Search Results
You are looking at 21 - 30 of 33 items for
- Author: Hui Li x
- Refine by access: All content x
Search for other papers by Jun Shao in
Google Scholar
PubMed
Search for other papers by Bing Zhang in
Google Scholar
PubMed
Search for other papers by Jia-Jun Yu in
Google Scholar
PubMed
Search for other papers by Chun-Yan Wei in
Google Scholar
PubMed
Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Fudan University, Shanghai, People’s Republic of China
Search for other papers by Wen-Jie Zhou in
Google Scholar
PubMed
Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Shanghai, People’s Republic of China
Search for other papers by Kai-Kai Chang in
Google Scholar
PubMed
Search for other papers by Hui-Li Yang in
Google Scholar
PubMed
Search for other papers by Li-Ping Jin in
Google Scholar
PubMed
Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Shanghai, People’s Republic of China
Search for other papers by Xiao-Yong Zhu in
Google Scholar
PubMed
Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Fudan University, Shanghai, People’s Republic of China
Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Shanghai, People’s Republic of China
Search for other papers by Ming-Qing Li in
Google Scholar
PubMed
Macrophages play an important role in the origin and development of endometriosis. Estrogen promoted the growth of decidual stromal cells (DSCs) by downregulating the level of interleukin (IL)-24. The aim of this study was to clarify the role and mechanism of IL-24 and its receptors in the regulation of biological functions of endometrial stromal cells (ESCs) during endometriosis. The level of IL-24 and its receptors in endometrium was measured by immunohistochemistry. In vitro analysis was used to measure the level of IL-24 and receptors and the biological behaviors of ESCs. Here, we found that the expression of IL-24 and its receptors (IL-20R1 and IL-20R2) in control endometrium was significantly higher than that in eutopic and ectopic endometrium of women with endometriosis. Recombinant human IL-24 (rhIL-24) significantly inhibited the viability of ESCs in a dosage-dependent manner. Conversely, blocking IL-24 with anti-IL-24 neutralizing antibody promoted ESCs viability. In addition, rhIL-24 could downregulate the invasiveness of ESCs in vitro. After co-culture, macrophages markedly reduced the expression of IL-24 and IL-20R1 in ESCs, but not IL-22R1. Moreover, macrophages significantly restricted the inhibitory effect of IL-24 on the viability, invasion, the proliferation relative gene Ki-67, proliferating cell nuclear antigen (PCNA) and cyclooxygenase2 (COX-2), and the stimulatory effect on the tumor metastasis suppressor gene CD82 in ESCs. These results indicate that the abnormally low level of IL-24 in ESCs possibly induced by macrophages may lead to the enhancement of ESCs’ proliferation and invasiveness and contribute to the development of endometriosis.
Search for other papers by Renjie Wang in
Google Scholar
PubMed
Search for other papers by Wei Pan in
Google Scholar
PubMed
Search for other papers by Lei Jin in
Google Scholar
PubMed
Search for other papers by Yuehan Li in
Google Scholar
PubMed
Search for other papers by Yudi Geng in
Google Scholar
PubMed
Search for other papers by Chun Gao in
Google Scholar
PubMed
Search for other papers by Gang Chen in
Google Scholar
PubMed
Search for other papers by Hui Wang in
Google Scholar
PubMed
Search for other papers by Ding Ma in
Google Scholar
PubMed
Search for other papers by Shujie Liao in
Google Scholar
PubMed
Artificial intelligence (AI) has experienced rapid growth over the past few years, moving from the experimental to the implementation phase in various fields, including medicine. Advances in learning algorithms and theories, the availability of large datasets and improvements in computing power have contributed to breakthroughs in current AI applications. Machine learning (ML), a subset of AI, allows computers to detect patterns from large complex datasets automatically and uses these patterns to make predictions. AI is proving to be increasingly applicable to healthcare, and multiple machine learning techniques have been used to improve the performance of assisted reproductive technology (ART). Despite various challenges, the integration of AI and reproductive medicine is bound to give an essential direction to medical development in the future. In this review, we discuss the basic aspects of AI and machine learning, and we address the applications, potential limitations and challenges of AI. We also highlight the prospects and future directions in the context of reproductive medicine.
