Redox properties of ginger extracts: Perspectives of use of Zingiber officinale Rosc. as antidiabetic agent

Lucia Račková PhD. 1 , Mária Cupáková 2 , Anton Ťažký 3 , Júlia Mičová 4 , Emil Kolek 5 , and Daniela Košťálová 2
  • 1 Institute of Experimental Pharmacology and Toxicology Slovak Academy of Sciences Dúbravská cesta 9, 841 04 Bratislava, Slovak Republic. TEL.: +421-2-59410659
  • 2 Department of Nutrition and Food Assesment, Institute of Biochemistry, Nutrition and Health Protection, Faculty of Chemical and Food Technology, Slovak University of Technology in Bratislava, Radlinského 9, SK-812 37 Bratislava, Slovak Republic
  • 3 Toxicological and Antidoping Centre, Comenius University, Faculty of Pharmacy, Odbojárov 10, SK-832 32 Bratislava, Slovak Republic
  • 4 Institute of Chemistry, Slovak Academy of Sciences, Dúbravská cesta 9, SK-845 38 Bratislava, Slovak Republic
  • 5 Department of Food Analysis, VÚP Food Research Institute, Priemyselná 4, SK-824 75, Bratislava, Slovak Republic

Abstract

In traditional medicine, several medicinal plants or their extracts have been used to treat diabetes. Zingiber officinale Roscoe, known commonly as ginger, is consumed worldwide in cookeries as a spice and flavouring agent. It has been used as the spice and medicine for thousands of years. The present study was undertaken to investigate the potential protective effect of Zingiber officinale Rosc. in a model of oxidative damage to pancreatic β cells. The free radical scavenging activities and composition of the isolated n-hexane and ethanolic extracts were confronted with their protective, antioxidant and cytotoxic effects in INS-1E β cells. Unlike the n-hexane extract (exerting, paradoxically, stronger antiradical capacity), both low cytotoxicity and remarkable protective effects on β cell viability, followed by lowering oxidative stress markers were found for the ethanolic extract Zingiber officinale Rosc. The present study is the first pilot study to assess the protective potential of Zingiber officinale Rosc. in a model of cytotoxic conditions imposed by diabetes in β cells.

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