The stingless bee honey protects against hydrogen peroxide-induced oxidative damage and lipopolysaccharide-induced inflammation in vitro

Oxidative stress inhibits osteoblast differentiation and function that lead to the development of osteoporosis. Casein-derived peptide VLPVPQK (PEP), a potent antioxidant, was isolated from β-casein of buffalo milk. We used an in vitro oxidative stress model induced by hydrogen peroxide (H2O2) in rat osteoblastic cells to investigate the protective effects of PEP against H2O2-induced dysfunction and oxidative damage. Cells were pretreated with PEP (50–200 ng/mL) for 2, 7 or 21 days followed by 0.3 mM H2O2 treatment for 24 h and then markers of osteogenic development, oxidative damage and apoptosis were examined. PEP significantly increased the viability and differentiation markers of osteoblast cells such as alkaline phosphatase and calcium mineralization. Moreover, PEP suppressed the production of reactive oxygen species (ROS), lipid peroxidation and ameliorated H2O2-induced reduction in glutathione, superoxide dismutase and catalase activities. In addition, PEP partially inhibited caspase-9 and-3 activities and reduced propidium iodide–positive cells. Altogether, our results demonstrated that PEP could protect rat osteoblast against H2O2-induced dysfunction and oxidative damage by reduction of ROS production, lipid peroxidation and increased antioxidant enzyme activities. Thus, our data suggest that PEP might be a valuable protective agent against oxidative stress–related diseases such as osteoporosis.

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Exopolysaccharides Produced by Lactobacillus rhamnosus GG Alleviate Hydrogen Peroxide-Induced Intestinal Oxidative Damage and Apoptosis through the Keap1/Nrf2 and Bax/Bcl-2 Pathways in Vitro

Food & Function ◽

10.1039/d1fo00277e ◽

2021 ◽

Author(s):

Anshan Shan ◽

Jinze Li ◽

Qiuke Li ◽

Nan Gao ◽

Zhihua Wang ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Epithelial Cells ◽

Oxidative Damage ◽

Lactobacillus Rhamnosus ◽

Lactobacillus Rhamnosus Gg

The purpose of the study was to explore the effect of exopolysaccharides (EPSs) of Lactobacillus rhamnosus GG (LGG) on the antioxidative and antiapoptotic activities of intestinal porcine epithelial cells (IPEC-J2)....

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Flavonoids as reductants of ferryl hemoglobin.

Acta Biochimica Polonica ◽

10.18388/abp.2009_2487 ◽

2009 ◽

Vol 56 (3) ◽

Cited By ~ 22

Author(s):

Lidia Gebicka ◽

Ewa Banasiak

Keyword(s):

Hydrogen Peroxide ◽

Oxidative Damage ◽

Beneficial Effect ◽

Rate Constants ◽

Plant Polyphenols ◽

Radical Site ◽

Derivatives Of ◽

Protein Moiety

The ferryl derivatives of hemoglobin are products of the reactions of oxy- and methemoglobin with hydrogen peroxide. Ferryl hemoglobins, either with or without a radical site on the protein moiety, are oxidizing species. Plant polyphenols, flavonoids, have been shown to act as antioxidants in vivo and in vitro. Reactions of met- and oxyhemoglobin with hydrogen peroxide in the presence of catechin, quercetin and rutin were studied. These flavonoids accelerated reduction of ferryl hemoglobin to methemoglobin. The rate constants of the reactions of ferryl hemoglobin with catechin, quercetin and rutin were in the order of 10(2) M(-1) s(-1), i.e. similar to the rate constants of ferryl hemoglobin with intracellular reducing compounds like urate or ascorbate. The beneficial effect of flavonoids against oxidative damage of hemoglobin caused by hydroperoxides, reported in the literature, is probably, at least in part, connected with the ability of flavonoids to scavenge ferryl hemoglobin.

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Vitamin E Can Ameliorate Oxidative Damage of Ovine Hepatocytes In Vitro by Regulating Genes Expression Associated with Apoptosis and Pyroptosis, but Not Ferroptosis

Molecules ◽

10.3390/molecules26154520 ◽

2021 ◽

Vol 26 (15) ◽

pp. 4520

Author(s):

Luyang Jian ◽

Ying Xue ◽

Yuefeng Gao ◽

Bo Wang ◽

Yanghua Qu ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Cell Death ◽

Vitamin E ◽

Oxidative Damage ◽

Treated Group ◽

Cellular Damage ◽

Control Group ◽

Group 4 ◽

Intracellular Ros

(1) Background: the current research was conducted to investigate the potential non-antioxidant roles of vitamin E in the protection of hepatocysts from oxidative damage. (2) Methods: primary sheep hepatocytes were cultured and exposed to 200, 400, 600, or 800 μmol/L hydrogen peroxide, while their viability was assessed using a CCK-8 kit. Then, cells were treated with 400 μmol/L hydrogen peroxide following a pretreatment with 50, 100, 200, 400, and 800 μmol/L vitamin E and their intracellular ROS levels were determined by means of the DCF-DA assay. RNA-seq, verified by qRT-PCR, was conducted thereafter: non-treated control (C1); cells treated with 400 μmol/L hydrogen peroxide (C2); and C2 plus a pretreatment with 100 μmol/L vitamin E (T1). (3) Results: the 200–800 μmol/L hydrogen peroxide caused significant cell death, while 50, 100, and 200 μmol/L vitamin E pretreatment significantly improved the survival rate of hepatocytes. ROS content in the cells pretreated with vitamin E was significantly lower than that in the control group and hydrogen-peroxide-treated group, especially in those pretreated with 100 μmol/L vitamin E. The differentially expressed genes (DEGs) concerning cell death involved in apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2), pyroptosis (NLRP3, IL-1β, and IRAK2), and ferroptosis (TFRC and PTGS2). The abundances of IL-1β, IRAK2, NLRP3, CASP8, CASP8AP2, RIPK1, and TLR7 were significantly increased in the C1 group and decreased in T1 group, while TFRC and PTGS2 were increased in T1 group. (4) Conclusions: oxidative stress induced by hydrogen peroxide caused cellular damage and death in sheep hepatocytes. Pretreatment with vitamin E effectively reduced intracellular ROS levels and protected the hepatocytes from cell death by regulating gene expression associated with apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2) and pyroptosis (NLRP3, IL-1β, and IRAK2), but not ferroptosis (TFRC and PTGS2).

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