Abstract
Mentha suaveolens is an aromatic herb that has a wide range of biological activities, including antimicrobial, antifungal, anti-inflammatory, and hepatoprotective properties. Although there are a few reports on the antioxidant property of M. suaveolens, its cytoprotective activity against oxidative stress has not been reported yet. The objective of this study was to determine the protective activity of M. suaveolens aqueous extract (MSAE) against hydrogen peroxide- (H2O2-) induced oxidative stress and apoptosis in human keratinocyte HaCaT cells. MSAE pretreatment decreased H2O2-induced cytotoxicity and suppressed H2O2-induced intracellular ROS generation. Furthermore, MSAE suppressed expression levels of H2O2-induced apoptotic genes such as cleaved caspase-3, caspase-9, and cleaved poly (ADP-ribose) polymerase (PARP). Pretreatment with MSAE induced expression of phase II enzyme such as HO-1 through translocation of NF-E2-related factor (Nrf2) upon H2O2 exposure. These results revealed that the cytoprotective effect of MSAE against oxidative stress-induced cell death was associated with activation of Nrf2-mediated phase II enzyme expression.
Highlights
Skin, the largest organ in human body, has direct contact with physical and chemical environmental factors
Viability of HaCaTcells pretreated with M. suaveolens aqueous extract (MSAE) followed by H2O2 treatment was higher than that of cells treated with H2O2 without such pretreatment (Figure 1(c))
Other expressions except of heme oxygenase-1 (HO-1) was not affected by treatment with MSAE. erefore, we focused on the cytoprotective mechanism of MSAE against H2O2− induced oxidative stress by assessing the expression of HO-1
Summary
The largest organ in human body, has direct contact with physical and chemical environmental factors. E production of ROS such as superoxide anion, hydroxyl radical, and hydrogen peroxide is the most important mediator of oxidative stress. It triggers apoptosis [2, 3]. Kelch-like ECH-associated protein 1 (Keap1)nuclear factor erythroid 2-related factor 2 (Nrf2) pathway is a key defense mechanism against oxidative stress [4]. Under conditions of oxidative stress, Nrf will dissociate with Keap, translocate into the nucleus, and bind to antioxidant response elements (ARE) present in the promoter region of antioxidant and detoxification genes including glutamatecysteine ligase (GCL), quinone oxidoreductase-1 (NQO1), and heme oxygenase-1 (HO-1) [5, 6]. HO-1 produces carbon monoxide (CO), biliverdin, and iron by catalysis of heme. ese products have protective roles against apoptosis [7, 8]
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