expression. It was shown that SA exhibited a protective effect against diethylnitrosamine (DEN)-induced hepatocellular carcinoma by reducing the serum liver marker levels and raising the expression of apoptotic proteins [36].

5. Anti-Diabetic Effects of Syringic Acid

Type 2 diabetes (T2D) encompasses over 90% of all diabetes cases. T2D leads to many micro- and macrovascular complications, resulting in psychological distress for patients [37]. Many in vivo studies have demonstrated that SA has anti-diabetic properties in diabetic animals [38], and have also revealed that a group treated with SA exhibited better kidney histopathological outcomes compared to the diabetic group [39]. Moreover, Muthukumaran et al. induced T2D in Wistar rats by a single intraperitoneal injection of alloxan. The experimental group received SA orally for 30 days. Plasma glucose levels exhibited a notable decrease alongside a significant increase in plasma insulin and C-peptide levels; in addition, the aberrant levels of plasma and tissue glycoprotein components were restored to a state closely resembling normal [38]. Further studies on Wistar rats, in which T2D was also induced by the administration of alloxan, proved that SA restores the perturbed levels of carbohydrate metabolic enzymes, hepatic enzymes, and renal marker enzymes back to normal levels [40]. Another research group studied the effects of SA on renal, cardiac, hepatic, and neuronal diabetic complications in streptozotocin-induced neonatal (nSTZ) rats [41]. Treatment with SA decreased hyperglycemia, as well as the symptoms of polydipsia, polyphagia, and polyuria. Additionally, it reduced relative organ weight, cardiac hypertrophic indices, inflammatory markers, cell injury markers, glycated hemoglobin levels, histopathological scores, and oxidative stress. Furthermore, SA treatment increased Na/K ATPase activity [41]. Wei et al. showed that SA derived from the orchid Herba dendrobii is effective in inhibiting the progression of diabetic cataracts in both in vivo and in vitro rat models. SA has the capacity to downregulate the expression of AR and lens structural proteins at the mRNA level [42]. SA has been also shown, in in vitro conditions, to bind with the serum albumin and to prevent glycation-associated complications [43]. Using molecular modeling and mass spectrometric studies, the authors proved that Lys 93,261,232, Arg 194 and Lys 93, Arg 194 are the responsible binding residues for SA [43]. Wu et al. orally administered rats with lotus seedpod oligomeric procyanidins (LSOPCs) and further investigated the anti-glycative activity of LSOPC itself as well as that of its metabolites. SA was one of the metabolites detected in rat’s urine. These urinary metabolites exhibited antioxidant, anti-glycation, and carbonyl-scavenging properties [44]. All these results suggest that SA provides beneficial health effects in T2D treatment.

6. Anti-Inflammatory Effects of Syringic Acid

The intricate processes of inflammation are orchestrated by an array of signaling molecules synthetized by immune cells such as leukocytes, macrophages, and mast cells [45]. It has been proven that SA exhibits anti-inflammatory, anti-obesity, and anti-steatotic properties [46]. Lee et al. studied isolated mouse peritoneal macrophages exposed to IFN-γ and LPS in vitro, with or without the presence of Taraxacum coreanum (TCC). Its chloroform fraction (SA and gallic acid (GA)) was employed for its anti-inflammatory properties [47]. In contrast to microphages without TCC treatment, macrophages treated with TCC in vitro exhibited significantly better inflammatory activation parameters, including the levels of iNOS, COX-2, IL-6, and TNF-α, and increased survival by 83% [47]. Another study presented by Costa et al. checked the anti-inflammatory properties of phenolic chemical compositions of Eugenia aurata and Eugenia punicifolia. Those extracts include SA. As a result of ex vivo and in vivo trials, both extracts were observed to hinder neutrophil migration, suppress cell adhesion, and mitigate the degranulation processes [48][49]. Ham et al. used mice as an animal model to examine the effects of SA on obese diet-induced hepatic dysfunction. Obesity in mice was induced by supplementation with HFD over 16 weeks. In the experimental group fed with SA, the body weight was lower, and visceral fat mass, serum levels of leptin, TNF-α, IFN-γ, IL-6 and MCP-1, insulin resistance, hepatic lipid content, droplets, and early fibrosis were reduced. The circulation level of adiponectin was higher when compared to the control group. SA also downregulated lipogenic genes and inflammatory genes, but upregulated fatty acid oxidation genes in the liver [50]. Another study using rats with carrageenan induced paw oedema showed the anti-inflammatory properties of SA, as a component of Hygrophila spinosa leaf extract [51]. The in vitro, biophysical, and in silico studies conducted by Dileep et al. examined the inhibitory potential of specific benzoic acid derivatives, including SA, against secretory phospholipase A2 (sPLA2), a key enzyme within the inflammatory pathway. They unveiled a consistent binding mode within the active site of sPLA2 and exhibited inhibitory effects at micromolar concentrations [52]. These studies suggested that SA has a number of favorable anti-inflammatory applications.

