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26 result(s) for "Medina-Campos, Omar Noel"
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Isoliquiritigenin Pretreatment Induces Endoplasmic Reticulum Stress-Mediated Hormesis and Attenuates Cisplatin-Induced Oxidative Stress and Damage in LLC-PK1 Cells
Isoliquiritigenin (IsoLQ) is a flavonoid with antioxidant properties and inducer of endoplasmic reticulum (ER) stress. In vitro and in vivo studies show that ER stress-mediated hormesis is cytoprotective; therefore, natural antioxidants and ER stress inducers have been used to prevent renal injury. Oxidative stress and ER stress are some of the mechanisms of damage involved in cisplatin (CP)-induced nephrotoxicity. This study aims to explore whether IsoLQ pretreatment induces ER stress and produces hormesis to protect against CP-induced nephrotoxicity in Lilly Laboratories Cell-Porcine Kidney 1 (LLC-PK1) cells. During the first stage of this study, both IsoLQ protective concentration and pretreatment time against CP-induced toxicity were determined by cell viability. At the second stage, the effect of IsoLQ pretreatment on cell viability, ER stress, and oxidative stress were evaluated. IsoLQ pretreatment in CP-treated cells induces expression of glucose-related proteins 78 and 94 kDa (GRP78 and GRP94, respectively), attenuates CP-induced cell death, decreases reactive oxygen species (ROS) production, and prevents the decrease in glutathione/glutathione disulfide (GSH/GSSG) ratio, free thiols levels, and glutathione reductase (GR) activity. These data suggest that IsoLQ pretreatment has a moderately protective effect on CP-induced toxicity in LLC-PK1 cells, through ER stress-mediated hormesis, as well as by the antioxidant properties of IsoLQ.
Protective Effect of Curcumin on D-Galactose-Induced Senescence and Oxidative Stress in LLC-PK1 and HK-2 Cells
D-galactose has been widely used as an inducer of cellular senescence and pathophysiological processes related to aging because it induces oxidative stress. On the other hand, the consumption of antioxidants such as curcumin can be an effective strategy to prevent phenotypes related to the enhanced production of reactive oxygen species (ROS), such as aging and senescence. This study aimed to evaluate the potential protective effect of curcumin on senescence and oxidative stress and endoplasmic reticulum stress induced by D-galactose treatment in Lilly Laboratories Culture-Porcine Kidney 1 (LLC-PK1) and human kidney 2 (HK-2) proximal tubule cell lines from pig and human, respectively. For senescence induction, cells were treated with 300 mM D-galactose for 120 h and, to evaluate the protective effect of the antioxidant, cells were treated with 5 µM curcumin for 24 h and subsequently treated with curcumin + D-galactose for 120 h. In LLC-PK1 cells, curcumin treatment decreased by 20% the number of cells positive for senescence-associated (SA)-β-D-galactosidase staining and by 25% the expression of 8-hydroxy-2′-deoxyguanosine (8-OHdG) and increased by 40% lamin B1 expression. In HK-2 cells, curcumin treatment increased by 60% the expression of proliferating cell nuclear antigen (PCNA, 50% Klotho levels, and 175% catalase activity. In both cell lines, this antioxidant decreased the production of ROS (20% decrease for LLC-PK1 and 10 to 20% for HK-2). These data suggest that curcumin treatment has a moderate protective effect on D-galactose-induced senescence in LLC-PK1 and HK-2 cells.
