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400 TSUN-THAI CHAI et al.punctatum and P. irregularis. The cytotoxicity of C.interruptus-derived coumarins against humannasopharyngeal carcinoma (KB) cell line was previouslyreported (14); however, this is the first accountof the fernís cytotoxicity toward K562 cell line.Different cancer cell lines respond differently evento treatment with the same cytotoxic agents (29).Hence, our study has added valuable information tocurrent knowledge of the anticancer potential of C.interruptus. Hot water extracts of all six ferns analyzedin this study were cytotoxic to K562 cancercell line. Thus, our findings suggest that these sixferns are promising sources of water-soluble andheat-stable cytotoxic agents. C. dentata, N. acutifolia,and P. irregularis are consumed as vegetables inMalaysia and India (16, 17, 30). Considering currentinterests to discover anticancer agents of food origin,future research to isolate and identify cytotoxicconstituents from the three ferns will be of greatvalue in the context of therapeutic agent development,especially for leukemia treatment.We report for the first time the in vitro antiglucosidaseactivity of C. arida, C. dentata, M. punctatum,N. acutifolia, and P. irregularis. Notably, edibleferns C. dentata, N. acutifolia, and P. irregularisdemonstrated stronger antiglucosidase activity thanthe other ferns. In line with current interests tosearch for food-derived antidiabetic natural productsand management of diabetes by dietary intervention(31-34), the three edible ferns deserve more attentionin future research. These ferns are not traditionallyused as antidiabetic remedies. Nevertheless,owing to their α-glucosidase inhibitory activity,these ferns, when consumed, may be beneficial tothe diets of diabetic patients. The water-soluble andthermally-stable nature of the α-glucosidaseinhibitors in the three ferns imply that such constituentscould be easily extracted with water andthat their activity is likely retained after cookingwith heat. In this study, we evaluated the antiglucosidaseactivity of the fern extracts by using yeastα-glucosidase. Yeast α-glucosidase is commerciallyavailable in pure form and has been routinely usedas a model for investigating antiglucosidase potentialof natural products (22, 35-37). Previous workhas shown that plant extracts which inhibited theactivity of yeast α-glucosidase also inhibited mammalianα-glucosidase. In addition, antiglucosidaseplant extracts can significantly dampen postprandialhyperglycemia in streptozocin-induced diabeticmice (37, 38).The presence of TP, THC, TF, and TPro in allthe fern extracts, except for the absence of TPro inM. punctatum, implies that the cytotoxic andantiglucosidase activities of the extracts may bepartly attributable to their phenolic constituents. P.irregularis extract, which was enriched in TF (37%by weight), showed potent cytotoxicity and concurrentlyexhibited relatively high antiglucosidaseactivity compared with the other ferns examined.Thus flavonoids may be a key group of bioactiveconstituents in P. irregularis. In this study, antiglucosidaseactivity of the ferns correlated with TP content,also implying that antiglucosidase activities ofthe ferns may be attributable to their phenolic constituents.No correlations were detected between thefour phytochemical parameters measured and thecytotoxic activities of the fern extracts. It is likelythat the fern extracts contained phenolic constituentsthat varied considerably in their efficacies or specificactivity per unit mass as cytotoxic agents.Consequently, their cytotoxic activities cannot bedirectly predicted from their phenolic contents.In conclusion, the cytotoxic effects of sixselected edible and medicinal ferns toward K562cell line were demonstrated for the first time. Thewater extracts of C. dentata, N. acutifolia, and P.irregularis were strong cytotoxic agents, with potencycomparable to that of anticancer drug 5-fluorouracil.Antiglucosidase activity was also detectedin five of these ferns for the first time. C. dentatahad the strongest antiglucosidase activity among theferns, which was stronger than acarbose but weakerthan myricetin. This study has provided preliminaryevidence that C. dentata is a promising source ofcytotoxic and antiglucosidase agents, which warrantmore in-depth investigations. To attest to theirpotential application as anticancer drugs, the effectsof cytotoxic constituents isolated from C. dentata onnormal cells should be confirmed. Correlationanalysis suggests that antiglucosidase activity of thefern extracts was attributable to their phenolic contents.Hence, future research can consider bioassayguidedisolation of glucosidase inhibitors from phenolicextracts of the ferns, especially C. dentata.REFERENCES1. Antignac E., Nohynek G.J., Re T., Clouzeau J.,Toutain H.: Food Chem. Toxicol. 49, 324(2011).2. Anastasi J.K., Chang M., Capili B.: J. NursePract. 7, 29 (2011).3. Iriti M., Faoro F.: Med. Hypotheses 67, 833(2006).4. Wijesinghe W.A.J.P., Jeon Y.-J.: Phytochem.Rev. 10, 431 (2011).5. Surh Y.-J.: Nat. Rev. Cancer 3, 768 (2003).