7. Hepatoprotective Effects of Syringic Acid

Hepatic disorders, acute and chronic, may result from various causes such as alcohol consumption (ALD: alcohol-induced liver disease; AFLD: alcoholic fatty liver disease) [53][54], obesity, metabolic syndrome (NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatotic hepatitis) [55][56], high doses of drugs (DILI: drug-induced liver injury) [57][58], and autoimmune diseases (autoimmune hepatitis) [59]. In studies using animal models, SA has shown anti-inflammatory, anti-oxidative, and anti-pathogenic activities [6][16][32][60]. Using a mice animal model, Itoh induced chronic liver injury by injecting CCl(4) and concanavalin (ConA). This caused an increase in ALT and AST levels and also excessive deposition of collagen fibrils. Furthermore, the TNF-α, IFN-γ, and IL-6 in the bloodstream exhibited a swift increase [16][32]. At the next stage of the study, mice were administered SA intravenously. An analysis of liver sections demonstrated that SA effectively reduced collagen accumulation, markedly lowered the hepatic hydroxyproline content, and notably suppressed the cytokine levels [16][32]. Another study was performed by Ramachandran et al., in which the authors used rats as an animal model for hepatoxicity. Hepatoxicity was induced by the intraperitoneal administration of acetaminophen (APAP). Next, the rats were supplemented with SA by an oral route. The administered SA markedly reduced the levels of hepatic and renal function markers upregulated by APAP, bringing them closer to normal values [60]. In turn, the effect of SA on thioacetamide-induced hepatic encephalopathy was investigated by Okkey et al. In rats treated with SA inflammatory markers, levels were restored to normal. In addition, reduced oxidative stress and ammonia were observed. SA generally reduced inflammatory injury. The structures of astrocytes and hepatocytes were preserved in rats treated with SA. SA was also shown to restore behavioral impairments [33]. A recent study conducted by Somade et al. examined the effect of SA against methyl cellosolve (MECE)-induced hepatotoxicity in rats. Treatment with SA significantly reduced the levels of cytosolic Nrf2, known to be a nuclear transcription factor playing an important role in cellular defense against oxidative stress. It also stimulated the activities of the endogenous antioxidant enzymes [61].These findings, taken together, indicate that SA offers substantial protective effects against liver injuries.


  1. Loos, R.J. From Nutrigenomics to Personalizing Diets: Are We Ready for Precision Medicine? Am. J. Clin. Nutr. 2019, 109, 1–2.
  2. Vo, Q.V.; Bay, M.V.; Nam, P.C.; Quang, D.T.; Flavel, M.; Hoa, N.T.; Mechler, A. Theoretical and Experimental Studies of the Antioxidant and Antinitrosant Activity of Syringic Acid. J. Org. Chem. 2020, 85, 15514–15520.
  3. Mittelstädt, G.; Negron, L.; Schofield, L.R.; Marsh, K.; Parker, E.J. Biochemical and Structural Characterisation of Dehydroquinate Synthase from the New Zealand Kiwifruit Actinidia Chinensis. Arch. Biochem. Biophys. 2013, 537, 185–191.
  4. Tzin, V.; Galili, G. New Insights into the Shikimate and Aromatic Amino Acids Biosynthesis Pathways in Plants. Mol. Plant 2010, 3, 956–972.
  5. Santos Sánchez, N.; Salas-Coronado, R.; Hernández-Carlos, B.; Villanueva, C. Shikimic Acid Pathway in Biosynthesis of Phenolic Compounds. In Plant Physiological Aspects of Phenolic Compounds; IntechOpen: London, UK, 2019; ISBN 978-1-78984-033-9.
  6. Srinivasulu, C.; Ramgopal, M.; Ramanjaneyulu, G.; Anuradha, C.M.; Suresh Kumar, C. Syringic Acid (SA)−A Review of Its Occurrence, Biosynthesis, Pharmacological and Industrial Importance. Biomed. Pharmacother. 2018, 108, 547–557.