Goats’ Feeding Supplementation with Acacia farnesiana Pods and Their Relationship with Milk Composition: Fatty Acids, Polyphenols, and Antioxidant Activity
Background: Research efforts have focused on the evaluation of the bioactive quality of animal products (milk, cheese, meat, and other by-products) contrasting various feeding strategies coming from different ecological zones. The study aimed to describe the fatty acids (FA), polyphenols (P), bioactive compounds (BC), and antioxidant activity (AA) of goat’s milk. Methods: Dairy goats were fed with five systems: (1) Grazing; (2) conventional diet (CD); (3) CD + 10% of Acacia farnesiana (AF) pods; (4) CD + 20% AF; and (5) CD + 30% AF. The fatty acid profile, health promoting and thrombogenic indexes were calculated. Milk extracts were evaluated by HPLC to determent phenolic compounds (gallic, caffeic, chlorogenic, and ferulic acids, catechin, epicatechin, and quercetin). Antioxidant activity of goat’s milk extract was evaluated using 2,2-diphenyl-1-picrylhydrazyl radical (DPPH•), oxygen radical absorbance capacity (ORAC), and the ferric reducing antioxidant power (FRAP) assays. Results: Conventional diet showed the highest content of polyunsaturated fatty acids while grazing showed the best n-6:n-3 and the linoleic:alpha linolenic acid ratio. Similarly, grazing and AF boosted the polyphenol content. Conclusions: Acacia farnesiana inclusion in the goats’ diets increased the presence of bioactive compounds and the antioxidant activity while diminishing the cholesterol content of goat’s milk.
NAC Pre-Administration Prevents Cardiac Mitochondrial Bioenergetics, Dynamics, Biogenesis, and Redox Alteration in Folic Acid-AKI-Induced Cardio-Renal Syndrome Type 3
The incidence of kidney disease is increasing worldwide. Acute kidney injury (AKI) can strongly favor cardio-renal syndrome (CRS) type 3 development. However, the mechanism involved in CRS development is not entirely understood. In this sense, mitochondrial impairment in both organs has become a central axis in CRS physiopathology. This study aimed to elucidate the molecular mechanisms associated with cardiac mitochondrial impairment and its role in CRS development in the folic acid-induced AKI (FA-AKI) model. Our results showed that 48 h after FA-AKI, the administration of N-acetyl-cysteine (NAC), a mitochondrial glutathione regulator, prevented the early increase in inflammatory and cell death markers and oxidative stress in the heart. This was associated with the ability of NAC to protect heart mitochondrial bioenergetics, principally oxidative phosphorylation (OXPHOS) and membrane potential, through complex I activity and the preservation of glutathione balance, thus preventing mitochondrial dynamics shifting to fission and the decreases in mitochondrial biogenesis and mass. Our data show, for the first time, that mitochondrial bioenergetics impairment plays a critical role in the mechanism that leads to heart damage. Furthermore, NAC heart mitochondrial preservation during an AKI event can be a valuable strategy to prevent CRS type 3 development.
Antioxidant Enzymes Haplotypes and Polymorphisms Associated with Obesity in Mexican Children
Obesity is a major health problem worldwide and constitutes a sanitary emergency in Mexico, especially childhood obesity. Several studies have proved the relationship between obesity and oxidative stress and the influence of genetic predisposition. This work was aimed to analyze the association of antioxidant enzyme polymorphisms with overweight and obesity in Mexican children and adolescents. A case-control study was performed in 585 children and adolescents aged 3 to 17 years, using two criteria to classify obesity: body mass index (BMI) and body fat percentage (BFP). Anthropometric and biochemical measurements were carried out, and malondialdehyde serum levels were determined. Genotyping was done with the Axiom Genome-Wide LAT microarray, including 68 single nucleotide polymorphisms (SNPs) of the glutathione peroxidase (GPX) and paraoxonase (PON) families. We found six haplotypes associated with obesity—two of them (one in GPX3 and the other in GPX5 and GPX6) in a protective direction when obesity was classified by BMI. The other four haplotypes were associated with obesity when classification was based on BFP—one of them in GPX3 in a protective direction and the others in PON genes conferring obesity risk. In addition, two SNPs, GPX3 rs922429 and GPX4 rs2074451 showed protection against obesity classified by BFP. This study showed genetic susceptibility to oxidative stress in relation to obesity in Mexican children and opens up the possibility that some genetic loci related to obesity are not identified when weight classification is based on BMI.
