The Experts below are selected from a list of 288 Experts worldwide ranked by ideXlab platform

M Myroshnychenko - One of the best experts on this subject based on the ideXlab platform.

  • features of an expression of smooth muscle actin by muscle cells of arterioles and venules of ureter and urinary bladder of newborns in modeling chronic Intrauterine Hypoxia
    Diagnostic Pathology, 2016
    Co-Authors: I Gorianikova, I Sorokina, M Myroshnychenko
    Abstract:

    Introduction/ Background Chronic Intrauterine Hypoxia, accompanied numerous complications of pregnancy, is one of the damaging factor of the organism of fetus and newborn. Aims The purpose – to reveal the features of expression of smooth muscle actin by muscle cells of arterioles and venules of ureter and urinary bladder of newborns under the influence of experimental chronic Intrauterine Hypoxia. Methods An experiment was conducted on modeling high mountain Hypoxia in rats of WAG line. Two groups were formed: I – newborns (n=11) born from 3 rats that were not subjected to high mountain Hypoxia; II – newborns (n=10) born from 4 rats that throughout pregnancy were exposed to a daily high mountain Hypoxia. The material of the study was the tissue of ureter and urinary bladder. It was used peroxidase reaction with the monoclonal antibodies to smooth muscle actin (DAKO, Denmark). The slides were studied in microscope «Olympus ВХ- 41». An experimental study was carried out in strict compliance with the requirements of the European convention (Strasbourg, 1986) on the housing, feeding and care of experimental animals, and their removal from the experiment. Mean values of indicators in groups were compared using a nonparametric U-criteria Mann-Whitney. Results In group I and II was observed expression of smooth muscle actin by muscle cells, forming muscle fibers and including in the tunica media of arterioles and venules of ureter and urinary bladder, in a clear cytoplasmic staining in brown. In group I the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (2,19±0,229)×10-6m and (1,38±0,189)×10-6m; in urinary bladder – (2,92±0,207)×10-6m and (2,11±0,160)×10-6m. In group II the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (1,67±0,270)×10-6m and (0,88±0,107)×10-6m; in urinary bladder – (2,20±0,198)×10-6m and (1,49±0,239)×10-6m. Analyzing and comparing the obtained values, it was observed that in group I and II was determined significant predominance (р 0,05) were absent. In group II in ureter and urinary bladder was a significant (р<0,05) decreasing of the mean values of indicators of thickness of muscle fibers in arterioles and venules in comparison with group I. Conclusion: Chronic Intrauterine Hypoxia leads to a thinning of the thickness of the muscle fibers in arterioles and venules of ureter and urinary bladder in newborns.

  • Features of an Expression of Smooth Muscle Actin by Muscle Cells of Arterioles and Venules of Ureter and Urinary Bladder of Newborns in Modeling Chronic Intrauterine Hypoxia
    Diagnostic Pathology, 2016
    Co-Authors: I Gorianikova, I Sorokina, M Myroshnychenko
    Abstract:

    Introduction/ Background Chronic Intrauterine Hypoxia, accompanied numerous complications of pregnancy, is one of the damaging factor of the organism of fetus and newborn. Aims The purpose – to reveal the features of expression of smooth muscle actin by muscle cells of arterioles and venules of ureter and urinary bladder of newborns under the influence of experimental chronic Intrauterine Hypoxia. Methods An experiment was conducted on modeling high mountain Hypoxia in rats of WAG line. Two groups were formed: I – newborns (n=11) born from 3 rats that were not subjected to high mountain Hypoxia; II – newborns (n=10) born from 4 rats that throughout pregnancy were exposed to a daily high mountain Hypoxia. The material of the study was the tissue of ureter and urinary bladder. It was used peroxidase reaction with the monoclonal antibodies to smooth muscle actin (DAKO, Denmark). The slides were studied in microscope «Olympus ВХ- 41». An experimental study was carried out in strict compliance with the requirements of the European convention (Strasbourg, 1986) on the housing, feeding and care of experimental animals, and their removal from the experiment. Mean values of indicators in groups were compared using a nonparametric U-criteria Mann-Whitney. Results In group I and II was observed expression of smooth muscle actin by muscle cells, forming muscle fibers and including in the tunica media of arterioles and venules of ureter and urinary bladder, in a clear cytoplasmic staining in brown. In group I the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (2,19±0,229)×10-6m and (1,38±0,189)×10-6m; in urinary bladder – (2,92±0,207)×10-6m and (2,11±0,160)×10-6m. In group II the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (1,67±0,270)×10-6m and (0,88±0,107)×10-6m; in urinary bladder – (2,20±0,198)×10-6m and (1,49±0,239)×10-6m. Analyzing and comparing the obtained values, it was observed that in group I and II was determined significant predominance (р 0,05) were absent. In group II in ureter and urinary bladder was a significant (р

