Protective Effect of Silymarin on Human Erythrocyte Against Tert-butyl Hydroperoxide Induced Oxidative Stress in vitro

2012 ◽  
Vol 2 (3) ◽  
pp. 167-174 ◽  
Author(s):  
Ratnesh Kumar Sharma ◽  
Nikhat J. Siddiqi ◽  
Bechan Sharma
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Human Erythrocyte ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide

The Effect of Tert-butyl Hydroperoxide on Peritoneal Macrophages and the Protective Effect of Protein-bound Polysaccharide Administered Intraperitoneally and Orally

1998 ◽  
Vol 26 (03n04) ◽  
pp. 301-310 ◽  
Author(s):  
Mei Zhou ◽  
Yuan Chen ◽  
Qian Ouyang ◽  
Shangxi Liu ◽  
Zhan-Jun Pang ◽  
...  
Keyword(s):  
Protective Effect ◽  
Morphological Changes ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Peritoneal Macrophages ◽  
Protective Effects ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide

Our previous studies have shown that a protein-bound polysaccharide, polysaccharide krestin (PSK), can protect macrophages from lipoperoxidative injury induced by tert-butyl hydroperoxide (tbOOH) and oxidatively modified low density lipoprotein (O-LDL). PSK was administered intraperitoneally to mice, and the peritoneal macrophages harvested were used as an experimental model. PSK does not reveal any protective effect on macrophages injured by tbOOH when incubated in vitro. In order to elucidate its mode of action, in the present study, the protective effects of PSK were further investigated using morphological changes and viability as indices. It was shown that, compared with the non-PSK group, the viability of macrophages was much higher in the PSK group, and the morphological changes in the PSK group were much less than those in the non-PSK group. The protective effect of PSK administered intraperitoneally and orally on macrophages injured by tbOOH was comparable. Furthermore, the serum of the PSK treated mice had the same protective effect.

Protective effect of extracts of Perilla frutescens treated with sucrose on tert-butyl hydroperoxide-induced oxidative hepatotoxicity in vitro and in vivo

2012 ◽  
Vol 133 (2) ◽  
pp. 337-343 ◽  
Author(s):  
Sung-Yong Yang ◽  
Chung-oui Hong ◽  
Hojoung Lee ◽  
Sang-yul Park ◽  
Byung-gyu Park ◽  
...  
Keyword(s):  
Protective Effect ◽  
Perilla Frutescens ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide

scholarly journals Protective Effect of Natural and Synthetic Anthocyanins against Tert-butyl-hydroperoxide-induced Oxidative Damages in Normal and β-thalassemic Major Human Erythrocytes In Vitro

2020 ◽  
Vol 17 (1) ◽  
pp. 38-47
Author(s):  
Naïma Charif ◽  
Nassima Mokhtari-Soulimane ◽  
Sabri Cherrak ◽  
Hafida Merzouk ◽  
Mourad Elhabiri
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thalassemia Major ◽  
Dpph Assay ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Oxidative Damages ◽  
Blood Disorder ◽  
Tert Butyl Hydroperoxide

Background: Even though β-thalassemia major is a genetic blood disorder, the damages endured by erythrocytes are mediated in part by oxidative stress. Antioxidants such as anthocyanins are capable to prevent the pro-oxidant effects induced by reactive oxygen species (ROS). Objective: This study aims to evaluate the in vitro preventive effects of one natural and two synthetic anthocyanins on normal and β-thalassemic erythrocytes on which toxicity has been induced by the free radical generator: tert-butyl-hydroperoxide TBHP. Methods: Erythrocytes isolated from fasting blood samples of healthy and β-thalassemic major individuals were treated either with TBHP alone or with TBHP after being pre-incubated with anthocyanins. Cell viability, reduced glutathione (GSH) and malondialdehyde (MDA) contents were measured after 90 minutes of incubation. In parallel, the antiradical scavenging capacities of the investigated anthocyanins were also estimated by using the 2,2-DiPhenyl-1-PicrylHydrazyl (DPPH•) assay. Results: The results clearly demonstrate that the treatment of erythrocytes with TBHP induces hemolysis along with marked redox state alteration (lipid peroxidation concomitant to GSH depletion) in both normal and β-thalassemia erythrocytes. During the pre-treatment with anthocyanins, erythrocytes become more resistant to oxidative impairments. Cyanin chloride and 6,7,3’,4’- tetrahydroxyflavylium chloride effectively prevent from TBHP-induced: hemolysis, lipid peroxidation and GSH depletion in normal and thalassemic erythrocytes, while 3’4’-dihdroxy-7-methoxyflavylium chloride had a lesser effect on MDA levels with thalassemic erythrocytes. These results are in agreement with those derived from the DPPH• assay. Conclusion: Our study contributes with important insights that tested anthocyanins may exert relevant potential in the alleviation of oxidative stress, especially the one affecting β-thalassemia erythrocytes.

scholarly journals Sinensetin Reduces Osteoarthritis Pathology in the Tert-Butyl Hydroperoxide-Treated Chondrocytes and the Destabilization of the Medial Meniscus Model Mice via the AMPK/mTOR Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Wenxian Zhou ◽  
Yifeng Shi ◽  
Hui Wang ◽  
Caiyu Yu ◽  
Huanqing Zhu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Potential Candidate ◽  
Mtor Signaling Pathway ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide

