ANTIOXIDATIVE PROPERTIES OF GEROPROTECTIVE PEPTIDES

2021 ◽  
pp. 707-714
Author(s):  
Л.С. Козина ◽  
В.А. Арутюнов ◽  
А.В. Арутюнян
Keyword(s):  
Environmental Factors ◽  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Regulatory Peptides ◽  
Whole Body ◽  
Insulin Degrading Enzyme ◽  
Expression Of Genes ◽  
Transport Chain ◽  
Total Peroxidase Activity ◽  
Activity Of Enzymes

Приведенные в работе результаты исследований об антиоксидантном действии ряда пептидных препаратов, которое наблюдается на различных уровнях, начиная от клеточного до организма в целом, свидетельствуют о важной роли низкомолекулярных пептидов в механизмах регуляции гомеостаза при старении. Антиоксидантные свойства регуляторных пептидов проявляются в экспериментах как на интактных половозрелых животных, так и особенно наглядно при старении или действии экстремальных факторов внешней среды (гипоксия, гипокинезия). Ряд исследуемых пептидов (AEDG, KE) оказывает мембраностабилизирующее действие, препятствуя осмотическому и кислотному гемолизу эритроцитов и снижая уровень содержания внеэритроцитарного гемоглобина и суммарной пероксидазной активности в плазме крови. Показано, что исследуемые пептиды способны оказывать нейропротекторный эффект путем стабилизации активности ферментов (неприлизин, инсулиндеградирующий фермент), играющих важную роль в катаболизме β-амилоида, и препятствовать его накоплению в мозге. Рассматривается участие регуляторных пептидов, обладающих антиоксидантными свойствами, на экспрессию генов, обеспечивающих стабилизацию митохондриальных мембран, функционирование электрон-транспортной цепи и активность антиоксидантных ферментов. The results of studies on the antioxidant effect of a number of peptide drugs, which is manifested at various levels, ranging from cells to the whole body, in adulthood and during aging, under the influence of extreme environmental factors, indicate the important role of low-molecular peptides in the mechanisms of regulating homeostasis during aging. The antioxidant properties of regulatory peptides are shown in experiments both on intact sexually mature animals, and especially clearly during aging or the action of extreme environmental factors (hypoxia, hypokinesia). A number of the studied substances (AEDG, KE) have a membrane-stabilizing effect, preventing osmotic and acid hemolysis of red blood cells and reducing the level of extra-erythrocyte hemoglobin and total peroxidase activity in blood plasma. It is shown that the studied peptides are able to have a neuroprotective effect by stabilizing the activity of enzymes (neprilysin, an insulin degrading enzyme) that play an important role in the catabolism of beta-amyloid, and prevent its accumulation in concentrations toxic to cells. The involvement of regulatory peptides with antioxidant properties on the expression of genes that ensure the stabilization of mitochondrial membranes, the functioning of the electron transport chain and the activity of antioxidant enzymes is considered.

scholarly journals The Potential Effects of Phytoestrogens: The Role in Neuroprotection

Molecules ◽  
2021 ◽  
Vol 26 (10) ◽  
pp. 2954
Author(s):  
Justyna Gorzkiewicz ◽  
Grzegorz Bartosz ◽  
Izabela Sadowska-Bartosz
Keyword(s):  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Estrogen Therapy ◽  
Neuroprotective Effects ◽  
Potential Health ◽  
Naturally Occurring ◽  
Epigenetic Effects ◽  
Estrogen Synthesis ◽  
Health Promoting ◽  
The Brain

Phytoestrogens are naturally occurring non-steroidal phenolic plant compounds. Their structure is similar to 17-β-estradiol, the main female sex hormone. This review offers a concise summary of the current literature on several potential health benefits of phytoestrogens, mainly their neuroprotective effect. Phytoestrogens lower the risk of menopausal symptoms and osteoporosis, as well as cardiovascular disease. They also reduce the risk of brain disease. The effects of phytoestrogens and their derivatives on cancer are mainly due to the inhibition of estrogen synthesis and metabolism, leading to antiangiogenic, antimetastatic, and epigenetic effects. The brain controls the secretion of estrogen (hypothalamus-pituitary-gonads axis). However, it has not been unequivocally established whether estrogen therapy has a neuroprotective effect on brain function. The neuroprotective effects of phytoestrogens seem to be related to both their antioxidant properties and interaction with the estrogen receptor. The possible effects of phytoestrogens on the thyroid cause some concern; nevertheless, generally, no serious side effects have been reported, and these compounds can be recommended as health-promoting food components or supplements.

