{"title":"Psychostimulants influence oxidative stress and redox signatures: the role of DNA methylation.","authors":"Vaishnavi Sundar, Tamizhselvi Ramasamy, Mayur Doke, Thangavel Samikkannu","doi":"10.1080/13510002.2022.2043224","DOIUrl":"10.1080/13510002.2022.2043224","url":null,"abstract":"<p><p><b>Objective:</b> Psychostimulant use induces oxidative stress and alters redox imbalance, influencing epigenetic signatures in the central nervous system (CNS). Among the various epigenetic changes, DNA methylation is directly linked to oxidative stress metabolism via critical redox intermediates such as NAD+, S-adenosylmethionine (SAM), and 2-oxoglutarate. Fluctuations in these intermediates directly influence epigenetic signatures, which leads to detectable alterations in gene expression and protein modification. This review focuses on recent advances in the impact of psychostimulant use on redox-imbalance-induced DNA methylation to develop novel epigenetics-based early interventions. <b>Methods:</b> This review is based on collective research data obtained from the PubMed, Science Direct, and Medline databases. The keywords used in the electronic search in these databases were redox, substance use disorder, psychostimulants, DNA methylation, and neurological diseases. <b>Results:</b> Instability in DNA methylation levels and redox expression effects are reported in various behavioral models stimulated by psychostimulants and opioids, indicating the widespread involvement of epigenetic changes in DNA methylation signatures in neurological disorders. <b>Discussion:</b> This review summarizes the need for more studies and experimental evaluations of DNA-methylation-based strategies that may help to understand the association between psychostimulant use and oxidative stress or redox-linked metabolic recalibration influencing neuronal impairments.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"27 1","pages":"53-59"},"PeriodicalIF":5.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8890556/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10265901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Damage-associated molecular patterns in vitiligo: igniter fuse from oxidative stress to melanocyte loss.","authors":"Jingying Wang, Yinghao Pan, Guangmin Wei, Hanxiao Mao, Rulan Liu, Yuanmin He","doi":"10.1080/13510002.2022.2123864","DOIUrl":"https://doi.org/10.1080/13510002.2022.2123864","url":null,"abstract":"<p><strong>Objectives: </strong>The pathogenesis of vitiligo remains unclear. In this review, we comprehensively describe the role of damage associated molecular patterns (DAMPs) during vitiligo pathogenesis.</p><p><strong>Methods: </strong>Published papers on vitiligo, oxidative stress and DAMPs were collected and reviewed via database searching on PubMed, MEDLINE and Embase, etc.</p><p><strong>Results: </strong>Oxidative stress may be an important inducer of vitiligo. At high oxidative stress levels, damage-associated molecular patterns (DAMPs) are released from keratinocytes or melanocytes in the skin and induce downstream immune responses during vitiligo. Treatment regimens targeting DAMPs can effectively improve disease severity.</p><p><strong>Discussion: </strong>DAMPs play key roles in initiating host defenses against danger signals, deteriorating the condition of vitiligo. DAMP levels in serum and skin may be used as biomarkers to indicate vitiligo activity and prognosis. Targeted therapies, incorporating HMGB1, Hsp70, and IL-15 could significantly improve disease etiology. Thus, novel strategies could be identified for vitiligo treatment by targeting DAMPs.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"27 1","pages":"193-199"},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9518600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9211143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-05-10DOI: 10.1080/13510002.2022.2074128
R. Akhigbe, D. T. Oluwole, T. E. Adegoke, M. Hamed, D. Anyogu, A. Ajayi
