Apigenin alleviates neomycin-induced oxidative damage via the Nrf2 signaling pathway in cochlear hair cells

2021 ◽  
Author(s):  
Gaogan Jia ◽  
Huanyu Mao ◽  
Yanping Zhang ◽  
Yusu Ni ◽  
Yan Chen
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Hair Cells ◽  
Cochlear Hair Cells ◽  
Nrf2 Signaling Pathway

scholarly journals Sirtuin-3 Protects Cochlear Hair Cells Against Noise-Induced Damage via the Superoxide Dismutase 2/Reactive Oxygen Species Signaling Pathway

2021 ◽  
Vol 9 ◽  
Author(s):  
Wenqi Liang ◽  
Chunli Zhao ◽  
Zhongrui Chen ◽  
Zijing Yang ◽  
Ke Liu ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Oxidative Damage ◽  
Hair Cell ◽  
Signaling Pathway ◽  
Hair Cells ◽  
Cell Injury ◽  
Cell Damage ◽  
Sirtuin 3 ◽  
Cochlear Hair Cells ◽  
Superoxide Dismutase 2

Mitochondrial oxidative stress is involved in hair cell damage caused by noise-induced hearing loss (NIHL). Sirtuin-3 (SIRT3) plays an important role in hair cell survival by regulating mitochondrial function; however, the role of SIRT3 in NIHL is unknown. In this study, we used 3-TYP to inhibit SIRT3 and found that this inhibition aggravated oxidative damage in the hair cells of mice with NIHL. Moreover, 3-TYP reduced the enzymatic activity and deacetylation levels of superoxide dismutase 2 (SOD2). Subsequently, we administered adeno-associated virus-SIRT3 to the posterior semicircular canals and found that SIRT3 overexpression significantly attenuated hair cell injury and that this protective effect of SIRT3 could be blocked by 2-methoxyestradiol, a SOD2 inhibitor. These findings suggest that insufficient SIRT3/SOD2 signaling leads to mitochondrial oxidative damage resulting in hair cell injury in NIHL. Thus, ameliorating noise-induced mitochondrial redox imbalance by intervening in the SIRT3/SOD2 signaling pathway may be a new therapeutic target for hair cell injury.

Effect of melatonin on attenuating the isoflurane-induced oxidative damage is related to PKCα/Nrf2 signaling pathway in developing rats

2018 ◽  
Vol 143 ◽  
pp. 9-18 ◽  
Author(s):  
Bei Li ◽  
Xiu Jing Feng ◽  
Xue Yuan Hu ◽  
Yong Ping Chen ◽  
Ji Chen Sha ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Nrf2 Signaling Pathway

scholarly journals Proanthocyanidins Protect against β-Hydroxybutyrate-Induced Oxidative Damage in Bovine Endometrial Cells

Molecules ◽  
2019 ◽  
Vol 24 (3) ◽  
pp. 400 ◽  
Author(s):  
Xi Cheng ◽  
Shuhua Yang ◽  
Chuang Xu ◽  
Lanzhi Li ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Manganese Superoxide Dismutase ◽  
Metabolic Diseases ◽  
Heme Oxygenase 1 ◽  
Endometrial Cells ◽  
Manganese Superoxide ◽  
Nrf2 Signaling Pathway ◽  
Mrna And Protein Expression ◽  
Stress Damage

Metabolic diseases, such as ketosis, are closely associated with decreased reproductive performance (such as delayed estrus and decreased pregnancy rate) in dairy cows. The change of β-hydroxybutyrate (BHBA) concentration in dairy cattle is an important mechanism leading to ketosis, and its blood concentration in ketotic cows is always significantly higher than in nonketotic cows. Many studies indicated that BHBA can induce oxidative damage in liver and other organs. Proanthocyanidins (PCs) have gained substantial attention in the last decade as strong antioxidative substances. This study aimed to demonstrate a protective effect of PCs against BHBA-induced oxidative stress damage in bovine endometrial (BEND) cells by activating the nuclear erythroid2-related factor2 (Nrf2) signaling pathway. Our research show that PCs could significantly increase activities of catalase (CAT) and glutathione peroxidase (GSH-PX), glutathione (GSH) content, and antioxidant capacity (T-AOC), while significantly decreasing malondialdehyde (MDA) content in BEND cells. Both mRNA and protein expression levels of Nrf2 were significantly increased in BEND cells, and glutamate–cysteine ligase catalytic subunit (GCLC), heme oxygenase 1 (HO-1), manganese superoxide dismutase (Mn-SOD), and NAD(P)H quinone dehydrogenase 1 (NQO-1) were also significantly increased. These results indicate that PCs can antagonize BHBA-induced oxidative damage by activating the Nrf2 signaling pathway to exert an antioxidant effect.