Tomato lipidic extract plus selenium decrease prostatic hyperplasia, dihydrotestosterone and androgen receptor expression versus finasteride in rats
PurposeEvaluate the therapeutic effect of a tomato lipidic extract (STE) in combination with selenium (Se) on rats with prostatic hyperplasia (PH) and to observe its possible mechanisms of action and synergism versus finasteride.Materials and methods54 male Wistar rats of nine weeks old were divided in Control (C), PH, Finasteride (F), STE, Se, F + STE, F + Se, STE + Se and F + STE + Se with testosterone enanthate (except C). After 4 weeks of treatment administration, prostate weight, bladder weight, diuresis, prooxidant and antioxidant activity, dihydrotestosterone (DHT), androgen receptor (AR) expression and anatomopathological analysis were determined.ResultsSTE + Se decreased prostate weight 53.8% versus 28% in F group, also STE + Se decreased significatively glandular hyperplasia, prooxidant activity, DHT and AR expression and increased diuresis and antioxidant activity versus finasteride which increased MDA in prostate.ConclusionsThese results demonstrate a greater therapeutic and beneficial effect of tomato lipidic extract in combination with Se in young rats with PH with respect to finasteride without increase prooxidant activity.
Selenium in combination with a tomato lipid extract as a therapy for benign prostatic hyperplasia and its alterations in rats with induced BPH
Benign prostatic hyperplasia (BPH) is the most common adenoma in old men. Tomatoes are a rich source of bioactive compounds that, as well as selenium (Se), possess antioxidant and antiproliferative activity. The aim was to evaluate the therapeutic effect of Se in combination with a tomato extract in aged rats with BPH. Aged male Wistar rats were divided in the following groups ( n  = 10 rats/group): Control (C), BPH, BPH + Finasteride (BPH + F), BPH + Tomato Lipidic Extract (BPH + E), BPH + Selenium (BPH + S) and BPH plus E plus S (BPH + E + S). After 4 weeks of treatment, prostate weight, diuresis, antioxidants enzymes, prooxidants and inflammatory markers, growth factors and androgens were determined. BPH + E + S reduced prostate weight by 59.29% and inhibited growth by 99.35% compared to BPH + F which only decreased weight and inhibited growth by 15.31% and 57.54%, respectively. Prooxidant markers were higher with BPH + F (49.4% higher vs. BPH), but BPH + E + S decreased these markers (94.27% vs. BPH) and increased antioxidant activity. Finally, diuresis was higher with the BPH + E + S combination and markers of inflammation and growth factors were significantly lower with respect to BPH + F. Our findings provide a beneficial and protective therapeutic option of E + S directed against androgens, oxidative stress and inflammation that regulates cell proliferation in the prostate gland.
Effect of Dietary Magnesium Content on Intestinal Microbiota of Rats
Background: Magnesium is a mineral that modulates several physiological processes. However, its relationship with intestinal microbiota has been scarcely studied. Therefore, this study aimed to assess the role of dietary magnesium content to modulate the intestinal microbiota of Wistar male rats. Methods: Rats were randomly assigned one of three diets: a control diet (C-Mg; 1000 mg/kg), a low magnesium content diet (L-Mg; 60 mg/kg), and a high magnesium content diet (H-Mg; 6000 mg/kg), for two weeks. After treatment, fecal samples were collected. Microbiota composition was assessed by sequencing the V3–V4 hypervariable region. Results: The C-Mg and L-Mg groups had more diversity than H-Mg group. CF231, SMB53, Dorea, Lactobacillus and Turibacter were enriched in the L-Mg group. In contrast, the phyla Proteobacteria, Parabacteroides, Butyricimonas, and Victivallis were overrepresented in the H-Mg group. PICRUSt analysis indicated that fecal microbiota of the L-Mg group were encoded with an increased abundance of metabolic pathways involving carbohydrate metabolism and butanoate metabolism. Conclusion: Dietary magnesium supplementation can result in intestinal dysbiosis development in a situation where there is no magnesium deficiency. Conversely, low dietary magnesium consumption is associated with microbiota with a higher capacity to harvest energy from the diet.