{"title":"Suppression of glutathione system and upregulation of caspase 3-dependent apoptosis mediate rohypnol-induced gastric injury","authors":"R. Akhigbe, D. T. Oluwole, T. E. Adegoke, M. Hamed, D. Anyogu, A. Ajayi","doi":"10.1080/13510002.2022.2074128","DOIUrl":"https://doi.org/10.1080/13510002.2022.2074128","url":null,"abstract":"ABSTRACT Objectives: This study investigated the impact of rohypnol on gastric tissue integrity. Methods: Forty male Wistar rats were randomized into control, low dose rohypnol-treated, high dose rohypnol-treated, low dose rohypnol-treated recovery and high dose rohypnol-treated recovery groups. Results: Rohypnol caused significant rise in gastric malondialdehyde (MDA), oxidized glutathione (GSSG), nitric oxide (NO), tumour necrotic factor-α (TNF-α), and interleukin-6 (IL-6) levels. Also, rohypnol caused reductions in gastric reduced glutathione (GSH) (as well as GSH/GSSG), and activities of superoxide dismutase (SOD), catalase, glutathione-S-transferase (GST), glutathione peroxidase (GPx), cyclo-oxygenase (COX-2). Furthermore, rohypnol upregulated caspase 3 activity and induced gastric DNA damage, evident by a rise in 8-hydroxydeoxyguanosine (8-OHdG) and DNA fragmentation index (DFI) in gastric tissue. These alterations were coupled with reduced gastric weight and distorted gastric cytoarchitecture. Cessation of rohypnol caused a significant but not complete reversal of rohypnol-induced gastric damage. Conclusion: This study revealed that rohypnol induced gastric injury by suppressing glutathione content and COX-2 activity, and upregulating caspase 3-dependent apoptosis, which was partly reversed by rohypnol withdrawal.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"3 1","pages":"111 - 118"},"PeriodicalIF":3.8,"publicationDate":"2022-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79873643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-04-28DOI: 10.1080/13510002.2022.2069534
Sen Zhu, Xuan Li, B. Dang, Fen-Shiun Wu, K. Gou, Chunming Wang, Changjun Lin
{"title":"Hydrogen sulfide protects retina from blue light-induced photodamage and degeneration via inhibiting ROS-mediated ER stress-CHOP apoptosis signal","authors":"Sen Zhu, Xuan Li, B. Dang, Fen-Shiun Wu, K. Gou, Chunming Wang, Changjun Lin","doi":"10.1080/13510002.2022.2069534","DOIUrl":"https://doi.org/10.1080/13510002.2022.2069534","url":null,"abstract":"ABSTRACT Background: Hydrogen sulfide (H2S) is a small reducing gas molecule with various biological functions such as anti-oxidative, anti-apoptotic and anti-inflammatory activities. In this study, we investigated the therapeutic effects of exogenous H2S in the experimental models of retinal photodamage in vivo and in vitro. Methods: Rats with open eyelids were pretreated with H2S (80~120 μmol/kg) for 10 days and then continuously exposed to blue light (435~445nm, 11.2W/m2) for 8 h to establish in vivo experimental model. ARPE-19 cells were pretreated with H2S and then exposed to blue light to establish in vitro experimental model. Results: In vivo experiments, H2S significantly ameliorated blue light-induced retinal oxidative stress, apoptosis and degeneration. Moreover, H2S inhibited the activation of blue light-induced endoplasmic reticulum (ER) stress CHOP apoptotic signaling. In vitro experiments, H2S improved blue light-induced oxidative stress and oxidative damage. H2S inhibited ROS-mediated activation of ER stress CHOP apoptotic signaling. H2S alleviated blue light-induced apoptosis and increases cell viability. The ER stress inhibitor 4-PBA alleviated blue light-induced apoptosis and increases cell viability. Conclusion: Taken together, these results indicate that H2S can inhibit ROS-mediated ER stress-CHOP apoptosis signal, thereby alleviating blue light-triggered retinal apoptosis and degeneration.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"1 1","pages":"100 - 110"},"PeriodicalIF":3.8,"publicationDate":"2022-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87430332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-03-31DOI: 10.1080/13510002.2022.2057707
Djurdja Jerotić, J. Ranin, Z. Bukumirić, Tatjana Djukic, V. Ćorić, A. Savić-Radojević, N. Todorović, M. Ašanin, M. Ercegovac, I. Milošević, M. Plješa-Ercegovac, G. Stevanović, M. Matić, Tatjana Simić