Henan Key Laboratory of Reproduction and Genetics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Henan Provincial Obstetrical and Gynecological Diseases (Reproductive Medicine) Clinical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Search for other papers by Hui Li in
Google Scholar
PubMed
Henan Key Laboratory of Reproduction and Genetics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Henan Provincial Obstetrical and Gynecological Diseases (Reproductive Medicine) Clinical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Search for other papers by Huan Wang in
Google Scholar
PubMed
Henan Key Laboratory of Reproduction and Genetics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Henan Provincial Obstetrical and Gynecological Diseases (Reproductive Medicine) Clinical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Search for other papers by Jianmin Xu in
Google Scholar
PubMed
Henan Key Laboratory of Reproduction and Genetics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Henan Provincial Obstetrical and Gynecological Diseases (Reproductive Medicine) Clinical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Search for other papers by Xinxin Zeng in
Google Scholar
PubMed
Henan Key Laboratory of Reproduction and Genetics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Henan Provincial Obstetrical and Gynecological Diseases (Reproductive Medicine) Clinical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Search for other papers by Yingpu Sun in
Google Scholar
PubMed
Henan Key Laboratory of Reproduction and Genetics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Henan Provincial Obstetrical and Gynecological Diseases (Reproductive Medicine) Clinical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Search for other papers by Qingling Yang in
Google Scholar
PubMed
In brief
Oocyte quality and its NAD+ level decrease with time during in vitro culture. This study shows that nicotinamide riboside (NR) supplementation improves early embryonic development potential in post-ovulatory oocytes by decreasing the reactive oxygen species (ROS) levels and reducing DNA damage and apoptosis which could potentially increase the success rate of assisted reproductive technology (ART).
Abstract
The quality of post-ovulatory oocytes deteriorates over time, impacting the outcome of early embryonic development during human ART. We and other groups have found that NAD+, a prominent redox cofactor and enzyme substrate, decreases in both aging ovaries and oocytes. In this study, we found that the NAD+ levels decreased in the post-ovulatory mouse oocytes during in vitro culture and this decrease was partly prevented by NR supplementation. NR treatmenty restored MII oocyte quality and enhanced the early embryonic development potential of post-ovulatory oocytes via alleviating mitochondrial dysfunction and maintaining normal spindle/chromosome structure. Also, treatment with NR decreased ROS levels and reduced DNA damage and apoptosis in post-ovulatory oocytes. Taken together, our findings indicated that NR supplementation increases the oocyte quality and early embryonic development potential in post-ovulatory oocytes which could potentially increase the success rate of ART.
Department of Histology and Embryology, College of Life Science, Department of Physiology, Harbin Medical University, 194 Xuefu Road, Nangang District, Harbin, Heilongjiang Province, China
Search for other papers by Xue Li in
Google Scholar
PubMed
Search for other papers by Zhi-Yan Shan in
Google Scholar
PubMed
Search for other papers by Yan-Shuang Wu in
Google Scholar
PubMed
Search for other papers by Xing-Hui Shen in
Google Scholar
PubMed
Search for other papers by Chun-Jia Liu in
Google Scholar
PubMed
Search for other papers by Jing-Ling Shen in
Google Scholar
PubMed
Search for other papers by Zhong-Hua Liu in
Google Scholar
PubMed
Search for other papers by Lei Lei in
Google Scholar
PubMed
Pig pluripotent cells may represent an advantageous experimental tool for developing therapeutic application in the human biomedical field. However, it has previously been proven to be difficult to establish from the early embryo and its pluripotency has not been distinctly documented. In recent years, induced pluripotent stem (iPS) cell technology provides a new method of reprogramming somatic cells to pluripotent state. The generation of iPS cells together with or without certain small molecules has become a routine technique. However, the generation of iPS cells from pig embryonic tissues using viral infections together with small molecules has not been reported. Here, we reported the generation of induced pig pluripotent cells (iPPCs) using the iPS technology in combination with valproic acid (VPA). VPA treatment significantly increased the expression of pluripotent genes and played an important role in early reprogramming. We showed that iPPCs resembled pig epiblast cells in their morphology and pluripotent markers, such as OCT4, NANOG, and SSEA1. It had a normal karyotype and could form embryoid bodies, which express three germ layer markers in vitro. In addition, the iPPCs might directly differentiate into neural progenitors after being induced with the retinoic acid and extracellular matrix. Our study established a reasonable method to generate pig pluripotent cells, which might be a new donor cell source for human neural disease therapy.
