Background:This study investigated the effect of melatonin(MT)on cell cycle(G1/S/G2/M)of parthenogenetic zygotes developed from vitrified-warmed mouse metaphase II(MII)oocytes and elucidated the potential mechanism of...Background:This study investigated the effect of melatonin(MT)on cell cycle(G1/S/G2/M)of parthenogenetic zygotes developed from vitrified-warmed mouse metaphase II(MII)oocytes and elucidated the potential mechanism of MT action in the first cleavage of embryos.Results:After vitrification and warming,oocytes were parthenogenetically activated(PA)and in vitro cultured(IVC).Then the spindle morphology and chromosome segregation in oocytes,the maternal mRNA levels of genes including Miss,Doc1r,Setd2 and Ythdf2 in activated oocytes,pronuclear formation,the S phase duration in zygotes,mitochondrial function at G1 phase,reactive oxygen species(ROS)level at S phase,DNA damage at G2 phase,early apoptosis in 2-cell embryos,cleavage and blastocyst formation rates were evaluated.The results indicated that the vitrification/warming procedures led to following perturbations 1)spindle abnormalities and chromosome misalignment,alteration of maternal mRNAs and delay in pronucleus formation,2)decreased mitochondrial membrane potential(MMP)and lower adenosine triphosphate(ATP)levels,increased ROS production and DNA damage,G1/S and S/G2 phase transition delay,and delayed first cleavage,and 3)increased early apoptosis and lower levels of cleavage and blastocyst formation.Our results further revealed that such negative impacts of oocyte cryopreservation could be alleviated by supplementation of warming,recovery,PA and IVC media with 10^(−9) mol/L MT before the embryos moved into the 2-cell stage of development.Conclusions:MT might promote cell cycle progression via regulation of MMP,ATP,ROS and maternal mRNA levels,potentially increasing the first cleavage of parthenogenetic zygotes developed from vitrified-warmed mouse oocytes and their subsequent development.展开更多
Objective:To explore the cardioprotective effect of hesperidin against arsenic trioxide-induced cardiac toxicity in rats.Methods:Cardiac toxicity was induced by oral administration of 4 mg/kg arsenic trioxide for 30 d...Objective:To explore the cardioprotective effect of hesperidin against arsenic trioxide-induced cardiac toxicity in rats.Methods:Cardiac toxicity was induced by oral administration of 4 mg/kg arsenic trioxide for 30 days.Hematological,biochemical,electrocardiography,echocardiography,and histopathological examinations were performed.Results:Hesperidin decreased the neutrophil-to-lymphocyte ratio,calcium,creatine kinase-myoglobin binding,lactate dehydrogenase,IL-6,and lipid peroxidation,as well as increased sodium and potassium concentration and superoxide dismutase and catalase activity in arsenic trioxide-intoxicated rats.Moreover,it reduced peak systolic velocity and end-diastolic velocity while increasing heart rate.Arsenic trioxide-induced histopathological damage to cardiac tissue was prominently alleviated by hesperidin treatment.Conclusions:Hesperidin attenuates arsenic trioxide-induced cardiac toxicity in rats.Therefore,it can be further explored as a cardioprotective agent.展开更多
基金supported by the National Natural Science Foundation of China(grant no.32072735,31572398)the Natural Science Fund of Qinghai Province(2020-ZJ-902)by the China Agriculture Research System(grant no.CARS-36).
文摘Background:This study investigated the effect of melatonin(MT)on cell cycle(G1/S/G2/M)of parthenogenetic zygotes developed from vitrified-warmed mouse metaphase II(MII)oocytes and elucidated the potential mechanism of MT action in the first cleavage of embryos.Results:After vitrification and warming,oocytes were parthenogenetically activated(PA)and in vitro cultured(IVC).Then the spindle morphology and chromosome segregation in oocytes,the maternal mRNA levels of genes including Miss,Doc1r,Setd2 and Ythdf2 in activated oocytes,pronuclear formation,the S phase duration in zygotes,mitochondrial function at G1 phase,reactive oxygen species(ROS)level at S phase,DNA damage at G2 phase,early apoptosis in 2-cell embryos,cleavage and blastocyst formation rates were evaluated.The results indicated that the vitrification/warming procedures led to following perturbations 1)spindle abnormalities and chromosome misalignment,alteration of maternal mRNAs and delay in pronucleus formation,2)decreased mitochondrial membrane potential(MMP)and lower adenosine triphosphate(ATP)levels,increased ROS production and DNA damage,G1/S and S/G2 phase transition delay,and delayed first cleavage,and 3)increased early apoptosis and lower levels of cleavage and blastocyst formation.Our results further revealed that such negative impacts of oocyte cryopreservation could be alleviated by supplementation of warming,recovery,PA and IVC media with 10^(−9) mol/L MT before the embryos moved into the 2-cell stage of development.Conclusions:MT might promote cell cycle progression via regulation of MMP,ATP,ROS and maternal mRNA levels,potentially increasing the first cleavage of parthenogenetic zygotes developed from vitrified-warmed mouse oocytes and their subsequent development.
文摘Objective:To explore the cardioprotective effect of hesperidin against arsenic trioxide-induced cardiac toxicity in rats.Methods:Cardiac toxicity was induced by oral administration of 4 mg/kg arsenic trioxide for 30 days.Hematological,biochemical,electrocardiography,echocardiography,and histopathological examinations were performed.Results:Hesperidin decreased the neutrophil-to-lymphocyte ratio,calcium,creatine kinase-myoglobin binding,lactate dehydrogenase,IL-6,and lipid peroxidation,as well as increased sodium and potassium concentration and superoxide dismutase and catalase activity in arsenic trioxide-intoxicated rats.Moreover,it reduced peak systolic velocity and end-diastolic velocity while increasing heart rate.Arsenic trioxide-induced histopathological damage to cardiac tissue was prominently alleviated by hesperidin treatment.Conclusions:Hesperidin attenuates arsenic trioxide-induced cardiac toxicity in rats.Therefore,it can be further explored as a cardioprotective agent.
