Yuling Mi

Zhejiang University, Hang-hsien, Zhejiang Sheng, China

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Publications (24)52.33 Total impact

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    ABSTRACT: Steroid hormones and their receptors play pivotal roles throughout vertebrate reproduction and development. Egg formation in avian species is a prime example. The synthesis of egg yolk proteins by the liver is highly estrogen dependent. Two major components of the yolk protein precursors, vitellogenin II (VTG II) and very low-density apolipoprotein II (ApoVLDL II) are synthesized in the liver of hens under estrogen stimulation and are subsequently transferred via the blood to the developing oocytes. Estrogen-inducible transcription can be mediated through estrogen receptors (ERα and ERβ) or through G protein-coupled receptor 30 (GPR30) but the exact participation of the individual receptor is not clear. Here we determine the relative contribution of each transduction pathway in VTG II and ApoVLDL II synthesis in the hepatocytes by using selective compounds that are known to specifically interact with each of the ERs and GPR30. 17β-estradiol and propyl-pyrazole-triol (PPT, ERα agonist) induced a dose-dependent increase in VTG II and ApoVLDL II mRNA expression. A high concentration of diarylpropionitrile (DPN, which preferentially motivates ERβ) slightly stimulated the expression of VTG II and ApoVLDL II mRNA. However, G-1 (a GPR30 agonist) failed to display any stimulating role. MPP (a highly selective ERα antagonist) fully blocked the expression of both yolk precursors which were up-regulated by 17β-estradiol, PPT and DPN. Considering that DPN can also provoke the action of ERα at high concentration, this excludes the participation of ERβ and supports the role of ERα. The above results indicate that estrogen stimulates the mRNA expression of VTG II and ApoVLDL II predominantly through ERα in the chicken liver.
    Theriogenology 01/2014; · 2.08 Impact Factor
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    ABSTRACT: The signaling molecule retinoic acid (RA) is known to triggers germ cells to enter meiosis. However, RA may not be the only secreted inducer of meiosis. Our previous data indicates that luteinizing hormone also promotes germ cell meiotic initiation by upregulating 3βHSDII transcription. Here, using chicken embryos, we investigate the role of progesterone (P4) in regulating germ cell meiotic initiation. P4 treatment at embryonic day 9.5 accelerated germ cell meiosis entry in the female chicken embryos. However, P4 treatment in vivo did no influence on testicular germ cells but triggered their meiotic initiation in the cultured testes. As treatment with a RA receptor (RAR) inhibitor did not block the stimulatory effect of P4 on germ cell meiotic initiation, this P4 stimulatory effect seems to be independent of RAR-mediated signaling. The abundance of RA metabolism-related enzymes and RA receptor (RARβ) mRNAs did not differ significantly between P4-treated and control individuals. The RA concentration in the ovaries remained unchanged by P4 treatment in vivo. Since no inhibition by the PR nuclear receptor antagonist mifepristone on P4 effect was observed in either in vitro or in vivo experiments, the effect of P4 on germ cell meiotic initiation is probably mediated by membrane progesterone receptors (mPR). The mPRα, mPRβ and mPRγ mRNAs were all expressed in the embryonic ovaries. The expression of mPRα and mPRβ were higher than that of mPRγ. Immunohistochemical results showed that mPRα-positive cells were mainly scattered in the ovarian cortex area where most germ cells were distributed. The mPRβ-positive cells were widely distributed in the ovaries and positive cells were clustered with a similar morphology to that of germ cell clusters. In conclusion, P4 may regulate embryonic germ cell meiotic initiation independent of RA signaling through the membrane PRs. This study provides a new insight into the mechanisms of germ cell meiotic initiation in the chicken.