I Gorianikova - One of the best experts on this subject based on the ideXlab platform.

  • features of an expression of smooth muscle actin by muscle cells of arterioles and venules of ureter and urinary bladder of newborns in modeling chronic Intrauterine Hypoxia
    Diagnostic Pathology, 2016
    Co-Authors: I Gorianikova, I Sorokina, M Myroshnychenko
    Abstract:

    Introduction/ Background Chronic Intrauterine Hypoxia, accompanied numerous complications of pregnancy, is one of the damaging factor of the organism of fetus and newborn. Aims The purpose – to reveal the features of expression of smooth muscle actin by muscle cells of arterioles and venules of ureter and urinary bladder of newborns under the influence of experimental chronic Intrauterine Hypoxia. Methods An experiment was conducted on modeling high mountain Hypoxia in rats of WAG line. Two groups were formed: I – newborns (n=11) born from 3 rats that were not subjected to high mountain Hypoxia; II – newborns (n=10) born from 4 rats that throughout pregnancy were exposed to a daily high mountain Hypoxia. The material of the study was the tissue of ureter and urinary bladder. It was used peroxidase reaction with the monoclonal antibodies to smooth muscle actin (DAKO, Denmark). The slides were studied in microscope «Olympus ВХ- 41». An experimental study was carried out in strict compliance with the requirements of the European convention (Strasbourg, 1986) on the housing, feeding and care of experimental animals, and their removal from the experiment. Mean values of indicators in groups were compared using a nonparametric U-criteria Mann-Whitney. Results In group I and II was observed expression of smooth muscle actin by muscle cells, forming muscle fibers and including in the tunica media of arterioles and venules of ureter and urinary bladder, in a clear cytoplasmic staining in brown. In group I the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (2,19±0,229)×10-6m and (1,38±0,189)×10-6m; in urinary bladder – (2,92±0,207)×10-6m and (2,11±0,160)×10-6m. In group II the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (1,67±0,270)×10-6m and (0,88±0,107)×10-6m; in urinary bladder – (2,20±0,198)×10-6m and (1,49±0,239)×10-6m. Analyzing and comparing the obtained values, it was observed that in group I and II was determined significant predominance (р 0,05) were absent. In group II in ureter and urinary bladder was a significant (р<0,05) decreasing of the mean values of indicators of thickness of muscle fibers in arterioles and venules in comparison with group I. Conclusion: Chronic Intrauterine Hypoxia leads to a thinning of the thickness of the muscle fibers in arterioles and venules of ureter and urinary bladder in newborns.