As a common degenerative disease, osteoarthritis (OA) usually causes disability in the elderly and socioeconomic burden. Previous studies have shown that proper autophagy has a protective effect on OA. Sinensetin (Sin) is a methylated flavonoid derived from citrus fruits. Studies have shown that Sin is a good autophagy inducer and has shown excellent therapeutic effects in a variety of diseases; however, its role in the treatment of OA is not fully understood. This study proved the protective effect of Sin on OA through a series of in vivo and in vitro experiments. In vitro experiments have shown that Sin may inhibit chondrocyte apoptosis induced by tert-butyl hydroperoxide (TBHP); at the same time, it might also inhibit the production of MMP13 and promote the production of aggrecan and collagen II. Mechanism studies have shown that Sin promotes chondrocyte autophagy by activating AMPK/mTOR signaling pathway. On the contrary, inhibition of autophagy can partially abolish the protective effect of Sin on TBHP-treated chondrocytes. In vivo experiments show that Sin may protect against DMM-induced OA pathogenesis. These results provide evidence that Sin serves as a potential candidate for the treatment of OA.

scholarly journals The Effect of Oxidative Stress on the Chicken Ovary: Involvement of Microbiota and Melatonin Interventions

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1422
Author(s):  
Jianping Wang ◽  
Ru Jia ◽  
Haojie Gong ◽  
Pietro Celi ◽  
Yong Zhuo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ovarian Function ◽  
Stress Factors ◽  
Ovary Cell ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide ◽  
Laying Performance ◽  
Chicken Ovary

The poultry ovary is used as a classic model to study ovarian biology and ovarian cancer. Stress factors induced oxidative stress to cause follicle atresia, which may be a fundamental reason for the reduction in fertility in older laying hens or in aging women. In the present study, we set out to characterize the relationships between oxidative stress and ovarian function. Layers (62 weeks of age; BW = 1.42 ± 0.12 kg) were injected with tert-butyl hydroperoxide (tBHP) at 0 (CON) and 800 μmol/kg BW (oxidative stress group, OS) for 24 days and the role of melatonin (Mel) on tBHP-induced ovary oxidative stress was assessed through ovary culture in vitro. The OS (800 μmol/kg BW tert-butyl hydroperoxide) treatment decreased the reproduction performance and ovarian follicle numbers. OS decreased the expression of SIRT1 and increased the P53 and FoxO1 expression of the ovary. A decreased Firmicutes to Bacteroidetes ratio, enriched Marinifilaceae (family), Odoribacter (genus) and Bacteroides_plebeius (species) were observed in the cecum of the OS group. Using Mel in vitro enhanced the follicle numbers and decreased the ovary cell apoptosis induced by tBHP. In addition, it increased the expression of SIRT1 and decreased the P53 and FoxO1 expression. These findings indicated that oxidative stress could decrease the laying performance, ovarian function and influence gut microbiota and body metabolites in the layer model, while the melatonin exerts an amelioration the ovary oxidative stress through SIRT1-P53/FoxO1 pathway.

scholarly journals In vitro Anti-Inflammatory and Anti-Oxidative Stress Activities of Kushenol C Isolated from the Roots of Sophora flavescens

Molecules ◽  
2020 ◽  
Vol 25 (8) ◽  
pp. 1768
Author(s):  
Byoung Ok Cho ◽  
Denis Nchang Che ◽  
Ji-Su Kim ◽  
Jang Hoon Kim ◽  
Jae Young Shin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Diseases ◽  
Hacat Cells ◽  
Sophora Flavescens ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Raw264.7 Macrophages ◽  
Tert Butyl Hydroperoxide ◽  
Anti Inflammatory

Kushenol C (KC) is a prenylated flavonoid isolated from the roots of Sophora flavescens aiton. Little is known about its anti-inflammatory and anti-oxidative stress activities. Here, we investigated the anti-inflammatory and anti-oxidative stress effects of KC in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages, and tert-butyl hydroperoxide (tBHP)-induced oxidative stress in HaCaT cells. The results demonstrated that KC dose-dependently suppressed the production of inflammatory mediators, including NO, PGE2, IL-6, IL1β, MCP-1, and IFN-β in LPS-stimulated RAW264.7 macrophages. The study demonstrated that the inhibition of STAT1, STAT6, and NF-κB activations by KC might have been responsible for the inhibition of NO, PGE2, IL-6, IL1β, MCP-1, and IFN-β in the LPS-stimulated RAW264.7 macrophages. KC also upregulated the expression of HO-1 and its activities in the LPS-stimulated RAW264.7 macrophages. The upregulation of Nrf2 transcription activities by KC in the LPS-stimulated RAW264.7 macrophages was demonstrated to be responsible for the upregulation of HO-1 expression and its activity in LPS-stimulated RAW264.7 macrophages. In HaCaT cells, KC prevented DNA damage and cell death by upregulating the endogenous antioxidant defense system involving glutathione, superoxide dismutase, and catalase, which prevented reactive oxygen species production from tert-butyl hydroperoxide (tBHP)-induced oxidative stress in HaCaT cells. The upregulated activation of Nrf2 and Akt in the PI3K-Akt signaling pathway by KC was demonstrated to be responsible for the anti-oxidative stress activity of KC in HaCaT cells. Collectively, the study suggests that KC can be further investigated as a potential anti-inflammatory candidate for the treatment of inflammatory diseases.

Sign in / Sign up

Export Citation Format

Share Document