{"title":"SOD2 rs4880 and GPX1 rs1050450 polymorphisms do not confer risk of COVID-19, but influence inflammation or coagulation parameters in Serbian cohort","authors":"Djurdja Jerotić, J. Ranin, Z. Bukumirić, Tatjana Djukic, V. Ćorić, A. Savić-Radojević, N. Todorović, M. Ašanin, M. Ercegovac, I. Milošević, M. Plješa-Ercegovac, G. Stevanović, M. Matić, Tatjana Simić","doi":"10.1080/13510002.2022.2057707","DOIUrl":"https://doi.org/10.1080/13510002.2022.2057707","url":null,"abstract":"ABSTRACT Objectives: Due to the role of oxidative stress in the pathophysiology of COVID-19, it is biologically plausible that inter-individual differences in patients’ clinical manifestations might be affected by antioxidant genetic profile. The aim of our study was to assess the distribution of antioxidant genetic polymorphisms Nrf2 rs6721961, SOD2 rs4880, GPX1 rs1050450, GPX3 rs8177412, and GSTP1 (rs1695 and rs1138272) haplotype in COVID-19 patients and controls, with special emphasis on their association with laboratory biochemical parameters. Methods: The antioxidant genetic polymorphisms were assessed by appropriate PCR methods in 229 COVID-19 patients and 229 matched healthy individuals. Results: Among examined polymorphisms, only GSTP1 haplotype was associated with COVID-19 risk (p = 0.009). Polymorphisms of SOD2 and GPX1 influenced COVID-19 patients’ laboratory biochemical profile: SOD2*Val allele was associated with increased levels of fibrinogen (p = 0.040) and ferritin (p = 0.033), whereas GPX1*Leu allele was associated with D-dimmer (p = 0.009). Discussion: Our findings regarding the influence of SOD2 and GPX1 polymorphisms on inflammation and coagulation parameters might be of clinical importance. If confirmed in larger cohorts, these developments could provide a more personalized approach for better recognition of patients prone to thrombosis and those for the need of targeted antioxidant therapy.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"42 1","pages":"85 - 91"},"PeriodicalIF":3.8,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90859089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-03-16DOI: 10.1080/13510002.2022.2051964
Hee Jo Han, H. Shin, Young-Chul Choi, S. M. Kim, Seung Woo Kim
{"title":"Serum uric acid level predicts the progression of amyotrophic lateral sclerosis following treatment with edaravone","authors":"Hee Jo Han, H. Shin, Young-Chul Choi, S. M. Kim, Seung Woo Kim","doi":"10.1080/13510002.2022.2051964","DOIUrl":"https://doi.org/10.1080/13510002.2022.2051964","url":null,"abstract":"ABSTRACT\u0000 Introduction Uric acid and edaravone might exert a neuroprotective effect in amyotrophic lateral sclerosis (ALS) by reducing oxidative stress. We analyzed whether the treatment effect of edaravone is pronounced in patients whose uric acid level increased after the treatment with edaravone. Materials and methods Forty patients with ALS who underwent treatment with edaravone were included. Baseline uric acid level and the rate of decline in uric acid after edaravone treatment were recorded. The rate of change of ALS functional rating scale-revised (ΔALSFRS-R/month) was calculated based on baseline ALSFRS-R score and ALSFRS-R score 6–24 weeks after the treatment. Results The serum uric acid levels decreased after treatment in 26 (65%) patients and increased in 12 (30%) patients. The ΔALSFRS-R/month was significantly faster in patients whose uric acid decreased (median 1.5 [Q1–Q3, 0.7–3.1]) than in patients whose uric acid increased (0.2 [0–1.0], p = 0.021). A high baseline uric acid level and low rate of decline in uric acid was associated with slower disease progression after adjusting for age, initial symptoms, and riluzole administration (p = 0.030 and p = 0.041, respectively). Discussion High baseline values and low rate of decline in uric acid may predict slow disease progression in ALS patients treated with edaravone.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"79 - 84"},"PeriodicalIF":3.8,"publicationDate":"2022-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76820560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-03-14DOI: 10.1080/13510002.2022.2050086
M. Atef, Noha M. Shafik, Y. Hafez, M. Watany, Amal A. Selim, Heba M. Shafik, Omnia Safwat El-Deeb