scholarly journals Molecular and Biochemical Pathways of Catalpol in Alleviating Diabetes Mellitus and Its Complications

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 323
Author(s):  
Subrat Kumar Bhattamisra ◽  
Hui Min Koh ◽  
Shin Yean Lim ◽  
Hira Choudhury ◽  
Manisha Pandey
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Complications ◽  
Inflammatory Markers ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Beneficial Effects ◽  
Ppar Γ ◽  
High Glucose Condition ◽  
Anti Inflammatory

Catalpol isolated from Rehmannia glutinosa is a potent antioxidant and investigated against many disorders. This review appraises the key molecular pathways of catalpol against diabetes mellitus and its complications. Multiple search engines including Google Scholar, PubMed, and Science Direct were used to retrieve publications containing the keywords “Catalpol”, “Type 1 diabetes mellitus”, “Type 2 diabetes mellitus”, and “diabetic complications”. Catalpol promotes IRS-1/PI3K/AKT/GLUT2 activity and suppresses Phosphoenolpyruvate carboxykinase (PEPCK) and Glucose 6-phosphatase (G6Pase) expression in the liver. Catalpol induces myogenesis by increasing MyoD/MyoG/MHC expression and improves mitochondria function through the AMPK/PGC-1α/PPAR-γ and TFAM signaling in skeletal muscles. Catalpol downregulates the pro-inflammatory markers and upregulates the anti-inflammatory markers in adipose tissues. Catalpol exerts antioxidant properties through increasing superoxide dismutase (sod), catalase (cat), and glutathione peroxidase (gsh-px) activity in the pancreas and liver. Catalpol has been shown to have anti-oxidative, anti-inflammatory, anti-apoptosis, and anti-fibrosis properties that in turn bring beneficial effects in diabetic complications. Its nephroprotective effect is related to the modulation of the AGE/RAGE/NF-κB and TGF-β/smad2/3 pathways. Catalpol produces a neuroprotective effect by increasing the expression of protein Kinase-C (PKC) and Cav-1. Furthermore, catalpol exhibits a cardioprotective effect through the apelin/APJ and ROS/NF-κB/Neat1 pathway. Catalpol stimulates proliferation and differentiation of osteoblast cells in high glucose condition. Lastly, catalpol shows its potential in preventing neurodegeneration in the retina with NF-κB downregulation. Overall, catalpol exhibits numerous beneficial effects on diabetes mellitus and diabetic complications.

scholarly journals Magnesium Deficiency Alters Expression of Genes Critical for Muscle Magnesium Homeostasis and Physiology in Mice

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2169
Author(s):  
Dominique Bayle ◽  
Cécile Coudy-Gandilhon ◽  
Marine Gueugneau ◽  
Sara Castiglioni ◽  
Monica Zocchi ◽  
...  
Keyword(s):  
Gastrocnemius Muscle ◽  
Magnesium Deficiency ◽  
Mitochondrial Dynamics ◽  
Body Weight Gain ◽  
Whole Body ◽  
Muscle Physiology ◽  
Deficient Diet ◽  
Muscle Weight ◽  
Magnesium Homeostasis ◽  
Expression Of Genes

Chronic Mg2+ deficiency is the underlying cause of a broad range of health dysfunctions. As 25% of body Mg2+ is located in the skeletal muscle, Mg2+ transport and homeostasis systems (MgTHs) in the muscle are critical for whole-body Mg2+ homeostasis. In the present study, we assessed whether Mg2+ deficiency alters muscle fiber characteristics and major pathways regulating muscle physiology. C57BL/6J mice received either a control, mildly, or severely Mg2+-deficient diet (0.1%; 0.01%; and 0.003% Mg2+ wt/wt, respectively) for 14 days. Mg2+ deficiency slightly decreased body weight gain and muscle Mg2+ concentrations but was not associated with detectable variations in gastrocnemius muscle weight, fiber morphometry, and capillarization. Nonetheless, muscles exhibited decreased expression of several MgTHs (MagT1, CNNM2, CNNM4, and TRPM6). Moreover, TaqMan low-density array (TLDA) analyses further revealed that, before the emergence of major muscle dysfunctions, even a mild Mg2+ deficiency was sufficient to alter the expression of genes critical for muscle physiology, including energy metabolism, muscle regeneration, proteostasis, mitochondrial dynamics, and excitation–contraction coupling.