    Theriogenology 01/2014; · 2.08 Impact Factor
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    ABSTRACT: The beneficial effects of quercetin on reproductive damage elicited by 4-nitrophenol (PNP) were studied in adult male mice. A six-week treatment of weekly intraperitoneal injections of PNP (50 mg/kg) resulted in severe damage to the seminiferous tubules, a remarkable increase in both hydroxyl radical and malondiadehyde production, and notably decreased glutathione peroxidase and superoxide dismutase activities. Moreover, PNP treatment induced germ cell apoptosis, inhibited Bcl-xl expression, and then activated Bax expression and the caspase-3 enzyme. Exposure to PNP also increased XBP-1 and HO-1 mRNAs levels. However, simultaneous supplementation with quercetin (75 mg/kg) attenuated the toxicity induced by PNP through renewal of the antioxidant enzyme's status, alleviating apoptosis by regulating the expressions of Bax and Bcl-xl, XBP-1 and HO-1mRNAs, and the regulation of caspase-3 activity. Taken together, these findings indicated that the antioxidant quercetin displays a potential preventive effect on PNP-induced oxidative damage in mouse testes and may represent an efficient supplement to attenuate reproductive toxicity from environmental toxicants in order to ensure reproductive health and sperm production. Anat Rec, 2013. © 2013 Wiley Periodicals, Inc.
    The Anatomical Record Advances in Integrative Anatomy and Evolutionary Biology 08/2013; · 1.34 Impact Factor
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    ABSTRACT: The interactive effect of insulin-like growth factor I (IGF-I) and prostaglandin E2 (PGE2) on the proliferation of theca externa cells (TECs) was investigated in the prehierarchical small yellow follicles of laying hens. IGF-I manifested a proliferating effect like PGE2 on TECs, but this stimulating effect was restrained by AG1024 (IGF-IR inhibitor), KP372-1 (PKB/AKT inhibitor) or NS398 (COX-2 inhibitor). AG1024, KP372-1 or NS398 abolished IGF-I-stimulated COX-2 expression and PGE2 production. Meanwhile, KP372-1, NS398 or AG1024 depressed the PGE2-stimulated expression of COX-2 and IGF-IR mRNA. Therefore, the IGF-I receptor pathway up-regulates COX-2 expression and PGE2 synthesis via PKB signaling cascade, and then PGE2 stimulates IGF-IR mRNA expression to promote TEC proliferation in an autocrine pattern. Overall, the reciprocal stimulation of intracellular PGE2 and IGF-I may enhance TEC proliferation and facilitate the development of chicken prehierarchical follicles.
    Prostaglandins & other lipid mediators 06/2013; · 2.42 Impact Factor
  • Bin He, Yuling Mi, Caiqiao Zhang
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    ABSTRACT: Gonadotropins are required for gametogenesis but in embryonic gonads this mechanism is not well understood. Here we use chicken embryos to investigate the mechanism that gonadotropins regulate the ovarian germ cell mitosis/meiosis decision. Treatment with follicle-stimulating hormone (FSH) delayed germ cell meiosis entry and promoted their proliferation. This action was blocked by an aromatase inhibitor. Treatment with luteinizing hormone (LH) accelerated germ cell meiosis entry and promoted transcription of 3βHSDII to increase progesterone (P4) production. In the cultured ovaries, P4 triggered meiotic initiation in germ cells. MiR181a*, which acts to downregulate the NR6A1 transcript to trigger the meiotic initiation, was upregulated by FSH and downregulated by LH. Collectively, gonadotropins regulate germ cells mitosis and meiotic initiation through steroid hormones and a miR181a*-mediated pathway. In particularly, FSH delays germ cell meiosis entry and promotes cell proliferation via estrogen while LH accelerates the meiotic initiation via elevated P4 production.
    Molecular and Cellular Endocrinology 02/2013; · 4.04 Impact Factor
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    ABSTRACT: The present study was designed to examine the effect of the grape seed proanthocyanidin extract (GSPE) on developing hepatic fibrosis that was induced by thioacetamide (TAA) in mice. Administration of TAA for 9 weeks led to a serious necrosis and apoptosis of the parenchymal cells, which resulted in an accumulation of excessive collagen in the liver and an increase of transformed hepatic stellate cells (HSCs). In addition, the mRNA expression of transforming growth factor β1 (TGF-β1), α-smooth muscle actin (α-SMA), as the marker of the activated HSCs, and α1-(I)-collagen were all up-regulated significantly when compared with the control. However, combined oral administration of GSPE at 100mg/kg suppressed the mRNA expression of TGF-β1 and α-SMA, with decreased collagen accumulation as demonstrated by histomorphological evaluation and quantitative RT-PCR. The mRNA expression of the pro-inflammatory factors, including inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), was remarkably enhanced by TAA treatment. However, their levels displayed a down-regulated trend beyond simultaneous GSPE treatment. Moreover, GSPE administration markedly suppressed lipid peroxidation. In conclusion, as a plant antioxidant, GSPE manifested effective hepatocellular protective action to ameliorate the developing liver fibrosis induced by chronic TAA administration in mice.