Cytotoxicity and antiglucosidase potential of six selected... 4016. Mata R., Cristians S., EscandÛn-Rivera S.,Ju·rez-Reyes K., Rivero-Cruz I.: J. Nat. Prod.76, 468 (2013).7. Ho R., Teai T., Bianchini J.-P., Lafont R.,Raharivelomanana P.: in Working with Ferns:Issues and Applications, Fern·ndez H., RevillaM.A., Kumar A. Eds., Springer, New York2010.8. Lee C.H., Shin S.L.: in Working with ferns:Issues and applications, Fern·ndez H., RevillaM.A., Kumar A. Eds., Springer, New York2010.9. Ali Asgar M.: Int. J. Food Prop. 16, 91 (2012).10. Karim S., Rahman M., Shahid S.B., Malek I.,Rahman A. et al.: Am.-Eurasian J. Sustain.Agric. 5, 405 (2011).11. Kumar M., Ramesh M., Sequiera S.: IndianFern J. 20, 1 (2003).12. Kumar S., Dash D.: Int. J. Pharm. Life Sci. 3,1631 (2012).13. Oyen L.P.A.: in Prota 16: Fibres/Plantes àfibres, Brink M., Achigan-Dako E.G. Eds.,PROTA, Wageningen, Netherlands 2010.14. Quadri-Spinelli T., Heilmann J., Rali T., SticherO.: Planta Med. 66, 728 (2000).15. Sharma U.K., Pegu S.: J. Ethnobiol. Ethnomed.7, 16 (2011).16. Voon B.H., Kueh H.S.: Asia Pac. J. Clin. Nutr.8, 24 (1999).17. Ong H.-C., Lina E., Milow P.: Sci. Res. Essays7, 441 (2012 ).18. Eswani N., Abd Kudus K., Nazre M., AwangNoor A.G., Ali M.: J. Agr. Sci. 2, 189 (2010).19. Ong H.-C., Chua S., Milow P.: Ethno. Med. 5,95 (2011).20. El Gharras H.: Int. J. Food Sci. Technol. 44,2512 (2009).21. Chai T.-T., Quah Y., Ooh K.-F., Mohd IsmailN.I., Ang Y.-V. et al.: Trop. J. Pharm. Res. 12,747 (2013).22. Chai T.-T., Elamparuthi S., Yong A.-L., QuahY., Ong H.-C. et al.: Bot. Stud. 54, 55 (2013).23. Tadera K., Minami Y., Takamatsu K.,Matsuoka T.: J. Nutr. Sci. Vitaminol. (Tokyo)52, 149 (2006).24. Derosa G., Maffioli P.: Arch. Med. Sci. 8, 899(2012).25. Waterhouse A.L.: in Current Protocols in FoodAnalytical Chemistry, Wrolstad R.E., AcreeT.E., An H., Decker E.A., Penner M.H. et al.Eds., John Wiley & Sons, Inc., New York 2001.26. Matkowski A., ZieliÒska S., OszmiaÒski J.,Lamer-Zarawska E.: Bioresour. Technol. 99,7892 (2008).27. Chai T.-T., Wong F.-C.: J. Med. Plants Res. 6,1730 (2012).28. Porter L.J., Hrstich L.N., Chan B.G.:Phytochemistry 25, 223 (1986).29. Lai H.Y., Lim Y.Y., Kim K.H.: BMCComplement. Altern. Med. 10, 15 (2010).30. Parihar P., Parihar L.: Nat. Prod. Rad. 5, 297(2006).31. Park H., Kim H.S.: J. Med. Food 17, 21 (2014).32. Lacroix I.M.E., Li-Chan E.C.Y.: Mol. Nutr.Food Res. 58, 61 (2014).33. Anuradha C.V.: Can. J. Physiol. Pharmacol. 91,397 (2013).34. Bahadoran Z., Mirmiran P., Azizi F.: J.Diabetes Metab. Disord. 12, 43 (2013).35. Schafer A., Hogger P.: Diabetes Res. Clin.Pract. 77, 41 (2007).36. Chai T.-T., Mohan M., Ong H.-C., Wong F.-C.:Trop. J. Pharm. Res. 13, 67 (2014).37. Zhang L., Hogan S., Li J., Sun S., Canning C. etal.: Food Chem. 126, 466 (2011).38. Hogan S., Zhang L., Li J., Sun S., Canning C.,Zhou K.: Nutr. Metab. 7, 71 (2010).Received: 13. 03. 2014
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PHARMACEUTICAL TECHNOLOGY347. £uka
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