scholarly journals Ultrasound Microbubbles Enhance the Neuroprotective Effect of Mouse Nerve Growth Factor on Intraocular Hypertension-Induced Neuroretina Damage in Rabbits

2016 ◽  
Vol 2016 ◽  
pp. 1-9
Author(s):  
Xiaoli Shen ◽  
Lina Huang ◽  
Dahui Ma ◽  
Jun Zhao ◽  
Yi Xie ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Blood Circulation ◽  
Neuroprotective Effect ◽  
Whole Body ◽  
Destruction Process ◽  
Optic Nerve Damage ◽  
Neuroprotective Drugs ◽  
Target Organs ◽  
Whole Body Metabolism ◽  
Ultrasound Microbubbles

Ultrasound microbubble combined optic protection drugs have obvious protective effect on optic nerve damage. This way of targeting drug delivery is becoming more simple, not through the whole body metabolism, avoiding drug via blood circulation when facing the decomposition and the environment in the interference and destruction process of drugs, to maximize the guarantee to reach target organs of drug concentration and to reache the maximum therapeutic effect. The technique of ultrasound microbubbles is safe, controllable, nonimmunogenic, and repeatable. It provides us with a novel idea in the administration of neuroprotective drugs.

scholarly journals Assessment of Nuclear and Mitochondrial DNA, Expression of Mitochondria-Related Genes in Different Brain Regions in Rats after Whole-Body X-ray Irradiation

2020 ◽  
Vol 21 (4) ◽  
pp. 1196 ◽  
Author(s):  
Serazhutdin Abdullaev ◽  
Nina Gubina ◽  
Tatiana Bulanova ◽  
Azhub Gaziev
Keyword(s):  
Mitochondrial Dna ◽  
Rat Brain ◽  
Mitochondrial Biogenesis ◽  
Copy Number ◽  
Brain Regions ◽  
The Other ◽  
Whole Body ◽  
X Ray ◽  
Expression Of Genes ◽  
Time Point

Studies of molecular changes occurred in various brain regions after whole-body irradiation showed a significant increase in terms of the importance in gaining insight into how to slow down or prevent the development of long-term side effects such as carcinogenesis, cognitive impairment and other pathologies. We have analyzed nDNA damage and repair, changes in mitochondrial DNA (mtDNA) copy number and in the level of mtDNA heteroplasmy, and also examined changes in the expression of genes involved in the regulation of mitochondrial biogenesis and dynamics in three areas of the rat brain (hippocampus, cortex and cerebellum) after whole-body X-ray irradiation. Long amplicon quantitative polymerase chain reaction (LA-QPCR) was used to detect nDNA and mtDNA damage. The level of mtDNA heteroplasmy was estimated using Surveyor nuclease technology. The mtDNA copy numbers and expression levels of a number of genes were determined by real-time PCR. The results showed that the repair of nDNA damage in the rat brain regions occurs slowly within 24 h; in the hippocampus, this process runs much slower. The number of mtDNA copies in three regions of the rat brain increases with a simultaneous increase in mtDNA heteroplasmy. However, in the hippocampus, the copy number of mutant mtDNAs increases significantly by the time point of 24 h after radiation exposure. Our analysis shows that in the brain regions of irradiated rats, there is a decrease in the expression of genes (ND2, CytB, ATP5O) involved in ATP synthesis, although by the same time point after irradiation, an increase in transcripts of genes regulating mitochondrial biogenesis is observed. On the other hand, analysis of genes that control the dynamics of mitochondria (Mfn1, Fis1) revealed that sharp decrease in gene expression level occurred, only in the hippocampus. Consequently, the structural and functional characteristics of the hippocampus of rats exposed to whole-body radiation can be different, most significantly from those of the other brain regions.

scholarly journals Pycnogenol® Induces Browning of White Adipose Tissue through the PKA Signaling Pathway in Apolipoprotein E-Deficient Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Huiying Cong ◽  
Wenxia Zhong ◽  
Yiying Wang ◽  
Shoichiro Ikuyama ◽  
Bin Fan ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Apolipoprotein E ◽  
Signaling Pathway ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Mrna Level ◽  
Antioxidant Properties ◽  
Expression Of Genes ◽  
Beige Adipocytes ◽  
Deficient Mice

