Abstract
Ultraviolet B (UV-B) radiation induces the extreme production of either reactive oxygen species (ROS) or inflammatory mediators. The aim of this study was to evaluate the antioxidant activities of 70% ethanolic extract of Lablab purpureus (LPE) and the underlying mechanisms using HaCaT cells exposed to UV-B. High-performance liquid chromatography (HPLC) confirmed the presence of gallic acid, catechin, and epicatechin in LPE. LPE was shown to have a very potent capacity to scavenge free radicals. The results showed that LPE prevented DNA damage and inhibited the generation of ROS in HaCaT cells without causing any toxicity. LPE increased the expression of endogenous antioxidant enzymes such as superoxide dismutase-1 and catalase. Furthermore, LPE treatment facilitates the nuclear translocation of nuclear factor (erythroid-derived 2)-like 2 (Nrf-2), boosting the phase II detoxifying enzyme heme oxygenase-1 (HO-1) leading to the combatting of oxidative stress. However, pretreatment of LPE also caused the phosphorylation of mitogen-activated protein kinases (MAPK kinase) (p38 kinase) and extracellular signal-regulated kinase (ERK), whereas treatment with p38 and ERK inhibitors substantially suppressed LPE-induced Nrf2 and heme oxygenase (HO)-1 expression. These findings suggest that LPE exhibits antioxidant activity via Nrf-2-mediated HO-1 signaling through the activation of p38 and ERK, indicating that LPE can potentially be used as a remedy to combat oxidative stress-induced disorder.
Highlights
Several skin diseases are developed and initiated by ultraviolet (UV) irradiation [1] through the generation of reactive oxygen species (ROS) such as hydroxyl radical, superoxide anion, hydrogen peroxide, and singlet oxygen [2]
We found that polyphenols and flavonoid contents were highest in Lablab purpureus (LPE) with values of 205.79 ± 0.11 mg gallic acid equivalent (GAE)/g and 296.56 ± 0.01 mg catechin equivalent (CAE)/g, respectively (Figure 1B)
The results showed that Nrf2 inhibition decreased the induction of heme oxygenase-1 (HO-1) by various concentrations of LPE (Figure 5), confirming the previous study that phase II enzymes are controlled by Nrf2
Summary
Several skin diseases are developed and initiated by ultraviolet (UV) irradiation [1] through the generation of reactive oxygen species (ROS) such as hydroxyl radical, superoxide anion, hydrogen peroxide, and singlet oxygen [2]. UV-B irradiation causes many detrimental effects, including deoxyribonucleic acid (DNA) and protein damage, oxidative stress, inflammation, and carcinogenesis. These events are mainly triggered by ROS and eventually lead to the development of various skin diseases [3,4]. Even though human skin tightly regulates its intracellular redox stability, UV-B can completely destroy the epidermal protective antioxidant system, which involves superoxide dismutase (SOD), catalase (CAT), and heme oxygenase-1 (HO-1) [9]
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