Search for other papers by Tao Yu in
Google Scholar
PubMed
Search for other papers by Shuai Lin in
Google Scholar
PubMed
Search for other papers by Rui Xu in
Google Scholar
PubMed
Search for other papers by Tian-Xi Du in
Google Scholar
PubMed
Search for other papers by Yang Li in
Google Scholar
PubMed
Search for other papers by Hui Gao in
Google Scholar
PubMed
Search for other papers by Hong-Lu Diao in
Google Scholar
PubMed
Search for other papers by Xiu-Hong Zhang in
Google Scholar
PubMed
Embryo implantation is a crucial step for the successful establishment of mammalian pregnancy. Cyclophilin A (CYPA) is a ubiquitously expressed intracellular protein and is secreted in response to inflammatory stimuli to regulate diverse cellular functions. However, there are currently no reports about the role of CYPA in embryo implantation. Here, we examine the expression pattern of CYPA during mouse early pregnancy and explore the potential role of CYPA during implantation. CYPA is expressed in the subluminal stroma surrounding the implanting blastocyst on day 5 of pregnancy, but not at inter-implantation sites. In ovariectomized mice, estrogen and progesterone significantly stimulate CYPA expression. When pregnant mice are injected intraperitoneally with CYPA inhibitor, the numbers of implantation sites are significantly reduced. Using an in vitro stromal cell culture system, Ppia siRNA knockdown of CYPA and CYPA-specific inhibitor treatment partially inhibits levels of CD147, MMP3 and MMP9. Decreased CYPA expression also significantly inhibits Stat3 activity and expands estrogen responsiveness. Taken together, CYPA may play an important role during mouse embryo implantation.
Search for other papers by Hui-Hui Shen in
Google Scholar
PubMed
Search for other papers by Cheng-Jie Wang in
Google Scholar
PubMed
Search for other papers by Xin-Yan Zhang in
Google Scholar
PubMed
Search for other papers by Yan-Ran Sheng in
Google Scholar
PubMed
Search for other papers by Shao-Liang Yang in
Google Scholar
PubMed
Search for other papers by Zi-Meng Zheng in
Google Scholar
PubMed
Search for other papers by Jia-Lu Shi in
Google Scholar
PubMed
Clinical Research Center, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, People’s Republic of China
Search for other papers by Xue-Min Qiu in
Google Scholar
PubMed
Search for other papers by Feng Xie in
Google Scholar
PubMed
Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
Department of Obstetrics and Gynecology, Maternal and Child Health Hospital of Longgang District, Shenzhen, Guangdong Province, People’s Republic of China
Search for other papers by Ming-Qing Li in
Google Scholar
PubMed
Heme oxygenase 1 (HO-1, encoded by the HMOX1 gene) is the rate-limiting enzyme that catalyzes heme degradation, and it has been reported to exert antioxidative effects. Recently, decidualization has been reported to confer resistance to environmental stress signals, protecting against oxidative stress. However, the effects and regulatory mechanism of HO-1 in decidual stromal cells (DSCs) during early pregnancy remain unknown. Here, we verified that the levels of HO-1 and heme in DSCs are increased compared with those in endometrial stromal cells. Additionally, the upregulation of HIF1A expression led to increased HMOX1 expression in DSCs possibly via nuclear factor erythroid 2-related factor (encoded by the NFE2L2 gene). However, addition of the competitive HO-1 inhibitor zinc protoporphyrin IX resulted in an increase in HIF1A expression. Hydrogen peroxide (H2O2) induced the production of reactive oxygen species (ROS), decreased the cell viability of DSCs in vitro, and upregulated the level of heme. As an HO-1 inducer, cobalt protoporphyrin IX decreased ROS production and significantly reversed the inhibitory effect of H2O2 on cell viability. More importantly, patients with unexplained spontaneous abortion had low levels of HO-1 that were insufficient to protect against oxidative stress. This study suggests that the upregulation of HO-1 expression via HIF1A protects DSCs against excessive heme-mediated oxidative stress. Furthermore, the excessive oxidative stress injury and impaired viability of DSCs associated with decreased HO-1 expression should be associated with the occurrence and/or development of spontaneous abortion.