Beige adipocytes in white adipose tissue (WAT) have received considerable recognition because of their potential protective effect against obesity. Pycnogenol (PYC), extracted from French maritime pine bark, has anti-inflammatory and antioxidant properties and can improve lipid profiles. However, the effect of PYC on obesity has never been explored. In this study, we investigated the effects of PYC on obesity and WAT browning in apolipoprotein E- (ApoE-) deficient mice. The results showed that PYC treatment clearly reversed body weight and the mass of eWAT gain resulting from a high-cholesterol and high-fat diet (HCD), but no difference in food intake. The morphology results showed that the size of the adipocytes in the PYC-treated mice was obviously smaller than that in the HCD-fed mice. Next, we found that PYC upregulated the expression of genes related to lipolysis (ATGL and HSL), while it decreased the mRNA level of PLIN1. PYC significantly increased the expression of UCP1 and other genes related to beige adipogenesis. Additionally, PYC increased the expression of proteins related to the protein kinase A (PKA) signaling pathway. The findings suggested that PYC decreased obesity by promoting lipolysis and WAT browning. Thus, PYC may be a novel therapeutic target for obesity.

scholarly journals Oleanolic Acid Exerts a Neuroprotective Effect Against Microglial Cell Activation by Modulating Cytokine Release and Antioxidant Defense Systems

Biomolecules ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 683 ◽  
Author(s):  
José M. Castellano ◽  
Silvia Garcia-Rodriguez ◽  
Juan M. Espinosa ◽  
María C. Millan-Linares ◽  
Mirela Rada ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oleanolic Acid ◽  
Cell Activation ◽  
Neuroprotective Effect ◽  
Cell Defense ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Antioxidant Defense Systems ◽  
Endogenous Antioxidant

Microglia respond to adverse stimuli in order to restore brain homeostasis and, upon activation, they release a number of inflammatory mediators. Chronic microglial overactivation is related to neuroinflammation in Alzheimer’s disease. In this work, we show that oleanolic acid (OA), a natural triterpene present in food and medicinal plants, attenuates the activation of BV2 microglial cells induced by lipopolysaccharide (LPS). Cell pretreatment with OA inhibited the release of IL-1β, IL-6, TNF-α, and NO, which was associated with the downregulation of the expression of genes encoding for these cytokines and inducible nitric oxide synthase (iNOS), and the reinforcement of the endogenous antioxidant cell defense. These findings advocate considering OA as a novel neuroprotective agent to inhibit oxidative stress and inflammatory response in activated microglia associated with Alzheimer’s disease.

scholarly journals Leathesia difformis Extract Inhibits α-MSH-Induced Melanogenesis in B16F10 Cells via Down-Regulation of CREB Signaling Pathway

2019 ◽  
Vol 20 (3) ◽  
pp. 536 ◽  
Author(s):  
Ga-Young Seo ◽  
Yuna Ha ◽  
Ah-Hyun Park ◽  
Oh Kwon ◽  
Youn-Jung Kim
Keyword(s):  
Therapeutic Agent ◽  
Antioxidant Properties ◽  
Inhibitory Effect ◽  
Melanin Synthesis ◽  
Melanocortin 1 Receptor ◽  
Dopachrome Tautomerase ◽  
Melanocyte Stimulating Hormone ◽  
B16f10 Cells ◽  
Expression Of Genes ◽  
Tyrosinase Related Protein

Leathesia difformis (L.) Areschoug (L. difformis) is a species of littoral brown algae of the class Phaeophyceae. Only a few studies on the apoptotic, antiviral, and antioxidant properties of L. difformis have been reported, and its inhibitory effect on melanin synthesis has not been studied. The aim of this study was to investigate the anti-melanogenic effect of L. difformis extract on α-melanocyte-stimulating hormone (α-MSH)-induced B16F10 melanocytes and its mechanism of action. L. difformis was extracted using 80% ethanol (LDE) and then fractioned between ethyl acetate (LDE-EA) and water (LDE-A). Our data demonstrated that LDE-EA significantly inhibited melanin level and cellular tyrosinase activity in α-MSH-stimulated B16 cells. In addition, the expression of genes associated with melanin synthesis, such as microphthalmia-associated transcription factor (Mitf), tyrosinase (Tyr), tyrosinase-related protein-1 (Trp-1), dopachrome tautomerase (Dct), and melanocortin 1 receptor (Mc1r) was down-regulated by LDE-EA treatment. Moreover, LDE-EA decreased p-CREB levels, which suggests that the inhibition of the cAMP/PKA/CREB pathways may be involved in the anti-melanogenic effect of LDE-EA. Thus, this study revealed that LDE-EA is an effective inhibitor of hyperpigmentation through inhibition of CREB pathways and may be considered as a potential therapeutic agent for hyperpigmentation disorders.