  • Features of an Expression of Smooth Muscle Actin by Muscle Cells of Arterioles and Venules of Ureter and Urinary Bladder of Newborns in Modeling Chronic Intrauterine Hypoxia
    Diagnostic Pathology, 2016
    Co-Authors: I Gorianikova, I Sorokina, M Myroshnychenko
    Abstract:

    Introduction/ Background Chronic Intrauterine Hypoxia, accompanied numerous complications of pregnancy, is one of the damaging factor of the organism of fetus and newborn. Aims The purpose – to reveal the features of expression of smooth muscle actin by muscle cells of arterioles and venules of ureter and urinary bladder of newborns under the influence of experimental chronic Intrauterine Hypoxia. Methods An experiment was conducted on modeling high mountain Hypoxia in rats of WAG line. Two groups were formed: I – newborns (n=11) born from 3 rats that were not subjected to high mountain Hypoxia; II – newborns (n=10) born from 4 rats that throughout pregnancy were exposed to a daily high mountain Hypoxia. The material of the study was the tissue of ureter and urinary bladder. It was used peroxidase reaction with the monoclonal antibodies to smooth muscle actin (DAKO, Denmark). The slides were studied in microscope «Olympus ВХ- 41». An experimental study was carried out in strict compliance with the requirements of the European convention (Strasbourg, 1986) on the housing, feeding and care of experimental animals, and their removal from the experiment. Mean values of indicators in groups were compared using a nonparametric U-criteria Mann-Whitney. Results In group I and II was observed expression of smooth muscle actin by muscle cells, forming muscle fibers and including in the tunica media of arterioles and venules of ureter and urinary bladder, in a clear cytoplasmic staining in brown. In group I the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (2,19±0,229)×10-6m and (1,38±0,189)×10-6m; in urinary bladder – (2,92±0,207)×10-6m and (2,11±0,160)×10-6m. In group II the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (1,67±0,270)×10-6m and (0,88±0,107)×10-6m; in urinary bladder – (2,20±0,198)×10-6m and (1,49±0,239)×10-6m. Analyzing and comparing the obtained values, it was observed that in group I and II was determined significant predominance (р 0,05) were absent. In group II in ureter and urinary bladder was a significant (р

Shaojie Yue - One of the best experts on this subject based on the ideXlab platform.

  • Analyzing the Effects of Intrauterine Hypoxia on Gene Expression in Oocytes of Rat Offspring by Single Cell Transcriptome Sequencing.
    Frontiers in genetics, 2019
    Co-Authors: Yang Liu, Ziqiang Luo, Mingjie Wang, Chuanding Cao, Zhengchang Liao, Ying Ding, Shaojie Yue, Ziling Lin
    Abstract:

    Intrauterine Hypoxia is one of the most frequently occurring complications during pregnancy, and the effects of antenatal Hypoxia in offspring are not restricted to the perinatal period. Previous studies have reported on this phenomenon, which is usually described as multigenerational or transgenerational inheritance. However, the exact mechanism of this type of inheritance is still not clear. Therefore, in the present study, we investigated the alteration in the gene expression of oocytes, derived from Intrauterine Hypoxia rats and their offspring, by transcriptome sequencing. Our results showed that 11 differentially expressed genes were inherited from the F1 to F2 generation. Interestingly, these differentially expressed genes were enriched in processes predominantly involved in lipid and insulin metabolism. Overall, our data indicated that alteration in the gene expression of oocytes may be associated with some metabolic diseases and could potentially be the basis of transgenerational or multigenerational inheritance, induced by an adverse perinatal environment.

  • excessive activation of nmda receptor inhibits the protective effect of endogenous bone marrow mesenchymal stem cells on promoting alveolarization in bronchopulmonary dysplasia
    American Journal of Physiology-cell Physiology, 2019
    Co-Authors: Yinyan Yue, Ziqiang Luo, Mingjie Wang, Chuanding Cao, Zhengchang Liao, Ying Ding, Liming Zhang, Shuai Liu, Feiyan Zhao, Shaojie Yue
    Abstract:

    We studied the role of bone marrow mesenchymal stem cells (MSCs) in our established model of bronchopulmonary dysplasia (BPD) induced by Intrauterine Hypoxia in the rat. First, we found that intrau...

