Anti-oxidative Activity of Hydrolysate from Rice Bran Protein in HepG2 Cells

Abstract

Glutathione (GSH) is an ubiquitous thiol-containing tripeptide, which plays important roles in cellular protection from oxidative stress. In our search for a dietary source that can increase GSH levels, we discovered that a 24 h treatment of HepG2 cells with rice bran protein hydrolysate (RBPH), prepared by Umamizyme G-catalyzed hydrolysis, increased the GSH content in a dose-dependent manner. RBPH elevated the expression levels of γ-glutamylcysteine synthetase (γ-GCS), which constitutes the rate-limiting enzyme of GSH synthesis, and of another two enzymes, hemeoxygenase-1 (HO-1) and reduced nicotinamide adenine dinucleotide (phosphate): quinone oxidoreductase 1 (NQO1). This induction was preceded by the accumulation of nuclear factor erythroid 2-related factor 2 (Nrf2) inside the nucleus, which is a key transcription factor for the expression of the γ-GCS, HO-1, and NQO1. Pre-treatment of cells with RBPH produced a significant protective effect against cytotoxicity caused by H 2 O 2 or ethanol. These results indicate that RBPH exerts a protective effect against oxidative stress by modulating GSH levels and anti-oxidative enzyme expression via the Nrf2 pathway.Key words rice bran; anti-oxidative; glutathione; nuclear factor erythroid 2-related factor 2 Rice is the most important cereal food in Japan. Rice bran (RB), which constitutes approximately 10% of the grain, is a major by-product of rice milling. RB is rich in protein, lipids, dietary fibers, and vitamins.1,2) Recently, RB was recognized as a functional ingredient, containing such antioxidants as tocopherols, tocotorienols, and γ-oryzanol.3,4) Moreover, enzymatically produced RB protein hydrolysates (RBPHs) were found to possess various biological functions with potential medical applications. In a previous study, we demonstrated that RBPH produced with Umamizyme G, a commercial protease from Aspergillus oryzae, from defatted RB protein exhibited the inhibitory activity of dipeptidylpetidase-IV (DPP-IV) that is a key regulator involved in the prevention and treatment of type 2 diabetes.5) RBPHs produced with other peptidases were shown to have an anti-proliferative effect on cancer cells, 6) and the ability to reduce micellar cholesterol levels. 7)

Sake lees hydrolysate protects against acetaminophen-induced hepatotoxicity via activation of the Nrf2 antioxidant pathway

“…Protein hydrolysates from rice, rice bran, eggshell membrane and chickpea have been reported to increase the intracellular glutathione levels and upregulate anti-oxidative enzymes in cells. ( 4 , 34 – 36 ) Since the active concentration ranged from 0.1 to 10 mg/ml, SLH showed similar bioactivity to the aforementioned hydrolysates (Fig. 4 A).…”

Protective Effects of Rice Peptide Oryza Peptide-P60 against Oxidative Injury through Activation of Nrf2 Signaling Pathway In Vitro and In Vivo

“…For example, treatment with 5 mg/mL rice bran-hydrolysate for 24 h increased intracellular GSH levels in HepG2 cells by ca. 2-fold . A 12 h treatment with 2.5 or 5 mg/mL FSGHF3 increased mRNA levels of γ-GCSh by ca.…”

“…We reported that rice bran protein hydrolysate increases intracellular GSH levels in the HepG2 human hepatoblastoma cells. 17 Additionally, rice-derived peptides and sake lees hydrolysate are hepatoprotective in the case of acetaminophen (APAP)-induced liver injury. 18,19 These antioxidative effects were suggested to be mediated through the Nrf2 antioxidant pathway.…”

Lamprey PHB2 maintains mitochondrial stability by tanslocation to the mitochondria under oxidative stress

“…Furthermore, numerous studies have demonstrated the extensive involvement of oxidative stress in ageing itself [4]. Oxidative stress represents an imbalance between toxic reactive oxygen species (ROS) and antioxidant systems, and high levels of ROS induce inflammation and cytotoxicity, which damages proteins, lipids, and DNA and subsequently disrupts mitochondrial structure and functions, ultimately resulting in cell death [5][6][7]. At present, most experts think it is related to the sudden onset of systemic inflammatory response syndrome in COVID-19 severe patients [8].…”