  7. Mirza, A.C.; Panchal, S.S. Safety Evaluation of Syringic Acid: Subacute Oral Toxicity Studies in Wistar Rats. Heliyon 2019, 5, e02129.
  8. Kapolou, A.; Karantonis, H.C.; Rigopoulos, N.; Koutelidakis, A.E. Association of Mean Daily Polyphenols Intake with Mediterranean Diet Adherence and Anthropometric Indices in Healthy Greek Adults: A Retrospective Study. Appl. Sci. 2021, 11, 4664.
  9. Kumar, N.; Goel, N. Phenolic Acids: Natural Versatile Molecules with Promising Therapeutic Applications. Biotechnol. Rep. 2019, 24, e00370.
  10. Radtke, J.; Linseisen, J.; Wolfram, G. Phenolic acid intake of adults in a Bavarian subgroup of the national food consumption survey. Z. Ernahrungswiss. 1998, 37, 190–197.
  11. Ovaskainen, M.-L.; Törrönen, R.; Koponen, J.M.; Sinkko, H.; Hellström, J.; Reinivuo, H.; Mattila, P. Dietary Intake and Major Food Sources of Polyphenols in Finnish Adults. J. Nutr. 2008, 138, 562–566.
  12. Pérez-Jiménez, J.; Fezeu, L.; Touvier, M.; Arnault, N.; Manach, C.; Hercberg, S.; Galan, P.; Scalbert, A. Dietary Intake of 337 Polyphenols in French Adults. Am. J. Clin. Nutr. 2011, 93, 1220–1228.
  13. Nascimento-Souza, M.A.; de Paiva, P.G.; Pérez-Jiménez, J.; do Carmo Castro Franceschini, S.; Ribeiro, A.Q. Estimated Dietary Intake and Major Food Sources of Polyphenols in Elderly of Viçosa, Brazil: A Population-Based Study. Eur. J. Nutr. 2018, 57, 617–627.
  14. Zamora-Ros, R.; Rothwell, J.A.; Scalbert, A.; Knaze, V.; Romieu, I.; Slimani, N.; Fagherazzi, G.; Perquier, F.; Touillaud, M.; Molina-Montes, E.; et al. Dietary Intakes and Food Sources of Phenolic Acids in the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Br. J. Nutr. 2013, 110, 1500–1511.
  15. Cikman, O.; Soylemez, O.; Ozkan, O.F.; Kiraz, H.A.; Sayar, I.; Ademoglu, S.; Taysi, S.; Karaayvaz, M. Antioxidant Activity of Syringic Acid Prevents Oxidative Stress in L-Arginine-Induced Acute Pancreatitis: An Experimental Study on Rats. Int. Surg. 2015, 100, 891–896.
  16. Itoh, A.; Isoda, K.; Kondoh, M.; Kawase, M.; Watari, A.; Kobayashi, M.; Tamesada, M.; Yagi, K. Hepatoprotective Effect of Syringic Acid and Vanillic Acid on CCl4-Induced Liver Injury. Biol. Pharm. Bull. 2010, 33, 983–987.
  17. Li, Y.; Zhang, L.; Wang, X.; Wu, W.; Qin, R. Effect of Syringic Acid on Antioxidant Biomarkers and Associated Inflammatory Markers in Mice Model of Asthma. Drug Dev. Res. 2019, 80, 253–261.
  18. Mihanfar, A.; Darband, S.G.; Sadighparvar, S.; Kaviani, M.; Mirza-Aghazadeh-Attari, M.; Yousefi, B.; Majidinia, M. In Vitro and in Vivo Anticancer Effects of Syringic Acid on Colorectal Cancer: Possible Mechanistic View. Chem.-Biol. Interact. 2021, 337, 109337.
  19. Mishra, V.; Jana, A.K.; Jana, M.M.; Gupta, A. Improvement of Selective Lignin Degradation in Fungal Pretreatment of Sweet Sorghum Bagasse Using Synergistic CuSO4-Syringic Acid Supplements. J. Environ. Manag. 2017, 193, 558–566.
  20. Brauer, G.M.; Stansbury, J.W. Materials Science Cements Containing Syringic Acid Esters- o-Ethoxybenzoic Acid and Zinc Oxide. J. Dent. Res. 1984, 63, 137–140.