  • Excessive Activation of NMDA Receptors Induced Neurodevelopmental Brain Damage and Cognitive Deficits in Rats Exposed to Intrauterine Hypoxia.
    Neurochemical research, 2017
    Co-Authors: Ziqiang Luo, Yang Liu, Mingjie Wang, Chuanding Cao, Zhengchang Liao, Ying Ding, Shaojie Yue
    Abstract:

    Intrauterine Hypoxia is one of the most common stressors in fetuses, which can lead to abnormal brain development and permanent neurological deficits in adulthood. Neurological disorder excitotoxicity induced by Hypoxia or ischemia may involve N-methyl-d-aspartate receptors (NMDARs), which are known to participate in the maturation and plasticity of developmental neurons. Inhibition of NMDARs has been reported to improve neurological outcomes in traumatic brain injuries and Alzheimer’s disease. Here, we investigated if antenatal blockade of NMDARs induced by memantine could alleviate neurodevelopmental brain damage and long-term cognitive deficits in Intrauterine Hypoxia rats. Pregnant rats were assigned to four groups: air control, air + memantine, Hypoxia, and Hypoxia + memantine. The rats were exposed to hypoxic conditions (FiO2 = 0.095–0.115) for 8 h/day (Hypoxia group) or given a daily memantine injection (5 mg/kg, i.p.) before Hypoxia exposure from pregnant day 19 (G19) to G20 (Hypoxia + memantine group).The influence of NMDARs antenatal blockade by memantine on Intrauterine Hypoxia-induced brain developmental damage and cognitive function was then studied. Intrauterine Hypoxia resulted in decreased fetal body weight, brain weight, cognitive function, hippocampal neuron numbers, and Ki-67 proliferation index in the hippocampus. Memantine preventive treatment in pregnant rats before Hypoxia exposure alleviated the aforementioned damage in vivo. Excessive activation of NMDARs contributes to fetal brain developmental damage and cognitive ability impairment induced by Intrauterine Hypoxia, which could be alleviated by antenatal memantine preventative treatment.

  • N-Methyl-D-aspartate Receptor Excessive Activation Inhibited Fetal Rat Lung Development In Vivo and In Vitro
    BioMed research international, 2016
    Co-Authors: Zhengchang Liao, Ziqiang Luo, Mingjie Wang, Chuanding Cao, Ying Ding, Huiyi Huo, Xiaocheng Zhou, Zeng Xiong, Shaojie Yue
    Abstract:

    Background. Intrauterine Hypoxia is a common cause of fetal growth and lung development restriction. Although N-methyl-D-aspartate receptors (NMDARs) are distributed in the postnatal lung and play a role in lung injury, little is known about NMDAR’s expression and role in fetal lung development. Methods. Real-time PCR and western blotting analysis were performed to detect NMDARs between embryonic days (E) 15.5 and E21.5 in fetal rat lungs. NMDAR antagonist MK-801’s influence on Intrauterine Hypoxia-induced retardation of fetal lung development was tested in vivo, and NMDA’s direct effect on fetal lung development was observed using fetal lung organ culture in vitro. Results. All seven NMDARs are expressed in fetal rat lungs. Intrauterine Hypoxia upregulated NMDARs expression in fetal lungs and decreased fetal body weight, lung weight, lung-weight-to-body-weight ratio, and radial alveolar count, whereas MK-801 alleviated this damage in vivo. In vitro experiments showed that NMDA decreased saccular circumference and area per unit and downregulated thyroid transcription factor-1 and surfactant protein-C mRNA expression. Conclusions. The excessive activation of NMDARs contributed to Hypoxia-induced fetal lung development retardation and appropriate blockade of NMDAR might be a novel therapeutic strategy for minimizing the negative outcomes of prenatal Hypoxia on lung development.

