Effects of Quercetin on Ovarian Function and Regulation of the Ovarian PI3K/Akt/FoxO3a Signalling Pathway and Oxidative Stress in a Rat Model of Cyclophosphamide‐Induced Premature Ovarian Failure

2021 ◽  
Author(s):  
Shaoyan Zheng ◽  
Mingying Ma ◽  
Yanxia Chen ◽  
Miaoxia Li
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Premature Ovarian Failure ◽  
Ovarian Function ◽  
Ovarian Failure ◽  
Signalling Pathway ◽  
And Oxidative Stress

scholarly journals Human Umbilical Cord Mesenchymal Stem Cells Therapy in Cyclophosphamide-Induced Premature Ovarian Failure Rat Model

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Dan Song ◽  
Yun Zhong ◽  
Chunfeng Qian ◽  
Qinyan Zou ◽  
Jian Ou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Rat Model ◽  
Premature Ovarian Failure ◽  
Ovarian Function ◽  
Hormone Secretion ◽  
Ovarian Failure ◽  
Human Umbilical Cord ◽  
Ovarian Cells

Premature ovarian failure (POF) is one of the most common causes of infertility in women. In our present study, we established cyclophosphamide- (CTX-) induced POF rat model and elucidated its effect on ovarian function. We detected the serum estrogen, follicle stimulating hormone, and anti-Müllerian hormone of mice models by ELISA and evaluated their folliculogenesis by histopathology examination. Our study revealed that CTX administration could severely disturb hormone secretion and influence folliculogenesis in rat. This study also detected ovarian cells apoptosis by deoxy-UTP-digoxigenin nick end labeling (TUNEL) and demonstrated marked ovarian cells apoptosis in rat models following CTX administration. In order to explore the potential of human umbilical cord mesenchymal stem cells (UCMSCs) in POF treatment, the above indexes were used to evaluate ovarian function. We found that human UCMSCs transplantation recovered disturbed hormone secretion and folliculogenesis in POF rat, in addition to reduced ovarian cell apoptosis. We also tracked transplanted UCMSCs in ovaries by fluorescencein situhybridization (FISH). The results manifested that the transplanted human UCMSCs could reside in ovarian tissues and could survive for a comparatively long time without obvious proliferation. Our present study provides new insights into the great clinical potential of human UCMSCs in POF treatment.

scholarly journals Intra-Ovarian Injection of Bone Marrow c-Kit+ Cells Induced Ovarian Rejuvenation in Menopausal Rats

2020 ◽  
Author(s):  
Sepideh Sheshpari ◽  
Mahnaz Shahnazi ◽  
Shahin Ahmadian ◽  
Mohammad Nouri ◽  
Mehran Mesgari Abbasi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Rat Model ◽  
Premature Ovarian Failure ◽  
Ovarian Function ◽  
Substantial Reduction ◽  
Ovarian Failure ◽  
Reproductive Age ◽  
Control Group ◽  
Premature Menopause ◽  
Post Transplantation

Abstract Background: Premature ovarian failure (POF) is a condition caused by ovarian insuffiency during the reproductive age that affects ~1% of women globally. Many attempts have been collected to find feasible and effective approach to reduce POF consequences in females. In this regard, cell-based therapies with certain cell types are touted as novel and hopeful therapeutic intervention in the clinical setting. Methods: To evaluate the restoration of ovarian function after intra-ovarian transplantation of bone marrow-derived c-Kit+ cells, a rat model of ovarian failure was produced. Rats were treated with 160 mg/kg/BW of 4-vinylcyclohexene dioxide (VCD) for 15 consecutive days. Using magnetic-activated cell sorting (MACS) technique, freshly isolated rat bone marrow-derived c-Kit+ and c-Kit- cells (4×105 cells/10 µL) were enriched and transplanted into the ovaries of treatment and control animals, respectively. Prior to transplantation as well as 2, 4, 6, and 8 weeks post-transplantation, randomly-selected rats were euthanized and ovarian tissues were subjected to pathohistological examinations and real-time PCR analyses.Results: Premature ovarian failure (POF) status was confirmed by the presence of pathological features and a decreased number of immature and mature follicles compared with control group (p<0.05). Histological examination revealed a substantial reduction of atretic follicles in POF rats receiving c-Kit+ cells in comparison with POF rats that did not receive these cells (p<0.05). Compared with control samples, angiogenesis-related genes, Angpt2 and KDR, showed increased and decreased expression in POF ovaries, respectively (p<0.05). c-Kit+ cells had potential to restore angiogenesis in the ovarian tissue to within normal ranges. Systemic levels of FSH did not significantly change in pre- or post-transplantation time points for any group (p>0.05). Notable reduction of collagen deposition was found in c-Kit treated rats. Transplantation of c-Kit+ cells also restored the reduced fertility rate (p<0.05).Conclusions: Our findings suggest that intra-ovarian administration of bone marrow-derived c-Kit+ cells can modulate angiogenesis signaling and pathological changes, leading to the rejuvenation of ovarian function of a rat model of premature menopause.

scholarly journals Curcumin exerts a protective effect against premature ovarian failure in mice

2018 ◽  
Vol 60 (3) ◽  
pp. 261-271 ◽  
Author(s):  
Zhengjie Yan ◽  
Youjin Dai ◽  
Heling Fu ◽  
Yuan Zheng ◽  
Dan Bao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Protective Effect ◽  
Premature Ovarian Failure ◽  
Ovarian Function ◽  
Ovarian Failure ◽  
Protective Agent ◽  
Primordial Follicles ◽  
Expression Levels ◽  
P16 Expression

This study was designed to investigate the protective effect of curcumin against d-galactose (d-gal)-induced premature ovarian failure (POF) in mice. A mouse POF model was induced by subcutaneous injection of d-gal (200 mg/kg/day) daily for 42 days. Mice in the curcumin group received both d-gal treatment and intraperitoneal injection of curcumin (100 mg/kg/day) for 42 days. Ovarian function, oxidative stress and apoptosis were evaluated. The P, E2 and SOD levels were higher, and the FSH, LH and MDA levels were significantly lower in the curcumin group than those in the d-gal group. The proportion of primordial follicles was also significantly higher in the curcumin group than that in the d-gal group. In addition, curcumin treatment after d-gal administration resulted in significantly lower Sod2, Cat, 8-OhdG, 4-HNE, NTY and senescence-associated protein P16 expression levels, higher Amh expression levels and less apoptosis in granulosa cells than was observed in the d-gal group. Moreover, the p-Akt, Nrf2 and HO-1 protein expression levels were significantly higher and the apoptosis-related cleaved caspase-3 and -9 protein expression levels were markedly lower in the curcumin group than in the d-gal group. In conclusion, curcumin effectively inhibited d-gal-induced oxidative stress, apoptosis and ovarian injury via a mechanism involving the Nrf2/HO-1 and PI3K/Akt signaling pathways, suggesting that curcumin is a potential protective agent against POF.

Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death

2021 ◽  
pp. 153537022199520
Author(s):  
Nanees F El-Malkey ◽  
Amira E Alsemeh ◽  
Wesam MR Ashour ◽  
Nancy H Hassan ◽  
Husam M Edrees
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Beclin 1 ◽  
Male Rats ◽  
Fetuin A ◽  
Intestinal Ischemia Reperfusion ◽  
And Oxidative Stress

Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson’s trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications.

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