Association between Serum Uric Acid Levels, Nutritional and Antioxidant Status in Patients on Hemodialysis
Purpose: To determine the relationship between uric acid (UA) and nutritional and antioxidant status in hemodialysis (HD) patients, given that hyperuricemia could be an indicator of good nutritional status possibly because of the antioxidant properties of UA. Methods: Cross-sectional study with 93 patients on HD. Hyperuricemia was considered as UA ≥6.0 mg/dL in females and ≥7.0 mg/dL in males. Nutritional variables were registered. Blood samples were taken before the dialysis session to determine oxidative damage as plasma malondialdehyde (MDA) content, and antioxidant capacity measuring 2,2-diphenyl-piclrylhidrazil radical (DPPH●) scavenging activity and oxygen radical absorbance capacity (ORAC) value. Results: Patients with hyperuricemia had higher creatinine (11.9 vs. 10.5 mg/dL; p = 0.004), potassium (5.5 vs. 5.0 mg/dL; p = 0.014) levels; phase angle (5.8 vs. 4.9; p = 0.005), protein consumption (normalized protein nitrogen appearance, nPNA, 1.03 vs. 0.83; p = 0.013) than normouricemic patients. DPPH● scavenging activity was higher in hyperuricemic subjects (1.139 vs. 1.049 mM Trolox equivalents; p = 0.007); likewise, hyperuricemic subjects had less oxidant damage measured by MDA (10.6 vs. 12.7 nmol/mL; p = 0.020). Subjects with normouricemia were at higher risk of having a reactance to height (Xc/H) ratio less than 35 (OR 2.79; 95% CI, 1.1–7.017, p = 0.028); nPNA < 1.0 (OR 3.78; 95% CI, 1.4–10.2, p = 0.007), diagnosis of cachexia (OR 2.95; 95% CI, 1156–7.518, p = 0.021), potassium levels <5 (OR 2.97; 95% CI, 1.136–7.772, p = 0.023) and PA < 5.5° (OR 3.38; 95% CI, 1.309–8.749, p = 0.012.) Conclusions: Patients with hyperuricemia had higher antioxidant capacity and better nutritional status. Purines and protein restrictions in HD patients with hyperuricemia need to be reviewed individually for each patient. More studies are needed to stablish a cut point of UA levels in renal population.
10-Gingerol Increases Antioxidant Enzymes and Attenuates Lipopolysaccharide-Induced Inflammation by Modulating Adipokines in 3T3-L1 Adipocytes
Background: Obesity increases reactive oxygen species production and alters adipokines levels, resulting in a low-grade chronic inflammation state, which contributes to tissue metabolic dysfunction. 10-gingerol, a phenol present in ginger, has shown potential anti-obesogenic effects in vitro. However, the antioxidant and anti-inflammatory properties of 10-gingerol have not been approached. The aim of this study was to investigate the effects of 10-gingerol on antioxidant enzymes’ expression and adipokine production in 3T3-L1 adipocytes in response to lipopolysaccharide (LPS)-induced inflammation. Methods: 10-gingerol antioxidant capacity was assessed through Oxygen Radical Absorbance Capacity (ORAC) , Ferric Reducing Antioxidant Power (FRAP), and radical scavenging activity of 2,2-diphenyl-2-picrylhydrazyl (DPPH) assays. 3T3-L1 cells were differentiated and stimulated with 100 ng/mL LPSs. Then, 15 µg/mL 10-gingerol was added for 48 h. The mRNA expression and protein abundance of antioxidant enzymes were evaluated by qPCR and Western blot, respectively. Adipokine levels were determined by ELISA. Results: 10-gingerol showed low FRAP and DPPH values but a moderate ORAC value. Moreover, 10-gingerol increased Gpx1 and Sod1 but downregulated Cat expression. Additionally, 10-gingerol significantly increased CAT and GPx1 levels but not SOD-1. Finally, adiponectin and leptin concentrations were increased while resistin and tumor necrosis factor alpha (TNFα) were decreased by 10-gingerol. Conclusions: 10-gingerol presented antioxidant potential by increasing antioxidant enzymes and attenuated LPS-induced inflammation by modulating adipokines in 3T3-L1 adipocytes.