Modulation of Oxidative Stress by 17 β-Estradiol and Genistein in Human Hepatic Cell Lines In Vitro

Surico, Daniela; Ercoli, Alfredo; Farruggio, Serena; Raina, Giulia; Filippini, Davide; Mary, David A.S.G.; Minisini, Rosalba; Surico, N; Pirisi, Mario; Grossini, Elena

doi:10.1159/000478752

Cited by 34 publications

(43 citation statements)

References 45 publications

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“…Gloria Gutiérrez-Venegas et al revealed that genistein was able to hinder the LPS-induced inflammatory response in H9c2 cells and decrease damage in myocardial cells due to LPS exposure [20]. Surico D et al reported that genistein and 17β-estradiol counteract the effects of peroxidation by an intracellular signal related to Akt and p38 MAPK and through the involvement of ERs and GPER [21]. In addition, Catmull S et al proposed that dietary genistein rescued reduced basal chloride in the diabetic Jejunum via sex-dependent mechanisms [22].…”

Section: Discussionmentioning

confidence: 99%

Genistein Inhibited Estradiol-Induced Vascular Endothelial Cell Injury by Downregulating the FAK/Focal Adhesion Pathway

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: In this study, we aimed to investigate the effects of genistein on the focal adhesion signaling pathway through its regulation of FAK. Genistein ultimately restored and alleviated estradiol-induced vascular endothelial injury. Methods: Microarray analysis was used to select differentially expressed genes. MTT assay was performed to detect the cell activity, and ROS test and NO test were performed to detect the degree of damage to HUVECs (human umbilical vein endothelial cells). The relative mRNA expression levels and protein expression levels of FAK were tested by western blot and qRT-PCR. GO functional analysis and KEGG pathway analysis were applied to predict the possible relationship between functions and related pathways, and transwell assay was used to detect cell invasion and migration. Results: FAK was highly expressed in the HUVECs treated with estradiol (HU-ESTs). Cell viability and NO level decreased, whereas ROS level increased in the HU-ESTs. Effective knockdown of FAK in HU-ESTs elevated cell viability and NO levels while suppressing ROS levels. In addition, inhibition of FAK greatly decreased cell invasion and migration, while the overexpression of FAK enhanced cell invasion and migration. KEGG further indicated focal adhesion pathways were activated. Genistein elevated HU-EST viability, and NO and ROS level increased in a concentration dependent manner. Transwell and western blot assays revealed that genistein could reduce the FAK expression levels and alleviate the damage to the HU-ESTs. Conclusion: FAK overexpression promoted invasion and migration of the HU-ESTs. However, genistein greatly suppressed FAK and estradiol-induced vascular endothelial cell injury.

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Section: Discussionmentioning

confidence: 99%

Genistein Inhibited Estradiol-Induced Vascular Endothelial Cell Injury by Downregulating the FAK/Focal Adhesion Pathway

Liu

et al. 2018

Cell Physiol Biochem

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“…Cell viability was examined by using the 1% 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT; Life Technologies, Italia, Monza, Italy) dye, as previously described [ 19 , 22 , 23 ] both in pre-adipocytes and in white adipocytes (treated with DM) and in brown adipocytes (treated with DM supplemented with 1 nM T3). Pre-adipocytes/adipocytes were treated in physiological and peroxidative conditions with adiponectin (100 µM; Sigma) and genistein at different doses (10 pM, 1 µM, 50 µM and 200 µM; Sigma) for 30 min.…”

Section: Methodsmentioning

confidence: 99%

“…Mitochondrial membrane potential measurement was performed with JC-1 assay as previously described for cell viability. After stimulation, the treatment medium was removed and cells were incubated with 5,51,6,61-tetrachloro-1,11,3,31 tetraethylbenzimidazolyl carbocyanine iodide (JC-1) 1X diluted in Assay Buffer 1X for 15 min at 37 °C, following the manufacturer’s instruction and as previously performed (Invitrogen, Life Technologies Europe BV, Monza, Italy) [ 19 , 22 , 23 ]. After incubation, the cells were washed twice with Assay Buffer 1× and then the mitochondrial membrane potential was determined by measuring the red (excitation 550 nm/emission 600 nm) and green (excitation 485 nm/emission 535 nm) fluorescence through a spectrometer (BS1000 Spectra Count).…”

Section: Methodsmentioning

confidence: 99%

“…After treatments, the reactions were stopped by removing the medium and washing with PBS, which was followed by staining with 10 µM H2DCFDA for 20 min at 37 °C. The fluorescence intensity of H2DCFDA was measured at an excitation and emission wavelength of 485 nm and 530 nm using a spectrometer, as previously performed (BS1000 Spectra Count) [ 19 , 22 , 23 ]. Experiments were repeated five times in pre-adipocytes taken from each patient.…”