Biogenic selenium nanoparticles synthesized by Lactobacillus casei ATCC 393 alleviate diquat-induced intestinal barrier dysfunction in C57BL/6 mice through their antioxidant activity

2020 ◽  
Vol 11 (4) ◽  
pp. 3020-3031 ◽  
Author(s):  
Lei Qiao ◽  
Xina Dou ◽  
Shuqi Yan ◽  
Baohua Zhang ◽  
Chunlan Xu
Keyword(s):  
Antioxidant Activity ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Lactobacillus Casei ◽  
Intestinal Barrier ◽  
Selenium Nanoparticles ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
Nrf2 Signaling Pathway ◽  
Biogenic Selenium Nanoparticles

Biogenic SeNPs synthesized by Lactobacillus casei ATCC 393 reversed diquat-induced oxidative damage to the epithelium by activating the Nrf2 signaling pathway.

scholarly journals Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H2O2-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 121 ◽  
Author(s):  
Lina Qi ◽  
Jingle Jiang ◽  
Jingfei Zhang ◽  
Lili Zhang ◽  
Tian Wang
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Protective Effects ◽  
Human Trophoblast ◽  
Nrf2 Signaling Pathway ◽  
Antioxidant Proteins ◽  
Pre Treatment ◽  
Induced Apoptosis ◽  
Excessive Accumulation

Pregnancy complications are associated with oxidative stress induced by accumulation of trophoblastic ROS in the placenta. We employed the human trophoblast HTR8/SVneo cell line to determine the effect of curcumin pre-treatment on H2O2-induced oxidative damage in HTR8/Sveo cells. Cells were pretreated with 2.5 or 5 μM curcumin for 24 h, and then incubated with 400 μM H2O2 for another 24 h. The results showed that H2O2 decreased the cell viability and induced excessive accumulation of reactive oxygen species (ROS) in HTR8/Sveo cells. Curcumin pre-treatment effectively protected HTR8/SVneo cells against oxidative stress-induced apoptosis via increasing Bcl-2/Bax ratio and decreasing the protein expression level of cleaved-caspase 3. Moreover, curcumin pre-treatment alleviated the excessive oxidative stress by enhancing the activity of antioxidative enzymes. The antioxidant effect of curcumin was achieved by activating Nrf2 and its downstream antioxidant proteins. In addition, knockdown of Nrf2 by Nrf2-siRNA transfection abolished the protective effects of curcumin on HTR8/SVneo cells against oxidative damage. Taken together, our results show that curcumin could protect HTR8/SVneo cells from H2O2-induced oxidative stress by activating Nrf2 signaling pathway.

Protective effect of seleno-amino-oligosaccharide on oxidative damage of IPEC-1 cells by activating Keap1/Nrf2 signaling pathway

2020 ◽  
Vol 155 ◽  
pp. 972-978 ◽  
Author(s):  
Xing-Wei Xiang ◽  
Zhong-Shan Zhang ◽  
Yu-Fang Zhou ◽  
Tian-Yi Zhou ◽  
Pei-Long Sun ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Nrf2 Signaling Pathway

scholarly journals Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Mengchuan Xu ◽  
Qiang Niu ◽  
Yunhua Hu ◽  
Gangling Feng ◽  
Haixia Wang ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Oxidative Stress Marker ◽  
Average Growth ◽  
Methylation Index ◽  
Arsenic Methylation ◽  
Nrf2 Signaling Pathway ◽  
Mrna And Protein Expression

Purpose. To investigate the effects of grape seed proanthocyanidin extract (GSPE) on oxidative damage and arsenic (As) methylation and to clarify the role of Nrf2 in the process. Methods. L-02 cells were treated with arsenic (25 μM) and GSPE (10, 25, and 50 mg/L) for 24 h. Cell viability was analyzed by MTT assay. Cell apoptosis and ROS fluorescence were detected by flow cytometry. Oxidative stress marker levels were measured using commercial kits. mRNA and protein expression were detected by qRT-PCR and western blotting. The cellular concentrations of methylation products were measured by HPLC-HGAFS. Arsenic methylation ability of cells was determined. Results. Cell survival rate was significantly lower in the As group than in the control group (P<0.05), while cell apoptosis increased and the number of apoptotic cells decreased gradually after GSPE intervention. Superoxide dismutase, glutathione, and sulfhydryl levels in the intervention group were significantly higher (P<0.05), while MDA and ROS levels were significantly lower (P<0.05) than those in the As group. The mRNA and protein expression of Nrf2, HO-1, NQO1, and glutathione-S-transferase increased in the As + GSPE group compared with that in the As group (P<0.05). GSPE significantly increased methylated As level, primary methylation index, secondary methylation index, average growth rate of methylation, and average methylation speed compared with the GSPE untreated group (P<0.05). After Nrf2 inhibition, the effect of GSPE decreased significantly. Conclusion. GSPE activates the Nrf2 signaling pathway to antagonize As-induced oxidative damage and to promote As methylation metabolism. Therefore, GSPE may be a potential agent for relieving As-induced hepatotoxicity.

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