  21. Bortolomeazzi, R.; Sebastianutto, N.; Toniolo, R.; Pizzariello, A. Comparative Evaluation of the Antioxidant Capacity of Smoke Flavouring Phenols by Crocin Bleaching Inhibition, DPPH Radical Scavenging and Oxidation Potential. Food Chem. 2007, 100, 1481–1489.
  22. Baker, C.J.; Mock, N.M.; Whitaker, B.D.; Roberts, D.P.; Rice, C.P.; Deahl, K.L.; Aver’yanov, A.A. Involvement of Acetosyringone in Plant–Pathogen Recognition. Biochem. Biophys. Res. Commun. 2005, 328, 130–136.
  23. Zhou, X.; Wu, F.; Xiang, W.S. Syringic Acid Inhibited Cucumber Seedling Growth and Changed Rhizosphere Microbial Communities. Plant Soil Environ. 2014, 60, 158–164.
  24. Gimeno, O.; Fernandez, L.A.; Carbajo, M.; Beltran, F.; Rivas, J. Photocatalytic Ozonation of Phenolic Wastewaters: Syringic Acid, Tyrosol and Gallic Acid. J. Environ. Sci. Health Part A 2008, 43, 61–69.
  25. Zhou, W.; Zhang, Y.; Ning, S.; Li, Y.; Ye, M.; Yu, Y.; Duan, G. Automated On-Line SPE/Multi-Stage Column-Switching and Benzoic Acid-Based QAMS/RODWs-HPLC for Oral Pharmacokinetics of Syringic Acid and Salicylic Acid in Rats. Chromatographia 2012, 75, 883–892.
  26. Liu, L.; Zhao, X.; Liu, Y.; Zhao, H.; Li, F. Dietary Addition of Garlic Straw Improved the Intestinal Barrier in Rabbits1. J. Anim. Sci. 2019, 97, 4248–4255.
  27. Kfoury, M.; Lounès-Hadj Sahraoui, A.; Bourdon, N.; Laruelle, F.; Fontaine, J.; Auezova, L.; Greige-Gerges, H.; Fourmentin, S. Solubility, Photostability and Antifungal Activity of Phenylpropanoids Encapsulated in Cyclodextrins. Food Chem. 2016, 196, 518–525.
  28. Yu, J.; Zhu, Y.; Wang, L.; Peng, M.; Tong, S.; Cao, X.; Qiu, H.; Xu, X. Enhancement of Oral Bioavailability of the Poorly Water-Soluble Drug Silybin by Sodium Cholate/Phospholipid-Mixed Micelles. Acta Pharmacol. Sin. 2010, 31, 759–764.
  29. Sabahi, Z.; Khoshnoud, M.J.; Hosseini, S.; Khoshraftar, F.; Rashedinia, M. Syringic Acid Attenuates Cardiomyopathy in Streptozotocin-Induced Diabetic Rats. Adv. Pharmacol. Pharm. Sci. 2021, 2021, 5018092.
  30. Kumar, S.; Prahalathan, P.; Raja, B. Syringic Acid Ameliorates L-NAME-Induced Hypertension by Reducing Oxidative Stress. Naunyn-Schmiedeberg’s Arch. Pharmacol. 2012, 385, 1175–1184.
  31. Jalili, T.; Carlstrom, J.; Kim, S.; Freeman, D.; Jin, H.; Wu, T.-C.; Litwin, S.; Symons, J. Quercetin-Supplemented Diets Lower Blood Pressure and Attenuate Cardiac Hypertrophy in Rats With Aortic Constriction. J. Cardiovasc. Pharmacol. 2006, 47, 531–541.
  32. Itoh, A.; Isoda, K.; Kondoh, M.; Kawase, M.; Kobayashi, M.; Tamesada, M.; Yagi, K. Hepatoprotective Effect of Syringic Acid and Vanillic Acid on Concanavalin A-Induced Liver Injury. Biol. Pharm. Bull. 2009, 32, 1215–1219.
  33. Ferah Okkay, I.; Okkay, U.; Gundogdu, O.L.; Bayram, C.; Mendil, A.S.; Ertugrul, M.S.; Hacimuftuoglu, A. Syringic Acid Protects against Thioacetamide-Induced Hepatic Encephalopathy: Behavioral, Biochemical, and Molecular Evidence. Neurosci. Lett. 2022, 769, 136385.