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Chao Du in
Google Scholar
PubMed
Omaha Veterans Affairs Medical Center, Omaha, Nebraska, USA
Search for other papers by John S Davis in
Google Scholar
PubMed
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Chao Chen in
Google Scholar
PubMed
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Zan Li in
Google Scholar
PubMed
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Ye Cao in
Google Scholar
PubMed
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Hui Sun in
Google Scholar
PubMed
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Bao-Shun Shao in
Google Scholar
PubMed
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Yu-Xin Lin in
Google Scholar
PubMed
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Yong-Sheng Wang in
Google Scholar
PubMed
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Li-Guo Yang in
Google Scholar
PubMed
College of Animal Science and Technology of Huazhong Agricultural University, Wuhan, China
Search for other papers by Guo-Hua Hua in
Google Scholar
PubMed
Fibroblast growth factor 2 (FGF2), a member of FGF family, binds with FGF receptors (FGFR) to initiate biological functions in various somatic cells. However, little is known regarding the role of FGF2/FGFR on oocyte meiosis. In this study, we investigated expression patterns and functions of FGF2/FGFR during in vitro maturation (IVM) of mouse cumulus-oocyte complexes (COCs). Among four FGFRs, Ffgr1 was the most abundant in COCs. The transcripts for Fgf2 and Ffgr1 in COCs increased during IVM. Ffgr1 was present in oocytes and cumulus cells, while Fgf2 was present in only cumulus cells. Treatment of COCs with the selective FGFR inhibitor SU5402 blocked oocyte meiotic progression and downregulated expression of Bmp15 and Gdf9. In contrast, supplement of FGF2 promoted oocyte meiotic progression and upregulated Bmp15 and Gdf9 expression. Inhibition of FGFR with SU5402 reduced cumulus expansion and expressions of Ptx3, Has2 and Tnfaip6. Treatment with FGF2 increased Ptx3 and Has2 expression. Inhibition of FGFR had no effect on meiotic progression of denuded oocytes (DOs). However, co-culture of DOs with COCs or supplementation with FGF2 promoted meiotic progression of DOs. Inhibition of FGF2/FGFR signaling also downregulated Ffgr1 expression, while supplemental FGF2 upregulated Fgfr1 expression. Furthermore, inhibition of FGFR in COCs interrupted the c-Mos/MAPK pathway and maturation-promoting factor (MPF), as indicated by downregulation of oocyte c-mos and Ccnb1 transcripts, respectively. Overall, this study suggests that FGF2 produced by cumulus cells, activates a FGF2/FGFR autocrine/paracrine loop within COCs to regulate cumulus expansion and oocyte meiosis. These findings reveal a novel role for FGF2/FGFR signaling during in vitro maturation of COCs.
Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
Search for other papers by Jia-Jun Yu in
Google Scholar
PubMed
Search for other papers by Hui-Ting Sun in
Google Scholar
PubMed
Search for other papers by Zhong-Fang Zhang in
Google Scholar
PubMed
Search for other papers by Ru-Xia Shi in
Google Scholar
PubMed
Search for other papers by Li-Bing Liu in
Google Scholar
PubMed
Search for other papers by Wen-Qing Shang in
Google Scholar
PubMed
Search for other papers by Chun-Yan Wei in
Google Scholar
PubMed
Search for other papers by Kai-Kai Chang in
Google Scholar
PubMed
Search for other papers by Jun Shao in
Google Scholar
PubMed
Search for other papers by Ming-Yan Wang in
Google Scholar
PubMed
Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Fudan University, Shanghai, People’s Republic of China
Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Shanghai, People’s Republic of China
Search for other papers by Ming-Qing Li in
Google Scholar
PubMed
Endometriosis (EMS) is associated with an abnormal immune response to endometrial cells, which can facilitate the implantation and proliferation of ectopic endometrial tissues. It has been reported that human endometrial stromal cells (ESCs) express interleukin (IL)15. The aim of our study was to elucidate whether or not IL15 regulates the cross talk between ESCs and natural killer (NK) cells in the endometriotic milieu and, if so, how this regulation occurs. The ESC behaviors in vitro were verified by Cell Counting Kit-8 (CCK-8), Annexin/PI, and Matrigel invasion assays, respectively. To imitate the local immune microenvironment, the co-culture system between ESCs and NK cells was constructed. The effect of IL15 on NK cells in the co-culture unit was investigated by flow cytometry (FCM). In this study, we found that ectopic endometrium from patients with EMS highly expressed IL15. Rapamycin, an autophagy inducer, decreased the level of IL15 receptors (i.e. IL15Rα and IL2Rβ). IL15 inhibits apoptosis and promotes the invasiveness, viability, and proliferation of ESCs. Meanwhile, a co-culture with ESCs led to a decrease in CD16 on NK cells. In the co-culture system, IL15 treatment downregulated the levels of Granzyme B and IFN-γ in CD16+NK cells, NKG2D in CD56dimCD16-NK cells, and NKP44 in CD56brightCD16-NK cells. On the one hand, these results indicated that IL15 derived from ESCs directly stimulates the growth and invasion of ESCs. On the other hand, IL15 may help the immune escape of ESCs by suppressing the cytotoxic activity of NK cells in the ectopic milieu, thereby facilitating the progression of EMS.
