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      Dietary hawthorn-leaves flavonoids improves ovarian function and liver lipid metabolism in aged breeder hens

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          Abstract

          Hawthorn-leaves flavonoids ( HF), extracted from hawthorn leaves, were reported to exert antioxidant, anti-inflammatory and hypolipidemic properties. The aim of our study was to investigate the effects of dietary HF on the reproduction performance and liver lipid metabolism of aged breeder hens. A total of 270 aged Qiling breeder hens (60-wk-old) were randomly divided into 3 treatments: 1) basic corn-soybean diet ( CON); 2) basic corn-soybean diet supplemented with 30 mg/kg HF ( LHF); 3) basic corn-soybean diet supplemented with 60 mg/kg HF ( HHF). The results showed that supplemented HF significantly improved the egg-laying rate and hatching rate of aged breeder hens ( P < 0.05). HF treatment reduced the serum TG, T-CHO and L-LDL levels ( P < 0.05), and upregulated the mRNA expressions of ESR1, ESR2, VTGⅡ, ApoB, and ApoVI in the liver ( P < 0.05). Serum estrogen levels in HF treated groups were elevated compared with the CON group ( P < 0.05). In the HHF group, the number of the primordial follicles was higher in comparison with the CON group ( P < 0.05). Furthermore, dietary supplementation with HF improved the activity of antioxidant enzymes (T-AOC, GSH-Pχ) ( P < 0.05), following with the reversed ovarian apoptosis and morphological damage. In addition, 60 mg/kg dietary HF upregulated the protein expression of PCNA and Nrf2 in the ovary ( P < 0.05). In summary, dietary supplementation with HF could improve the reproduction performance through regulating liver lipid metabolism and improving ovarian function in aged breeder hens.

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          From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis.

          Estrogen deficiency has been considered the seminal mechanism of osteoporosis in both women and men, but epidemiological evidence in humans and recent mechanistic studies in rodents indicate that aging and the associated increase in reactive oxygen species (ROS) are the proximal culprits. ROS greatly influence the generation and survival of osteoclasts, osteoblasts, and osteocytes. Moreover, oxidative defense by the FoxO transcription factors is indispensable for skeletal homeostasis at any age. Loss of estrogens or androgens decreases defense against oxidative stress in bone, and this accounts for the increased bone resorption associated with the acute loss of these hormones. ROS-activated FoxOs in early mesenchymal progenitors also divert ss-catenin away from Wnt signaling, leading to decreased osteoblastogenesis. This latter mechanism may be implicated in the pathogenesis of type 1 and 2 diabetes and ROS-mediated adverse effects of diabetes on bone formation. Attenuation of Wnt signaling by the activation of peroxisome proliferator-activated receptor gamma by ligands generated from lipid oxidation also contributes to the age-dependent decrease in bone formation, suggesting a mechanistic explanation for the link between atherosclerosis and osteoporosis. Additionally, increased glucocorticoid production and sensitivity with advancing age decrease skeletal hydration and thereby increase skeletal fragility by attenuating the volume of the bone vasculature and interstitial fluid. This emerging evidence provides a paradigm shift from the "estrogen-centric" account of the pathogenesis of involutional osteoporosis to one in which age-related mechanisms intrinsic to bone and oxidative stress are protagonists and age-related changes in other organs and tissues, such as ovaries, accentuate them.
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            A novel and compact review on the role of oxidative stress in female reproduction

            In recent years, the study of oxidative stress (OS) has become increasingly popular. In particular, the role of OS on female fertility is very important and has been focused on closely. The occurrence of OS is due to the excessive production of reactive oxygen species (ROS). ROS are a double-edged sword; they not only play an important role as secondary messengers in many intracellular signaling cascades, but they also exert indispensable effects on pathological processes involving the female genital tract. ROS and antioxidants join in the regulation of reproductive processes in both animals and humans. Imbalances between pro-oxidants and antioxidants could lead to a number of female reproductive diseases. This review focuses on the mechanism of OS and a series of female reproductive processes, explaining the role of OS in female reproduction and female reproductive diseases caused by OS, including polycystic ovary syndrome (PCOS), endometriosis, preeclampsia and so on. Many signaling pathways involved in female reproduction, including the Keap1-Nrf2, NF-κB, FOXO and MAPK pathways, which are affected by OS, are described, providing new ideas for the mechanism of reproductive diseases.
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              Melatonin ameliorates myocardial ischemia reperfusion injury through SIRT3-dependent regulation of oxidative stress and apoptosis.

              Sirtuins are a family of highly evolutionarily conserved nicotinamide adenine nucleotide-dependent histone deacetylases. Sirtuin-3 (SIRT3) is a member of the sirtuin family that is localized primarily to the mitochondria and protects against oxidative stress-related diseases, including myocardial ischemia/reperfusion (MI/R) injury. Melatonin has a favorable effect in ameliorating MI/R injury. We hypothesized that melatonin protects against MI/R injury by activating the SIRT3 signaling pathway. In this study, mice were pre-treated with or without a selective SIRT3 inhibitor and then subjected to MI/R operation. Melatonin was administered intraperitoneally (20 mg/kg) 10 min before reperfusion. Melatonin treatment improved post-ischemic cardiac contractile function, decreased infarct size, diminished lactate dehydrogenase release, reduced the apoptotic index and ameliorated oxidative damage. Notably, MI/R induced a significant decrease in myocardial SIRT3 expression and activity, whereas the melatonin treatment upregulated SIRT3 expression and activity, and thus decreased the acetylation of superoxide dismutase 2 (SOD2). In addition, melatonin increased Bcl-2 expression and decreased Bax, Caspase-3 and cleaved Caspase-3 levels in response to MI/R. However, the cardioprotective effects of melatonin were largely abolished by the selective SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl)pyridine (3-TYP), suggesting that SIRT3 plays an essential role in mediating the cardioprotective effects of melatonin. In vitro studies confirmed that melatonin also protected H9c2 cells against simulated ischemia/reperfusion injury (SIR) by attenuating oxidative stress and apoptosis, while SIRT3-targeted siRNA diminished these effects. Taken together, our results demonstrate for the first time that melatonin treatment ameliorates MI/R injury by reducing oxidative stress and apoptosis via activating the SIRT3 signaling pathway. This article is protected by copyright. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Poult Sci
                Poult Sci
                Poultry Science
                Elsevier
                0032-5791
                1525-3171
                21 September 2021
                December 2021
                21 September 2021
                : 100
                : 12
                : 101499
                Affiliations
                [0001]College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China
                Author notes
                [2 ]Corresponding author: fxshi@ 123456njau.edu.cn
                [1]

                These authors contributed equally to this work.

                Article
                S0032-5791(21)00521-6 101499
                10.1016/j.psj.2021.101499
                8572884
                34731736
                86dd5489-213a-4d3b-8a9c-c04ba60d853a
                © 2021 Published by Elsevier Inc. on behalf of Poultry Science Association Inc.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 5 September 2020
                : 17 September 2021
                Categories
                PHYSIOLOGY AND REPRODUCTION

                hawthorn leaves flavonoids,reproduction performance,lipid metabolism,antioxidant

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