  • MicroRNA expression profile in Intrauterine Hypoxia-induced pulmonary hypoplasia in rats.
    Experimental and therapeutic medicine, 2014
    Co-Authors: Huiyi Huo, Ziqiang Luo, Mingjie Wang, Zhengchang Liao, Xiaocheng Zhou, Shaojie Yue
    Abstract:

    Hypoxia is necessary for fetal development; however, excess Hypoxia is detrimental. The mechanisms underlying the effects of Hypoxia on lung development remain unclear, although important roles of microRNAs (miRNAs) during lung development have recently been established. However, the effect on lung development at an miRNA expression level, following changes in oxygen tension, have not yet been studied. In the present study, pregnant rats were exposed to a fraction of inspired oxygen of 10.5 or 21% for two days on gestation day 19, following which the body weight, lung wet weight, radial alveolar count (RAC) and mean linear intercept (Lm) of the newborn pups were analyzed on postnatal day 1. To define the role of miRNAs during lung development following Intrauterine Hypoxia exposure, the miRNA expression pattern was profiled using a miRNA microarray. The newborn rats in the hypoxic group exhibited statistically significant decreases in body weight, lung weight and the RAC, as well as a marked increase in the Lm. A total of 69 miRNAs were identified to have significant changes in expression, including 55 upregulated and 14 downregulated miRNAs. Quantitative polymerase chain reaction was used to validate the microarray results of six selected miRNAs. Therefore, the results indicated that late gestation Intrauterine Hypoxia exposure may cause lung injury and miRNAs may play important roles in this process.

I Sorokina - One of the best experts on this subject based on the ideXlab platform.

  • features of an expression of smooth muscle actin by muscle cells of arterioles and venules of ureter and urinary bladder of newborns in modeling chronic Intrauterine Hypoxia
    Diagnostic Pathology, 2016
    Co-Authors: I Gorianikova, I Sorokina, M Myroshnychenko
    Abstract:

    Introduction/ Background Chronic Intrauterine Hypoxia, accompanied numerous complications of pregnancy, is one of the damaging factor of the organism of fetus and newborn. Aims The purpose – to reveal the features of expression of smooth muscle actin by muscle cells of arterioles and venules of ureter and urinary bladder of newborns under the influence of experimental chronic Intrauterine Hypoxia. Methods An experiment was conducted on modeling high mountain Hypoxia in rats of WAG line. Two groups were formed: I – newborns (n=11) born from 3 rats that were not subjected to high mountain Hypoxia; II – newborns (n=10) born from 4 rats that throughout pregnancy were exposed to a daily high mountain Hypoxia. The material of the study was the tissue of ureter and urinary bladder. It was used peroxidase reaction with the monoclonal antibodies to smooth muscle actin (DAKO, Denmark). The slides were studied in microscope «Olympus ВХ- 41». An experimental study was carried out in strict compliance with the requirements of the European convention (Strasbourg, 1986) on the housing, feeding and care of experimental animals, and their removal from the experiment. Mean values of indicators in groups were compared using a nonparametric U-criteria Mann-Whitney. Results In group I and II was observed expression of smooth muscle actin by muscle cells, forming muscle fibers and including in the tunica media of arterioles and venules of ureter and urinary bladder, in a clear cytoplasmic staining in brown. In group I the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (2,19±0,229)×10-6m and (1,38±0,189)×10-6m; in urinary bladder – (2,92±0,207)×10-6m and (2,11±0,160)×10-6m. In group II the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (1,67±0,270)×10-6m and (0,88±0,107)×10-6m; in urinary bladder – (2,20±0,198)×10-6m and (1,49±0,239)×10-6m. Analyzing and comparing the obtained values, it was observed that in group I and II was determined significant predominance (р 0,05) were absent. In group II in ureter and urinary bladder was a significant (р<0,05) decreasing of the mean values of indicators of thickness of muscle fibers in arterioles and venules in comparison with group I. Conclusion: Chronic Intrauterine Hypoxia leads to a thinning of the thickness of the muscle fibers in arterioles and venules of ureter and urinary bladder in newborns.