    Toxicology Letters 07/2012; 213(3):353-60. · 3.15 Impact Factor
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    ABSTRACT: Meiosis is a process unique to the differentiation of germ cells and exhibits sex-specific in timing. Previous studies showed that retinoic acid (RA) as the vitamin A metabolite is crucial for controlling Stra8 (Stimulated by retinoic acid gene 8) expression in the gonad and to initiate meiosis; however, the mechanism by which retinoid-signaling acts has remained unclear. In the present study, we investigated the role of the enzyme retinaldehyde dehydrogenase 2 (RALDH2) which catalyzes RA synthesizes by initiating meiosis in chicken ovarian germ cells. Meiotic germ cells were first detected at day 15.5 in chicken embryo ovary when the expression of synaptonemal complex protein 3 (Scp3) and disrupted meiotic cDNA 1 homologue (Dmc1) became elevated, while Stra8 expression was specifically up-regulated at day 12.5 before meiosis onset. It was observed from the increase in Raldh2 mRNA expression levels and decreases in Cyp26b1 (the enzyme for RA catabolism) expression levels during meiosis that requirement for RA accumulation is essential to sustain meiosis. This was also revealed by RA stimulation of the cultured ovaries with the initiation of meiosis response, and the knocking down of the Raldh2 expression during meiosis, leading to abolishment of RA-dependent action. Altogether, these studies indicate that RA synthesis by the enzyme RALDH2 and signaling through its receptor is crucial for meiosis initiation in chicken embryonic ovary.
    Amino Acids 06/2012; · 3.91 Impact Factor
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    ABSTRACT: As embryonic progenitors for the gametes, PGCs (primordial germ cells) proliferate and develop under strict regulation of numerous intrinsic and external factors. As the most active natural metabolite of vitamin A, all-trans RA (retinoic acid) plays pivotal roles in regulating development of various cells. The proliferating action of RA on PGCs was investigated along with the intracellular PI3K (phosphoinositide 3-kinase)/Akt (protein kinase B; also known as Akt)-mediated NF-κB (nuclear factor κB) signalling cascade. The results show that RA significantly promoted PGC proliferation in a dose- and time-dependent manner, confirmed by BrdU (bromodeoxyuridine) incorporation and cell cycle analysis. However, this promoting effect was attenuated by sequential inhibitors of LY294002 for PI3K, KP372-1 for Akt and SN50 for NF-κB respectively. Western blot analysis showed increased Akt phosphorylation (Ser473) of PGCs after stimulation with RA, but this was abolished by LY294002 or KP372-1. Treatment with RA increased expression of NF-κB and decreased IκBα (inhibitory κBα) expression, which were inhibited by SN50. Blockade of PI3K or Akt activity inhibited NF-κB translocation from the cytoplasm to the nucleus. Finally, mRNA expression of cell cycle regulating genes [cyclin D1 and E, CDK6 (cyclin-dependent kinase 6) and CDK2] was up-regulated in the RA-treated cells. This stimulation was also markedly retarded by combined treatment with LY294002, KP372-1 and SN50. These results suggest that RA activates the PI3K/Akt and NF-κB signalling cascade to promote proliferation of the cultured chicken PGCs.