  34. Velu, P.; Vinothkumar, V.; Babukumar, S.; Ramachandhiran, D. Chemopreventive Effect of Syringic Acid on 7,12-Dimethylbenz(a)Anthracene Induced Hamster Buccal Pouch Carcinogenesis. Toxicol. Mech. Methods 2017, 27, 631–640.
  35. Pei, J.; Velu, P.; Zareian, M.; Feng, Z.; Vijayalakshmi, A. Effects of Syringic Acid on Apoptosis, Inflammation, and AKT/mTOR Signaling Pathway in Gastric Cancer Cells. Front. Nutr. 2021, 8, 788929.
  36. Lavanya, M.; Srinivasan, P.; Padmini, R. Unveiling the Anticancer Effect of Syringic Acid and Its Derivatives in Hepatocellular Carcinoma. Int. J. App. Pharm. 2023, 15, 114–124.
  37. Yeung, A.W.K.; Tzvetkov, N.T.; Durazzo, A.; Lucarini, M.; Souto, E.B.; Santini, A.; Gan, R.-Y.; Jozwik, A.; Grzybek, W.; Horbańczuk, J.O.; et al. Natural Products in Diabetes Research: Quantitative Literature Analysis. Nat. Prod. Res. 2021, 35, 5813–5827.
  38. Muthukumaran, J.; Srinivasan, S.; Venkatesan, R.S.; Ramachandran, V.; Muruganathan, U. Syringic Acid, a Novel Natural Phenolic Acid, Normalizes Hyperglycemia with Special Reference to Glycoprotein Components in Experimental Diabetic Rats. J. Acute Dis. 2013, 2, 304–309.
  39. Rashedinia, M.; Khoshnoud, M.J.; Fahlyan, B.K.; Hashemi, S.-S.; Alimohammadi, M.; Sabahi, Z. Syringic Acid: A Potential Natural Compound for the Management of Renal Oxidative Stress and Mitochondrial Biogenesis in Diabetic Rats. Curr. Drug Discov. Technol. 2021, 18, 405–413.
  40. Srinivasan, S.; Muthukumaran, J.; Muruganathan, U.; Venkatesan, R.S.; Jalaludeen, A.M. Antihyperglycemic Effect of Syringic Acid on Attenuating the Key Enzymes of Carbohydrate Metabolism in Experimental Diabetic Rats. Biomed. Prev. Nutr. 2014, 4, 595–602.
  41. Mirza, A.C.; Panchal, S.S.; Allam, A.A.; Othman, S.I.; Satia, M.; Mandhane, S.N. Syringic Acid Ameliorates Cardiac, Hepatic, Renal and Neuronal Damage Induced by Chronic Hyperglycaemia in Wistar Rats: A Behavioural, Biochemical and Histological Analysis. Molecules 2022, 27, 6722.
  42. Wei, X.; Chen, D.; Yi, Y.; Qi, H.; Gao, X.; Fang, H.; Gu, Q.; Wang, L.; Gu, L. Syringic Acid Extracted from Herba Dendrobii Prevents Diabetic Cataract Pathogenesis by Inhibiting Aldose Reductase Activity. Evid. Based Complement. Alternat. Med. 2012, 2012, 426537.
  43. Bhattacherjee, A.; Datta, A. Mechanism of Antiglycating Properties of Syringic and Chlorogenic Acids in in Vitro Glycation System. Food Res. Int. 2015, 77, 540–548.
  44. Wu, Q.; Li, S.; Li, X.; Fu, X.; Sui, Y.; Guo, T.; Xie, B.; Sun, Z. A Significant Inhibitory Effect on Advanced Glycation End Product Formation by Catechin as the Major Metabolite of Lotus Seedpod Oligomeric Procyanidins. Nutrients 2014, 6, 3230–3244.
  45. Aoki, K.; Tajima, T.; Yabushita, Y.; Nakamura, A.; Nezu, U.; Takahashi, M.; Kimura, M.; Terauchi, Y. A Novel Initial Codon Mutation of the Thiazide-Sensitive Na-Cl Cotransporter Gene in a Japanese Patient with Gitelman’s Syndrome. Endocr. J. 2008, 55, 557–560.
  46. Guo, H.; Callaway, J.B.; Ting, J.P.-Y. Inflammasomes: Mechanism of Action, Role in Disease, and Therapeutics. Nat. Med. 2015, 21, 677–687.