scholarly journals Consequences of prenatal and preweaning growth for yield of beef primal cuts from 30-month-old Piedmontese- and Wagyu-sired cattle

2009 ◽  
Vol 49 (6) ◽  
pp. 468 ◽  
Author(s):  
P. L. Greenwood ◽  
L. M. Cafe ◽  
H. Hearnshaw ◽  
D. W. Hennessy ◽  
S. G. Morris
Keyword(s):  
Growth Rate ◽  
Environmental Factors ◽  
Tissue Distribution ◽  
Early Life ◽  
Low Birthweight ◽  
Carcass Weight ◽  
Whole Body ◽  
Target Market ◽  
Subsequent Growth

Cattle sired by Piedmontese or Wagyu bulls were bred and grown within pasture-based nutritional systems followed by feedlot finishing. Effects of low (mean 28.6 kg, n = 120) and high (38.8 kg, n = 120) birthweight followed by slow (mean 554 g/day, n = 119) or rapid (875 g/day, n = 121) growth to weaning on beef primal cut weights at ~30 months of age were examined. Cattle of low birthweight or grown slowly to weaning had smaller primal cuts at 30 months as a result of reduced liveweight and smaller carcasses compared with their high birthweight or rapidly grown counterparts. Hence they require additional nutritional and economic inputs to reach target market weights. At equivalent carcass weights (380 kg), cattle restricted in growth from birth to weaning yielded slightly more beef and were somewhat leaner than their rapidly grown counterparts, resulting in primal cuts being up to 4% heavier in the slowly grown compared with the rapidly grown cattle. Compositional differences due to birthweight were less apparent at the same carcass weight, although low birthweight cattle had a slightly (~2%) heavier forequarter and slightly lower (~1%) hindquarter retail yield, and less shin-shank meat (~2%) than high birthweight cattle, suggesting only minor effects on carcass tissue distribution. There were few interactions between sire genotype and birthweight or preweaning growth, and interactions between birthweight and preweaning growth were not evident for any variables. However, variability between cohorts in their long-term responses to growth early in life suggests other environmental factors during early-life and/or subsequent growth influenced carcass yield characteristics. Overall, this study shows that effects of birthweight and preweaning growth rate on carcass compositional and yield characteristics were mostly explained by variation in carcass weight and, hence, in whole body growth to 30 months of age.

scholarly journals 3,5-T2 alters murine genes relevant for xenobiotic, steroid, and thyroid hormone metabolism

2016 ◽  
Vol 56 (4) ◽  
pp. 311-323 ◽  
Author(s):  
Julika Lietzow ◽  
Janine Golchert ◽  
Georg Homuth ◽  
Uwe Völker ◽  
Wenke Jonas ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Phase Iii ◽  
Whole Body ◽  
High Dose ◽  
Thyroid Hormone Metabolism ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Novel Target

The endogenous thyroid hormone (TH) metabolite 3,5-diiodo-l-thyronine (3,5-T2) acts as a metabolically active substance affecting whole-body energy metabolism and hepatic lipid handling in a desirable manner. Considering possible adverse effects regarding thyromimetic action of 3,5-T2 treatment in rodents, the current literature remains largely controversial. To obtain further insights into molecular mechanisms and to identify novel target genes of 3,5-T2 in liver, we performed a microarray-based liver tissue transcriptome analysis of male lean and diet-induced obese euthyroid mice treated for 4 weeks with a dose of 2.5 µg/g bw 3,5-T2. Our results revealed that 3,5-T2 modulates the expression of genes encoding Phase I and Phase II enzymes as well as Phase III transporters, which play central roles in metabolism and detoxification of xenobiotics. Additionally, 3,5-T2 changes the expression of TH responsive genes, suggesting a thyromimetic action of 3,5-T2 in mouse liver. Interestingly, 3,5-T2 in obese but not in lean mice influences the expression of genes relevant for cholesterol and steroid biosynthesis, suggesting a novel role of 3,5-T2 in steroid metabolism of obese mice. We concluded that treatment with 3,5-T2 in lean and diet-induced obese male mice alters the expression of genes encoding hepatic xenobiotic-metabolizing enzymes that play a substantial role in catabolism and inactivation of xenobiotics and TH and are also involved in hepatic steroid and lipid metabolism. The administration of this high dose of 3,5-T2 might exert adverse hepatic effects. Accordingly, the conceivable use of 3,5-T2 as pharmacological hypolipidemic agent should be considered with caution.

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