    Cell Biology International 05/2012; 36(8):705-12. · 1.64 Impact Factor
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    ABSTRACT: Basic fibroblast growth factor (bFGF or FGF2) plays diverse roles in regulating cell proliferation, migration and differentiation during embryo development. In this study, the effect of bFGF on ovarian germ cell development was investigated in the embryonic chicken by in vitro and in vivo experiments. Results showed that a remarkable decrease in bFGF expression in the ovarian cortex was manifested during meiosis progression. With ovary organ culture, we revealed that meiosis was initiated after retinoic acid (RA) treatment alone but was decreased after combined bFGF treatment that was detected by real time RT-PCR, fluorescence immunohistochemistry and Giemsa staining. Further, no significant difference in mRNA expression of either RA metabolism-related enzymes (Raldh2 and Cyp26b1) or RA receptors was displayed after bFGF challenge. This result suggests that the suppression of bFGF on meiosis was unlikely through inhibition of RA signaling. In addition, as a mitogen, bFGF administration increased germ cell proliferation (via BrdU incorporation) in cultured organ or cells in vitro and also in developing embryos in vivo. In contrast, blockade of bFGF action by SU5402 (an FGFR1 antagonist) or inhibition of protein kinase C signaling showed inhibited effect of bFGF on mitosis. In conclusion, bFGF suppresses RA-induced entry of germ cells into meiosis to ensure embryonic ovarian germ cells to maintain at undifferentiated status and accelerate germ cell proliferation by binding with FGFR1 involving PKC activation in the chicken.
    General and Comparative Endocrinology 01/2012; 176(2):173-81. · 2.82 Impact Factor
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    ABSTRACT: The proliferating effect of basic fibroblast growth factor (bFGF) on granulosa cells from ovarian pre-hierarchical follicles was evaluated in the laying chickens. Expression of bFGF receptor 1 (FGFR1) from small yellow follicles was determined by immunohistochemistry and RT-PCR. The FGFR1 protein and mRNA were intensively expressed in the granulosa layer. After 8- to 24-h treatment with bFGF (0.1-100 ng/ml), the proliferation of cultured granulosa cells was remarkably enhanced in a dose- and time-dependent manner. The FGFR1 antagonist SU5402 inhibited bFGF-induced cell proliferation. This stimulating effect was further confirmed by 5-bromo-2-deoxyuridine incorporation and terminal transferase dUTP nick end-labelling assay. Immunocytochemistry of protein kinases A (PKA) and C (PKC) showed that the pro-proliferation action of bFGF predominantly activated PKC expression. Meanwhile, the bFGF-induced cell proliferation was significantly promoted by PKC activator PMA and inhibited by PKC inhibitor H(7) (p < 0.05). In addition, the bFGF-elicited cell proliferation was accompanied with increased mRNA expression of the cell cycle-regulating genes including cyclins D1 and E1, cyclin-dependent kinases 2 and 6. In conclusion, bFGF promoted the proliferation of ovarian granulosa cells through binding with FGFR1 and involving PKC pathway in the pre-hierarchical follicles of the laying chickens.
    Reproduction in Domestic Animals 05/2011; 47(1):135-42. · 1.39 Impact Factor
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    ABSTRACT: Cadmium is a toxic heavy metal that is widely distributed in the environment. As a critical process, oxidative toxicity mediates the morphological and functional damages in germ cells after cadmium exposure. In this study, the protective effect of quercetin on cadmium-induced oxidative toxicity was investigated in mouse testicular germ cells. After oral administration of cadmium chloride at 4 mg/kg body weight for 2 weeks, damages in spermatozoa occurred in the early stage of spermatogenesis. Cadmium treatment significantly decreased the testicular antioxidant system, including decreases in the glutathione (GSH) level, superoxide dismutase (SOD), and GSH peroxidase (GSH-Px) activities. Moreover, exposure to cadmium resulted in an increase of hydrogen peroxide production and lipid peroxidation in testes. In addition, cadmium provoked germ cell apoptosis by upregulating expression of the proapoptotic proteins Bax and caspase-3 and downregulating expression of the antiapoptotic protein Bcl-XL. However, combined administration of a common flavonoid quercetin at 75 mg/kg body weight significantly attenuated cadmium-induced germ cell apoptosis by suppressing the hydrogen peroxide production and lipid peroxidation in testicular tissue. Simultaneous supplementation of quercetin markedly restored the decrease in GSH level and SOD and GSH-Px activities elicited by cadmium treatment. Additionally, quercetin protected germ cells from cadmium-induced apoptosis by downregulating the expression of Bax and caspase-3 and upregulating Bcl-XL expression. These results indicate that quercetin, due to its antioxidative and antiapoptotic characters, may manifest effective protective action against cadmium-induced oxidative toxicity in mouse testicular germ cells.