  47. Lee, M.-H.; Kang, H.; Lee, K.; Yang, G.; Ham, I.; Bu, Y.; Kim, H.; Choi, H.-Y. The Aerial Part of Taraxacum Coreanum Extract Has an Anti-Inflammatory Effect on Peritoneal Macrophages in Vitro and Increases Survival in a Mouse Model of Septic Shock. J. Ethnopharmacol. 2013, 146, 1–8.
  48. Costa, M.F.; Jesus, T.I.; Lopes, B.R.P.; Angolini, C.F.F.; Montagnolli, A.; Gomes, L.d.P.; Pereira, G.S.; Ruiz, A.L.T.G.; Carvalho, J.E.; Eberlin, M.N.; et al. Eugenia Aurata and Eugenia Punicifolia HBK Inhibit Inflammatory Response by Reducing Neutrophil Adhesion, Degranulation and NET Release. BMC Complement. Altern. Med. 2016, 16, 403.
  49. Gierlikowska, B.; Stachura, A.; Gierlikowski, W.; Demkow, U. Phagocytosis, Degranulation and Extracellular Traps Release by Neutrophils-The Current Knowledge, Pharmacological Modulation and Future Prospects. Front. Pharmacol. 2021, 12, 666732.
  50. Ham, J.R.; Lee, H.-I.; Choi, R.-Y.; Sim, M.-O.; Seo, K.-I.; Lee, M.-K. Anti-Steatotic and Anti-Inflammatory Roles of Syringic Acid in High-Fat Diet-Induced Obese Mice. Food Funct. 2016, 7, 689–697.
  51. Patra, A.; Jha, S.; Pn, M.; Aher, V.; Chattopadhyay, P.; Roy, D. Anti-Inflammatory and Antipyretic Activities of Hygrophilaspinosa T. Anders Leaves (Acanthaceae). Trop. J. Pharm. Res. 2009, 8, 133–137.
  52. Dileep, K.V.; Remya, C.; Cerezo, J.; Fassihi, A.; Pérez-Sánchez, H.; Sadasivan, C. Comparative Studies on the Inhibitory Activities of Selected Benzoic Acid Derivatives against Secretory Phospholipase A2, a Key Enzyme Involved in the Inflammatory Pathway. Mol. Biosyst. 2015, 11, 1973–1979.
  53. Chopyk, D.M.; Grakoui, A. Contribution of the Intestinal Microbiome and Gut Barrier to Hepatic Disorders. Gastroenterology 2020, 159, 849–863.
  54. Schwartz, J.M.; Reinus, J.F. Prevalence and Natural History of Alcoholic Liver Disease. Clin. Liver Dis. 2012, 16, 659–666.
  55. Safari, Z.; Gérard, P. The Links between the Gut Microbiome and Non-Alcoholic Fatty Liver Disease (NAFLD). Cell Mol. Life Sci. 2019, 76, 1541–1558.
  56. Younossi, Z.M. Non-Alcoholic Fatty Liver Disease—A Global Public Health Perspective. J. Hepatol. 2019, 70, 531–544.
  57. García-Cortés, M.; Ortega-Alonso, A.; Lucena, M.I.; Andrade, R.J. Spanish Group for the Study of Drug-Induced Liver Disease Drug-Induced Liver Injury: A Safety Review. Expert Opin. Drug Saf. 2018, 17, 795–804.
  58. Iorga, A.; Dara, L.; Kaplowitz, N. Drug-Induced Liver Injury: Cascade of Events Leading to Cell Death, Apoptosis or Necrosis. Int. J. Mol. Sci. 2017, 18, 1018.
  59. Komori, A. Recent Updates on the Management of Autoimmune Hepatitis. Clin. Mol. Hepatol. 2021, 27, 58–69.
  60. Ramachandran, V.; Raja, B. Protective Effects of Syringic Acid against Acetaminophen-Induced Hepatic Damage in Albino Rats. J. Basic Clin. Physiol. Pharmacol. 2010, 21, 369–385.
  61. Somade, O.T.; Oyinloye, B.E.; Ajiboye, B.O.; Osukoya, O.A. Methyl Cellosolve-Induced Hepatic Oxidative Stress: The Modulatory Effect of Syringic Acid on Nrf2-Keap1-Hmox1-NQO1 Signaling Pathway in Rats. Phytomed. Plus 2023, 3, 100434.
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to : , , , ,
View Times: 138
Revisions: 2 times (View History)
Update Date: 27 Feb 2024