Section: Methodsmentioning

confidence: 99%

“…The protective effects elicited by genistein could be related to its effect on adipogenesis, which would be inhibited by mechanisms related to 5’ adenosine monophosphate-activated protein kinase α/β (AMPKα/β), [ 1 , 16 , 17 ]. Also, the anti-inflammatory and antioxidant properties exerted by genistein in different cell types [ 18 , 19 , 20 ] could represent a mechanism leading to its protective effects. So far however, information about those issue is scarce.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Genistein on Differentiation and Viability of Human Visceral Adipocytes

et al. 2018

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Obesity can lead to pathological growth of adipocytes by inducing inflammation and oxidative stress. Genistein could be a potential candidate for the treatment of obesity due to its antioxidant properties. Specific kits were used to examine the effects of genistein vs adiponectin on human visceral pre-adipocytes differentiation, cell viability, mitochondrial membrane potential, and oxidative stress in pre-adipocytes and in white/brown adipocytes. Western Blot was performed to examine changes in protein activation/expression. Genistein increased human visceral pre-adipocytes differentiation and browning, and caused a dose-related improvement of cell viability and mitochondrial membrane potential. Similar effects were observed in brown adipocytes and in white adipocytes, although in white cells the increase of cell viability was inversely related to the dose. Moreover, genistein potentiated AMP-activated protein kinase (AMPK)/mitofusin2 activation/expression in pre-adipocytes and white/brown adipocytes and protected them from the effects of hydrogen peroxide. The effects caused by genistein were similar to those of adiponectin. The results obtained showed that genistein increases human visceral pre-adipocytes differentiation and browning, protected against oxidative stress in pre-adipocytes and white/brown adipocytes through mechanisms related to AMPK-signalling and the keeping of mitochondrial function.

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Connectivity of the Cerebello-Thalamo-Cortical Pathway in Survivors of Childhood Leukemia Treated With Chemotherapy Only

et al. 2020

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IMPORTANCE Treatment with contemporary chemotherapy-only protocols is associated with risk for neurocognitive impairment among survivors of childhood acute lymphoblastic leukemia (ALL). OBJECTIVE To determine whether concurrent use of methotrexate and glucocorticoids is associated with interference with the antioxidant system of the brain and damage and disruption of glucocorticoid-sensitive regions of the cerebello-thalamo-cortical network. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study was conducted from December 2016 to July 2019 in a single pediatric cancer tertiary care center. Participants included survivors of childhood ALL who were more than 5 years from cancer diagnosis, age 8 years or older, and treated on an institutional chemotherapy-only protocol. Age-matched community members were recruited as a control group. Data were analyzed from August 2017 to August 2020. EXPOSURE ALL treatment using chemotherapy-only protocols. MAIN OUTCOMES AND MEASURES This study compared brain volumes between survivors and individuals in a community control group and examined associations among survivors of methotrexate and dexamethasone exposure with neurocognitive outcomes. Functional and effective connectivity measures were compared between survivors with and without cognitive impairment. The Rey-Osterrieth complex figure test, a neurocognitive evaluation in which individuals are asked to copy a figure and then draw the figure from memory, was scored according to published guidelines and transformed into age-adjusted z scores based on nationally representative reference data and used to measure organization and planning deficits. β values for neurocognitive tests represented the amount of change in cerebellar volume or chemotherapy exposure associated with 1 SD change in neurocognitive outcome by z score (mm 3 /1 SD in z score for cerebellum, mm 3 /[g×hr/L] for dexamethasone and methotrexate AUC, and mm 3 /intrathecal count for total intrathecal count). RESULTS Among 302 eligible individuals, 218 (72%) participated in the study and 176 (58%) had usable magnetic resonance imaging (MRI) results. Among these, 89 (51%) were female participants and the mean (range) age was 6.8 (1-18) years at diagnosis and 14.5 (8-27) years at evaluation. Of 100 community individuals recruited as the control group, 82 had usable MRI results; among these, 35 (43%) were female individuals and the mean (range) age was 13.8 (8-26) years at evaluation. There was no significant difference in total brain volume between survivors and individuals in the control group. Survivors of both sexes showed decreased mean (SD) cerebellar volumes compared with the control population (female: 70 568 [6465] mm 3 vs 75 134 [6780] mm 3 ; P < .001; male: 77 335 [6210] mm 3 vs 79 020 [7420] mm 3 ; P < .001). In female survivors, decreased cerebellar volume was associated with worse performance in Rey-Osterrieth complex figure test (left cerebellum: β = 55.54;

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Modulation of Oxidative Stress by 17 β-Estradiol and Genistein in Human Hepatic Cell Lines In Vitro

Cited by 34 publications

References 45 publications

Genistein Inhibited Estradiol-Induced Vascular Endothelial Cell Injury by Downregulating the FAK/Focal Adhesion Pathway

Genistein Inhibited Estradiol-Induced Vascular Endothelial Cell Injury by Downregulating the FAK/Focal Adhesion Pathway

Effects of Genistein on Differentiation and Viability of Human Visceral Adipocytes

Connectivity of the Cerebello-Thalamo-Cortical Pathway in Survivors of Childhood Leukemia Treated With Chemotherapy Only

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