    The Anatomical Record Advances in Integrative Anatomy and Evolutionary Biology 03/2011; 294(3):520-6. · 1.34 Impact Factor
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    ABSTRACT: The attenuating effect of quercetin on cadmium-induced oxidative damage and apoptosis was investigated in cultured granulosa cells from chicken ovarian follicles. Results showed that exposure to 5 μM CdCl(2) induced a decrease in granulosa cell number and viability, caused chromatin condensation and DNA fragmentation. Moreover, cadmium treatment markedly increased malondialdehyde level and decreased glutathione peroxidase and superoxide dismutase activities. Furthermore, cadmium provoked higher BAX expression, inhibited expression of BCL2 and X-linked inhibitor of apoptosis protein (XIAP) and activated caspase-3. However, simultaneous supplementation with 1 μg/ml quercetin protected granulosa cells against cadmium-induced cytotoxicity through attenuating lipid peroxidation, renewing antioxidant enzymes activities and alleviating apoptosis by modulating XIAP, BAX and BCL2 expression, and inhibiting caspase-3 activity. Therefore, these results suggested that quercetin, as a widely distributed dietary antioxidant, contributes potentially to prevent cadmium-induced cytotoxicity in granulosa cells through attenuating lipid peroxidation, elevating intracellular antioxidant status and inhibiting apoptosis to ensure reproductive health.
    Reproductive Toxicology 01/2011; 31(4):477-85. · 3.14 Impact Factor
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    ABSTRACT: The effect of GS (ginsenosides) on proliferation of chicken GCs (granulosa cells) from prehierarchical SYF (small yellow follicles) was evaluated, and involvement of the PKC (protein kinase C) signalling pathway as well as mRNA expression of cyclins and CDK (cyclin-dependent kinase) were investigated. Whole SYF or GCs isolated from SYF were cultured in Medium 199 supplemented with 0.5% FCS (fetal calf serum). After 16 h, the cells were challenged with GS alone or in combination with PKC inhibitor H7 or activator PMA (phorbol 12-myristate 13-acetate) for 24 h in serum-free medium. Results showed that in both whole follicles and pure GCs monolayer culture system, GS (0.1-10 microg/ml) significantly increased the number of GCs in SYF in a dose-dependent manner, and this stimulatory effect was inhibited by H7, but enhanced by PMA. Meanwhile, the PCNA-LI (proliferating cell nuclear antigen labelling index) of GCs displayed similar changes with the cell number. Mechanism of GS action was further evaluated in cultured GCs separated from SYF. Western blot analysis showed that 10 microg/ml GS increased PKC translocation from cytoplasm to the plasma membrane of the GCs to become the active state. This effect was blocked by H7. Furthermore, GS up-regulated the expression of cyclin D1/CDK6 and cyclin E/CDK2 mRNAs in GCs; however, inhibition of PKC with H7 attenuated this stimulatory effect. These results indicated that GS could stimulate proliferation of chicken GCs through activated PKC-involved up-regulation of cyclin D1/CDK6 and cyclin E/CDK2 genes, subsequently promoting development of the chicken prehierarchical follicles.
    Cell Biology International 07/2010; 34(7):769-75. · 1.64 Impact Factor
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    ABSTRACT: The 4-nitrophenol (PNP) in diesel exhaust particles (DEP) has been identified as a vasodilator and is a known degradation product of the insecticide parathion. In this study, the protective effect of quercetin, a potent oxygen free radical scavenger and metal chelator, against the oxidative damage of PNP on cultured testicular cells was studied in male embryonic chickens. Testicular cells from Day 18 embryos were cultured in serum-free McCoy's 5A medium and challenged with quercetin (1.0 microg/ml) alone or in combinations with PNP (10(-7)-10(-5) M) for 48 h. The oxidative damage was estimated by measuring cell viability, content of malondialdehyde (MDA), activity of superoxide dismutase (SOD) and glutathione peroxidation (GSH-Px) activity. The results showed that exposure to PNP (10(-5) M) induced condensed nuclei, vacuolated cytoplasm and a decrease in testicular cell viability and spermatogonial cell number. Exposure to PNP induced lipid peroxidation by elevation of the content of MDA. Exposure to PNP also decreased GSH-Px activity and SOD activity. However, simultaneous supplementation with quercetin restored these parameters to the same levels as the control. Consequently, PNP induced oxidative stress in spermatogonial cells, and dietary quercetin may attenuate the reproductive toxicity of PNP to restore the intracellular antioxidant system in the testicular cells of embryonic chickens.
