Abstract
Equisetum ramosissimum, a genus of Equisetaceae, is a medicinal plant that can be separated into ethyl acetate (EA), dichloromethane (DM), n-hexane (Hex), methanol (MeOH), and water extracts. EA extract was known to have potent antioxidative properties, reducing power, DPPH scavenging activity, and metal ion chelating activity. This study compared these five extracts in terms of their inhibiting effects on three human malignant melanomas: A375, A375.S2, and A2058. MTT assay presented the notion that both EA and DM extracts inhibited melanoma growth but did not affect the viabilities of normal dermal keratinocytes (HaCaT) or fibroblasts. Western blot analyses showed that both EA and DM extracts induced overexpression of caspase proteins in all three melanomas. To determine their roles in melanogenesis, this study analyzed their in vitro suppressive effects on mushroom tyrosinase. All extracts except for water revealed moderate suppressive effects. None of the extracts affected B16-F10 cells proliferation. EA extract inhibited cellular melanin production whereas DM extract unexpectedly enhanced cellular pigmentation in B16-F10 cells. Data for modulations of microphthalmia-associated transcription factor, tyrosinase, tyrosinase-related protein 1, and tyrosinase-related protein 2 showed that EA extract inhibited protein expression mentioned above whereas DM extract had the opposite effect. Overall, the experiments indicated that the biofunctional activities of EA extract contained in food and cosmetics protect against oxidation, melanoma, and melanin production.
Highlights
Mitochondria, chloroplasts, and peroxisomes produce reactive oxygen species (ROS) through respiration and photosynthesis [1, 2]
Even though free radicals are needed for normal healthy biochemical processes in the body, they have severe negative health effects [18, 19]
ethyl acetate (EA) and DM extracts affected the viabilities of melanoma cells and showed low toxicity in both normal human cells, HaCaT cells and fibroblasts
Summary
Mitochondria, chloroplasts, and peroxisomes produce reactive oxygen species (ROS) through respiration and photosynthesis [1, 2]. Studies suggested that the changes in cellular homeostasis caused by high ROS levels can result in oxidative damage [3]. To avoid ROS oxidative injuries, the defense radical scavenging systems used by the human being were separated into enzymatic and nonenzymatic mechanisms. Antioxidant enzymes and substances could reduce oxidative damage by decreasing production of ROS and radicals [2]. These agents include glutathione and catalase, glutathione reductase, superoxide dismutase, and glutathione peroxidase. The above antioxidative materials are applied in synergic ways with each other against various free radical types [1,2,3]
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