| dc.description.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. | en_US |