Tongji University School of Medicine, Shanghai, People’s Republic of China
NHC Key Lab of Reproduction Regulation (Shanghai Institute of Planned Parenthood Research), Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
Search for other papers by Sha-Ting Lei in
Google Scholar
PubMed
Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
Search for other papers by Ming-Qing Li in
Google Scholar
PubMed
Search for other papers by Yan-Ling Cao in
Google Scholar
PubMed
Tongji University School of Medicine, Shanghai, People’s Republic of China
Search for other papers by Shu-Hui Hou in
Google Scholar
PubMed
Tongji University School of Medicine, Shanghai, People’s Republic of China
Search for other papers by Hai-Yan Peng in
Google Scholar
PubMed
Search for other papers by Dong Zhao in
Google Scholar
PubMed
Search for other papers by Jing Sun in
Google Scholar
PubMed
Endometriosis (EMS) is a chronic benign inflammatory disease characterized by the growth of endometrial-like tissue in aberrant locations outside of the uterine cavity. Angiogenesis and abnormal immune responses are the fundamental requirements of endometriotic lesion survival in the peritoneal cavity. Follistatin-like I (FSTL1) is a secreted glycoprotein that exhibits varied expression levels in cardiovascular disease, cancer and arthritis. However, the role of FSTL1 in the development of EMS remains to be fully elucidated. Results of the present study demonstrated that the expression of FSTL1 was significantly increased in ectopic endometrial stromal cells (ESCs) and peritoneal fluid from patients with EMS, compared to the control group. Both conditions of hypoxia and estrogen treatment induced human ESCs to produce increased levels of FSTL1 and disco-interacting protein 2 homolog A (DIP2A). Furthermore, the expression levels of DIP2A, IL8 and IL1β were increased in FSTL1 overexpressed HESCs. Additionally, FSTL1 treatment increased the proliferation of HUVECs in a dose-dependent manner in vitro and markedly increased the tube formation of HUVECs. Moreover, treatment with FSTL1 facilitated M1 polarization of macrophages, increased the secretion of proinflammatory factors and inhibited the expression of scavenger receptor CD36. Results of the present study suggested that the elevated expression of FSTL1 may play a key role in accelerating the development of EMS via enhancing the secretion of proinflammatory factors and promoting angiogenesis.
Key Laboratory of Animal Genetics and Breeding of the Ministry of Agriculture, College of Animal Sciences and Technology, College of Veterinary Medicine, Department of Obstetrics and Gynecology, College of Animal Sciences and Technology, China Agricultural University, Beijing 100094, People's Republic of China
Search for other papers by Wen-Min Cheng in
Google Scholar
PubMed
Search for other papers by Lei An in
Google Scholar
PubMed
Search for other papers by Zhong-Hong Wu in
Google Scholar
PubMed
Search for other papers by Yu-Bo Zhu in
Google Scholar
PubMed
Search for other papers by Jing-Hao Liu in
Google Scholar
PubMed
Search for other papers by Hong-Mei Gao in
Google Scholar
PubMed
Search for other papers by Xi-He Li in
Google Scholar
PubMed
Search for other papers by Shi-Jun Zheng in
Google Scholar
PubMed
Search for other papers by Dong-Bao Chen in
Google Scholar
PubMed
Search for other papers by Jian-Hui Tian in
Google Scholar
PubMed
We recently reported that electrical activation followed by secondary chemical activation greatly enhanced the developmental competence of in vitro matured porcine oocytes fertilized by intracytoplasmic sperm injection (ICSI). We hypothesized that sperm treatment with disulfide bond reducing agents will enhance the development competence of porcine embryos produced by this ICSI procedure. We examined the effects of glutathione (GSH), dithiothreitol (DTT), GSH or DTT in combination with heparin on sperm DNA structure, paternal chromosomal integrity, pronuclear formation, and developmental competence of in vitro matured porcine oocytes after ICSI. Acridine orange staining and flow cytometry based sperm chromatin structure assay were used to determine sperm DNA integrity by calculating the cells outside the main population (COMP αT). No differences were observed in COMP αT values among GSH-treated and control groups. COMP αT values in GSH-treated groups were significantly lower than that in DTT-treated groups. Following ICSI, GSH treatments did not significantly alter paternal chromosomal integrity. Paternal chromosomal integrity in sperm treated with DTT plus or minus heparin was also the lowest among all groups. GSH-treated sperm yielded the highest rates of normal fertilization and blastocyst formation, which were significantly higher than that of control and DTT-treated groups. The majority of blastocysts derived from control and GSH-treated spermatozoa were diploid, whereas blastocysts derived from DTT-treated spermatozoa were haploid. In conclusion, sperm treatment with GSH enhanced the developmental capacity of porcine embryos produced by our optimized ICSI procedure.