    Journal of Reproduction and Development 04/2010; 56(2):195-9. · 1.76 Impact Factor
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    ABSTRACT: Quercetin, an antioxidant flavonoid, is considered beneficial for human and animal health. In this study, the protective effect of quercetin on oxidative damage to testicular cells was studied in embryonic chickens after treatment with 4-nitro-3-phenylphenol (PNMPP) derived from diesel exhaust particles. Testicular cells were challenged with PNMPP (10(-8)-10(-6) M) alone and in combination with quercetin for 48 h. The results showed that quercetin manifested no deleterious effect on spermatogonial cells up to 1.0 microg/ml. Exposure to PNMPP (10(-6) M) induced condensed nuclei and vacuolated cytoplasm and reductions in testicular cell viability and spermatogonial cell numbers (p<0.05). It also induced lipid peroxidation by an elevation of thiobarbituric acid reactive substances and decreased glutathione peroxidase activity and superoxide dismutase activity (p<0.05). Simultaneous supplementation with quercetin restored these parameters to the same levels as in the control. These data indicate that quercetin protects spermatogonial cells from oxidative damage in embryonic chickens intoxicated with PNMPP.
    Bioscience Biotechnology and Biochemistry 01/2010; 74(5):934-8. · 1.27 Impact Factor
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    ABSTRACT: Diesel exhaust particles (DEP) are considered to be one of the most important air pollutants. In this study, the protective effect of quercetin, an antioxidant flavonoid, on oxidative damage of testicular cells was studied by analysis of the intracellular antioxidant system of embryonic chickens after treatment with 3-methyl-4-nitrophenol (PNMC) derived from DEP. Testicular cells from 18-day-old embryos were cultured in serum-free McCoys'5A medium and challenged with PNMC (10(-7) to 10(-5)M) alone or in combinations with quercetin (1.0 microg/ml) for 48h. Results showed that exposure to PNMC (10(-5)M) induced condensed nuclei and vacuolated cytoplasm, a decrease in testicular cell viability and spermatogonial cell number. Exposure to PNMC induced lipid peroxidation by an elevation of thiobarbituric acid reactive substances as well as decreasing glutathione peroxidation activity and superoxide dismutase activity. However, simultaneous supplementation with quercetin restored these parameters to the similar levels as the control. PNMC is therefore concluded to have induced the oxidative stress of the spermatogonial cells, which can be attenuated by combined quercetin treatment. Our results support the therapeutic use of quercetin in the prevention or treatment of the reproductive toxicity by environmental toxicant PNMC.
    Toxicology Letters 08/2009; 190(1):61-5. · 3.15 Impact Factor
  • Comparative Biochemistry and Physiology C-toxicology & Pharmacology - COMP BIOCHEM PHYSIOL PT C. 01/2008; 148(4):460-460.