  • Features of an Expression of Smooth Muscle Actin by Muscle Cells of Arterioles and Venules of Ureter and Urinary Bladder of Newborns in Modeling Chronic Intrauterine Hypoxia
    Diagnostic Pathology, 2016
    Co-Authors: I Gorianikova, I Sorokina, M Myroshnychenko
    Abstract:

    Introduction/ Background Chronic Intrauterine Hypoxia, accompanied numerous complications of pregnancy, is one of the damaging factor of the organism of fetus and newborn. Aims The purpose – to reveal the features of expression of smooth muscle actin by muscle cells of arterioles and venules of ureter and urinary bladder of newborns under the influence of experimental chronic Intrauterine Hypoxia. Methods An experiment was conducted on modeling high mountain Hypoxia in rats of WAG line. Two groups were formed: I – newborns (n=11) born from 3 rats that were not subjected to high mountain Hypoxia; II – newborns (n=10) born from 4 rats that throughout pregnancy were exposed to a daily high mountain Hypoxia. The material of the study was the tissue of ureter and urinary bladder. It was used peroxidase reaction with the monoclonal antibodies to smooth muscle actin (DAKO, Denmark). The slides were studied in microscope «Olympus ВХ- 41». An experimental study was carried out in strict compliance with the requirements of the European convention (Strasbourg, 1986) on the housing, feeding and care of experimental animals, and their removal from the experiment. Mean values of indicators in groups were compared using a nonparametric U-criteria Mann-Whitney. Results In group I and II was observed expression of smooth muscle actin by muscle cells, forming muscle fibers and including in the tunica media of arterioles and venules of ureter and urinary bladder, in a clear cytoplasmic staining in brown. In group I the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (2,19±0,229)×10-6m and (1,38±0,189)×10-6m; in urinary bladder – (2,92±0,207)×10-6m and (2,11±0,160)×10-6m. In group II the mean values of indicators of thickness of muscle fibers in arterioles and venules of ureter were respectively (1,67±0,270)×10-6m and (0,88±0,107)×10-6m; in urinary bladder – (2,20±0,198)×10-6m and (1,49±0,239)×10-6m. Analyzing and comparing the obtained values, it was observed that in group I and II was determined significant predominance (р 0,05) were absent. In group II in ureter and urinary bladder was a significant (р

Yajun Zhao - One of the best experts on this subject based on the ideXlab platform.

  • Impact of Intrauterine Hypoxia on adolescent and adult cognitive function in rat offspring: sexual differences and the effects of spermidine intervention.
    Acta pharmacologica Sinica, 2020
    Co-Authors: Meng Mao, Lin Yang, Zhuo Jin, Yan-ru Wang, Yajun Zhao
    Abstract:

    Intrauterine Hypoxia (IUH) affects the growth and development of offspring. It remains unclear that how long the impact of IUH on cognitive function lasts and whether sexual differences exist. Spermidine (SPD) has shown to improve cognition, but its effect on the cognitive function of IUH offspring remains unknown. In the present study we investigated the influence of IUH on body weight and neurological, motor and cognitive function and the expression of APP, BACE1 and Tau5 proteins in brain tissues in 2- and 4-month-old IUH rat offspring, as well as the effects of SPD intervention on these parameters. IUH rat model was established by treating pregnant rats with intermittent Hypoxia on gestational days 15-21, meanwhile pregnant rats were administered SPD (5 mg·kg-1·d-1;ip) for 7 days. Neurological deficits were assessed in the Longa scoring test; motor and cognitive functions were evaluated in coat hanger test and active avoidance test, respectively. We found that IUH decreased the body weight of rats in both sexes but merely impaired motor and cognitive function in female rats without changing neurological function in the rat offspring of either sex at 2 months of age. For 4-month-old offspring, IUH decreased body weight in males and impaired neurological function and increased cognitive function in both sexes. IUH did not affect APP, BACE1 or Tau5 protein expression in either the hippocampus or cortex of all offspring; however, it increased the cortical Tau5 level in 2-month-old female offspring. Surprisingly, SPD intervention prevented weight loss. SPD intervention reversed the motor and cognitive decline caused by IUH in 2-month-old female rat offspring. Taken together, IUH-induced cognitive decline in rat offspring is sex-dependent during puberty and can be recovered in adult rats. SPD intervention improves IUH-induced cognitive and neural function decline.

