Black soybeans protect human keratinocytes from oxidative stress‐induced cell death

Abstract

Black soybeans are functional foods containing a variety of bioactives such as isoflavones, carotenoids, tocopherols, phenolic acid as well as anthocyanins. Here, we examined whether Cheongja#3 black soybean extract has a protective effect on oxidative stress‐induced cell death in human keratinocytes HaCaT. First, we identified fat‐soluble bioactives in three varieties of soybean extracts (Saedanbaek, Daechan, and Cheongja#3). In particular, black soybean Cheongja#3 had high amounts of lutein than other varieties. We demonstrated that Cheongja#3 extract reduced intracellular reactive oxygen species levels in HaCaT cells. Furthermore, Cheongja#3 protected cells from hydrogen peroxide (H2O2)‐induced oxidative stress and triggered cell death determined by cell viabilities and apoptotic caspase activities. Next, we identified the underlying mechanism is due to increased Nrf2 antioxidant system by Cheongja#3, thus increasing the expression of heme oxygenases (HO)‐1. These results indicated that Cheongja#3 soybean extract has protective role against oxidative stress by upregulating the Nrf‐2 antioxidant system in human keratinocyte HaCaT cells.

Antioxidant Activities and Protective Effects of Dendropachol, a New Bisbibenzyl Compound from Dendrobium pachyglossum, on Hydrogen Peroxide-Induced Oxidative Stress in HaCaT Keratinocytes

“…The result showed that the viabilities of HaCaT cells decreased in a dose-dependent manner, and the highest concentration (500 µmol/L) caused about 50% of cell survival ( Figure 3 A). Our results agreed with previous studies showing that H 2 O 2 at 500 μmol/L reduced cell viability in the range between 50–65% compared to the untreated group [ 37 , 38 , 39 ]. In the present study, the cytotoxicity of compounds 1–5 was evaluated on HaCaT keratinocytes before the preventive effect mechanism study.…”

Cytotoxicity of Ficus Crocata Extract on Cervical Cancer Cells and Protective Effect against Hydrogen Peroxide-Induced Oxidative Stress in HaCaT Non-Tumor Cells

“…The cytotoxic effect of H 2 O 2 on HaCaT cells was in agreement with that previously reported, and the reduction in cell viability corresponds to the oxidative damage caused by the increase in H 2 O 2 concentration [ 20 , 23 , 24 , 25 ]. Considering that mitochondrial homeostasis plays a key role in cell viability and survival [ 26 ], the cytotoxic effect has been associated with mitochondrial dysfunction and H 2 O 2 -induced apoptotic events [ 20 , 23 , 24 , 25 ]. Properly functioning mitochondria produce ATP and modulate cellular redox balance to ensure cell metabolism [ 27 , 28 ].…”

“…H 2 O 2 -induced oxidative damage in HaCaT cells has been reported to induce mitochondrial dysfunction by increasing concentrations of ROS, decreasing antioxidant defenses (SOD, GPx, and GSH), and increasing the release of cytochrome C into the cytoplasm and nucleus [ 24 ]. On the other hand, exposure to H 2 O 2 is known to promote apoptosis, because it increases the expression and activation of pro-apoptotic proteins, such as Bax and caspases 3, 6, 7, 8, and 9, and reduces the expression of the anti-apoptotic protein Bcl-2 [ 21 , 24 , 25 ]. These events could explain the H 2 O 2 -induced oxidative damage and cytotoxicity in HaCaT cells.…”

Protective Effect of Merbau (Intsia bijuga) Extract on Hydrogen Peroxide-Treated HaCaT Human Keratinocytes and Its Formulation as Antioxidant Cream

“…20,21 This method has been widely used to evaluate antioxidant activities and has advantages over the other in vitro assays, including DPPH, ferric reducing antioxidant power (FRAP), and trolox equivalent antioxidant capacity (TEAC). 2,[22][23] Keratinocytes are the major cells that make up the skin epidermis, which have a similar topology as the outer layer of the skin. Therefore, the antioxidant assay on HaCaT cells is more representative than the other in vitro methods.…”

“…ROS formation is the main cause of skin aging which is characterized by increased wrinkling, sagging, laxity, skin dryness, and pigmentation of the skin. 1,2 Oxidative stress produced by ROS also contributes to the development of various diseases and skin disorders. 3,4 ROS triggers melanogenesis in the skin, and it is known that melanocytes undergoing melanogenesis have a much lower capacity to repair DNA against oxidative damage, leading to skin carcinogenesis.…”