{"title":"The evolving role of long noncoding RNA HIF1A-AS2 in diabetic retinopathy: a cross-link axis between hypoxia, oxidative stress and angiogenesis via MAPK/VEGF-dependent pathway","authors":"M. Atef, Noha M. Shafik, Y. Hafez, M. Watany, Amal A. Selim, Heba M. Shafik, Omnia Safwat El-Deeb","doi":"10.1080/13510002.2022.2050086","DOIUrl":"https://doi.org/10.1080/13510002.2022.2050086","url":null,"abstract":"ABSTRACT Background Diabetic retinopathy (DR) signifies a frequent serious diabetic complication influencing retinal structure and function. Dysregulation of lncRNAs drives a wide array of human diseases especially diabetes; thus, we aimed to study lncRNA HIF1A-AS2 role and its interplay with hypoxia, oxidative stress (OS), and angiogenesis in DR. Materials and methods 60 DM patients in addition to 15 healthy subjects. were enrolled. LncRNA HIF1A-AS2 mRNA relative gene expression was assessed. Hypoxia inducible factor 1-alpha (HIF-1α), vascular endothelial growth factor (VEGF), mitogen activated protein kinase (MAPK), and endoglin levels were assessed. Detection of DNA damage using comet assay, and Redox status parameters were also detected. Results LncRNA HIF1A-AS2 expression was significantly increased in diabetic patients with the highest levels in proliferative DR patients. Moreover, HIFα, VEGF, MAPK, and Endogolin levels were significantly higher in the diabetic patients compared to control group with the highest levels in in proliferative DR patients. Significant DNA damage in comet assay was observed to be the highest in this group. Conclusion We observed for the first time the imminent role of long noncoding RNA HIF1A-AS2 in DR throughout its stages and its interplay with hypoxia, OS, and angiogenesis via MAPK/VEGF-dependent pathway.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"27 Suppl 1 1","pages":"70 - 78"},"PeriodicalIF":3.8,"publicationDate":"2022-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80302761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-03-04DOI: 10.1080/13510002.2022.2046425
Omnia Safwat El-Deeb, Rasha Osama El-Esawy, H. Al-Shenawy, H. Ghanem
{"title":"Modulating gut dysbiosis and mitochondrial dysfunction in oxazolone-induced ulcerative colitis: the restorative effects of β-glucan and/or celastrol","authors":"Omnia Safwat El-Deeb, Rasha Osama El-Esawy, H. Al-Shenawy, H. Ghanem","doi":"10.1080/13510002.2022.2046425","DOIUrl":"https://doi.org/10.1080/13510002.2022.2046425","url":null,"abstract":"ABSTRACT Objectives Microbiome–Mitochondria interaction is gaining a significant attention; thus, studying its mechanism emerges as a must to provide restorative lines in managing diseases. The aim is to study the mechanistic effects of β-Glucan and/or Celastrol in oxazolone-induced ulcerative colitis (UC). Methods 75 Wistar rats were allocated into 5 equal groups. Group I: control group. Group II: UC group, Group III: β-Glucan-treated UC group, Group IV: Celastrol-treated UC group & Group V: mutual treatment group. All groups were subjected to the detection of free fatty acid receptor 2 (FFAR-2) and peroxisome proliferator-activated receptor gamma co-activator1α (PGC-1α) mRNA gene expressions. Citrate synthase (CS) activity, mitochondrial membrane potential (MMP), ATP concentration, reactive oxygen species (ROS) were detected. Trimethylamine N-oxide (TMAO) concentration was measured. Results After treatment we monitored significant upregulation of FFAR-2 and PGC-1α mRNA expression. Likewise, ATP level and CS activity were significantly increased. On the contrary, there was a significant lessening in ROS and TMAO levels with improvement of MMP. Conclusion Mutual use of β- Glucan and Celastrol had a greater effect than each alone against UC, which is considered a novel finding highlighting the ameliorative effects of this combined treatment in modulating Microbiome/Mitochondria axis, thus launching promising avenues for UC.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"89 2 1","pages":"60 - 69"},"PeriodicalIF":3.8,"publicationDate":"2022-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83629372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2021-12-01DOI: 10.1080/13510002.2021.2004047