  • Corrigendum to "Spermidine Prevents Heart Injury in Neonatal Rats Exposed to Intrauterine Hypoxia by Inhibiting Oxidative Stress and Mitochondrial Fragmentation".
    Oxidative medicine and cellular longevity, 2019
    Co-Authors: Nannan Chai, Hao Zhang, Yan Liu, Yan Lin, Lina Wang, Jiamin Yan, Sazonova Elena Nikolaevna, Yajun Zhao
    Abstract:

    Intrauterine Hypoxia (IUH) is a common Intrauterine dysplasia that can cause programming of the offspring cardiovascular system. In this study, we hypothesized that placental treatment with spermidine (SPD) can prevent heart injury in neonatal offspring exposed to IUH. Pregnant rats were exposed to 21% O2 or 10% O2 (Hypoxia) for 7 days prior to term or were exposed to Hypoxia and intraperitoneally administered SPD or SPD+difluromethylornithine (DFMO) on gestational days 15-21. Seven-day-old offspring were then sacrificed to assess several parameters. Our results demonstrated that IUH led to decreased myocardial ornithine decarboxylase (ODC) and increased spermidine/spermine N1-acetyltransferase (SSAT) expression in the offspring. IUH also resulted in decreased offspring body weight, heart weight, cardiomyocyte proliferation, and antioxidant capacity and increased cardiomyocyte apoptosis and fibrosis. Furthermore, IUH caused mitochondrial structure abnormality, dysfunction, and decreased biogenesis and led to a fission/fusion imbalance in offspring hearts. In vitro, Hypoxia induced mitochondrial ROS accumulation, decreased membrane potential, and increased fragmentation. Notably, all Hypoxia-induced changes analyzed in this study were prevented by SPD. Thus, in utero SPD treatment is a potential strategy for preventing IUH-induced neonatal cardiac injury.

  • Spermidine Prevents Heart Injury in Neonatal Rats Exposed to Intrauterine Hypoxia by Inhibiting Oxidative Stress and Mitochondrial Fragmentation
    Hindawi Limited, 2019
    Co-Authors: Nannan Chai, Hao Zhang, Yan Liu, Yan Lin, Lina Wang, Jiamin Yan, Sazonova Elena Nikolaevna, Yajun Zhao
    Abstract:

    Intrauterine Hypoxia (IUH) is a common Intrauterine dysplasia that can cause programming of the offspring cardiovascular system. In this study, we hypothesized that placental treatment with spermidine (SPD) can prevent heart injury in neonatal offspring exposed to IUH. Pregnant rats were exposed to 21% O2 or 10% O2 (Hypoxia) for 7 days prior to term or were exposed to Hypoxia and intraperitoneally administered SPD or SPD+difluromethylornithine (DFMO) on gestational days 15-21. Seven-day-old offspring were then sacrificed to assess several parameters. Our results demonstrated that IUH led to decreased myocardial ornithine decarboxylase (ODC) and increased spermidine/spermine N1-acetyltransferase (SSAT) expression in the offspring. IUH also resulted in decreased offspring body weight, heart weight, cardiomyocyte proliferation, and antioxidant capacity and increased cardiomyocyte apoptosis and fibrosis. Furthermore, IUH caused mitochondrial structure abnormality, dysfunction, and decreased biogenesis and led to a fission/fusion imbalance in offspring hearts. In vitro, Hypoxia induced mitochondrial ROS accumulation, decreased membrane potential, and increased fragmentation. Notably, all Hypoxia-induced changes analyzed in this study were prevented by SPD. Thus, in utero SPD treatment is a potential strategy for preventing IUH-induced neonatal cardiac injury