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    ABSTRACT: Quercetin, an antioxidant flavonoid, is considered beneficial to human and animal health. In this study, the protective effects of quercetin in relation to oxidative damage of testicular cells were studied by analysis of the intracellular antioxidant system after treatment of embryonic chickens with hypoxanthine-xanthine oxidase (HX-XO) or 2,4-dichlorophenoxyacetic acid (2,4-D). Testicular cells from Day 18 embryos were challenged with quercetin alone or in combinations with HX-XO or 2,4-D for 48 h in culture. The results showed that quercetin manifested no deleterious effects on spermatogonial cells at concentrations up to 1.0 microg/ml. Exposure to HX-XO or 2,4-D (50 microg/ml) induced condensed nuclei and vacuolated cytoplasm and a decrease in testicular cell viability and spermatogonial cell number. Membrane integrity was damaged by elevated lactate dehydrogenase leakage. Exposure to HX-XO or 2,4-D also elicited lipid peroxidation by elevation of thiobarbituric acid reactive substances and decreased glutathione content and superoxide dismutase activity. However, simultaneous supplementation with quercetin restored these parameters to the levels in the controls. Consequently, HX-XO and 2,4-D induced oxidative stress in spermatogonial cells; however, dietary quercetin may attenuate the negative effects of environmental toxicants and restore the antioxidant system in testicular cells.
    Journal of Reproduction and Development 08/2007; 53(4):749-54. · 1.76 Impact Factor
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    ABSTRACT: Primordial germ cells (PGCs) are undifferentiated pluripotent stem cells, whose proliferation is influenced by many internal and external factors. In the present study, a PGC-somatic cell co-culture model was established to evaluate effects of the flavonoids daidzein (DAI) and quercetin (QUE) on proliferation of PGCs from embryonic chickens. PGCs were isolated from the germinal ridge of 3.5-4day embryos and cultured in 5% fetal calf serum (FCS)-supplemented Medium 199. PGC subculture was carried out on chicken embryonic fibroblast feeder (CEF) or follicular granulosa cell feeder (GCF) layers. The subcultured PGCs were challenged with flavonoids alone or in combination with a reactive oxygen substance (ROS)-producing system on CEF for 48h. The results showed a better supporting effect of CEF than GCF. Flavonoids (1microg/ml) significantly promoted PGC proliferation, which could be markedly inhibited by ROS. The oxidative damage by ROS was further manifest by decreased superoxide dismutase activity and glutathione levels. In addition, activation of protein kinase A (PKA) by forskolin significantly stimulated PGC proliferation, but PKA inhibitor H89 inhibited the proliferating effects induced by DAI and QUE. These results indicated that cultured PGCs respond to exogenous agents on proliferation and that antioxidant flavonoids could restore the intracellular antioxidant system and promote PGC proliferation via their antioxidant action involving the PKA signaling pathway.
    Cell Biology International 06/2006; 30(5):445-51. · 1.64 Impact Factor
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    ABSTRACT: The effect of androgen on germ cell proliferation was evaluated by a chicken ovarian germ-somatic cell co-culture model and the mechanisms were explored. Ovarian cells were dispersed from 18-day-old embryos, cultured in serum-free McCoy's 5A medium and challenged with testosterone (T) alone or in combinations with androgen receptor antagonist Flutamide, estrogen receptor antagonist Tamoxifen or aromatase inhibitor Letrozole for 48 h. Germ cells were identified by c-kit immunocytochemistry. The number of germ cells was counted and the proliferating cells were identified by immunocytochemistry of proliferating cell nuclear antigen (PCNA). The labeling index (LI) was determined for germ cells. Results showed that T (10(-7) to 10(-6)M) significantly increased the number of germ cells (P<0.05) and this stimulating effect was inhibited by Flutamide (10-1000 ng/ml), Tamoxifen (10-1000 ng/ml) or Letrozole (10(-9) to 10(-7)M) in a dose-dependent manner. Furthermore, PCNA-LI of germ cells displayed similar changes with the numbers of germ cells. These results indicated that T-stimulated proliferation of cultured ovarian germ cells through both, androgenic and estrogenic actions in embryonic chickens.
    Domestic Animal Endocrinology 05/2005; 28(4):451-62. · 2.38 Impact Factor

Publication Stats

129 Citations
52.33 Total Impact Points

Institutions

  • 2004–2014
    • Zhejiang University
      • • College of Animal Sciences
      • • Department of Veterinary Medicine
      Hang-hsien, Zhejiang Sheng, China
  • 2013
    • Chinese Academy of Fishery Sciences
      北江, Zhejiang Sheng, China
  • 2009–2010
    • Tokyo University of Agriculture and Technology
      • Department of Veterinary Medicine
      Tokyo, Tokyo-to, Japan