Guang-Min Yu, Li-Feng Zhou, Bi-Xia Zeng, Jing-Jun Huang, Xiao-Jun She
{"title":"The antioxidant effect of triptolide contributes to the therapy in a collagen-induced arthritis rat model.","authors":"Guang-Min Yu, Li-Feng Zhou, Bi-Xia Zeng, Jing-Jun Huang, Xiao-Jun She","doi":"10.1080/13510002.2021.2004047","DOIUrl":"10.1080/13510002.2021.2004047","url":null,"abstract":"<p><strong>Background: </strong>As a chronic autoimmune disease, rheumatoid arthritis (RA) is related to oxidative stress, which may lead to the occurrence and persistence of inflammation in RA. The purpose of this study is to evaluate the potential antioxidant effect of triptolide in collagen-induced arthritis (CIA) rat model.</p><p><strong>Methods: </strong>We examined the severity of arthritis, levels of local and systemic oxidative stress, periarticular bone erosion and weight of organs in CIA rats treated with triptolide.</p><p><strong>Results: </strong>We found that triptolide decreased the paw thickness and clinical arthritis score, significantly. The mRNA expression and activity of myeloperoxidase and inducible nitric oxide synthase were remarkably decreased in the paws of the CIA rats after triptolide treatment. Triptolide significantly inhibited the levels of nitrite and nitrate in serum, as well as the urinary level of dityrosine. Triptolide treatment also markedly increased bone volume of tibia, but suppressed epiphyseal plate thickness of both femur and tibia. In addition, there was no significant difference in the weight of organs after the therapy, except decreased spleen weight.</p><p><strong>Conclusions: </strong>These results suggested that the local and systemic oxidative stress was enhanced in the CIA rats and the therapeutic dose of triptolide had a definite antioxidant effect.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"26 1","pages":"197-202"},"PeriodicalIF":5.2,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8604496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39740958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2021-12-01DOI: 10.1080/13510002.2021.1871814
Nabila Jahan, Apu Chowdhury, Ting Li, Ke Xu, Fen Wei, Sicen Wang
{"title":"Neferine improves oxidative stress and apoptosis in benign prostate hyperplasia via Nrf2-ARE pathway.","authors":"Nabila Jahan, Apu Chowdhury, Ting Li, Ke Xu, Fen Wei, Sicen Wang","doi":"10.1080/13510002.2021.1871814","DOIUrl":"https://doi.org/10.1080/13510002.2021.1871814","url":null,"abstract":"<p><strong>Background: </strong>Progression of Benign Prostate hyperplasia (BPH) is vulnerable to oxidative stress (OS) and prostatic enlargement among the aging males through apoptosis deregulation. Our present study aimed to investigate the effect of neferine (NF) in the regulation of oxidative stress and apoptosis in human BPH-1 cells.</p><p><strong>Methods: </strong>BPH epithelial cell line BPH-1 was treated with NF for 24 and 48 h. To measure oxidative stress (OS) we investigated MDA, SOD, and GST expression along with Nrf2 and its downstream gene and protein expression. Cell proliferation and apoptosis regulation was assayed with respective methods.</p><p><strong>Results: </strong>Investigation revealed NF remarkably activate Nrf2 and its downstream proteins HO-1 and NQO1 at 48 h more substantially. Nrf2/Keap1 relative gene and protein expression indicated that NF might trigger Nrf2 upregulation by decreasing Keap1 expression. Both NF concentrations (3 µM and 9 µM) were able to deplete ROS and lipid peroxidation, concurrently, up-regulated SOD and GST. NF reduced cell proliferation significantly along with the regulation of apoptotic proteins Bax, Bcl2, Cyt-C, Caspase 9, and Caspase 3 at the same time (48 h).</p><p><strong>Conclusion: </strong>This study is the first to manifest that NF may potentially regulate BPH by counterbalancing between OS and apoptosis through the activation of Nrf2-ARE pathway.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"26 1","pages":"1-9"},"PeriodicalIF":3.8,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/13510002.2021.1871814","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38795382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}