FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2005901598> ?p ?o ?g. }

• W2005901598 endingPage "468" @default.
• W2005901598 startingPage "461" @default.
• W2005901598 abstract "We constructed a model of apoptosis in mouse preimplantation embryos and investigated the effect of the flavonol icariin on embryonic development in vitro in embryos with reduced microRNA-21 (miR-21). The model was generated by microinjecting an miR-21 inhibitor into the cytoplasm of mouse pronuclear embryos, which were cultured in vitro using modified CZB (mCZB) basal medium (model group), or using mCZB medium with 0.6 μg/mL icariin as an experimental group (model-Ica). These were compared with embryos collected in vivo (vivo group) or not microinjected (control group). Developmental rates in vitro of two- and four-cell embryos and blastocysts were observed, and Hoechst 33342 and terminal deoxynucleotidyl transferase dUTP nick end labeling staining were used to count blastocyst cell numbers and apoptotic cell numbers and percentages. The transcriptional levels of miR-21, the apoptotic genes caspase 3 and phosphatase and tensin homolog deleted on chromosome ten (PTEN), and the antiapoptotic gene Bcl-2 were detected by quantitative polymerase chain reaction (qPCR). Western immunoblotting was used to detect the protein levels of caspase 3, PTEN, and Bcl-2. Compared with the model group, icariin treatment significantly improved blastocyst development in vitro (58.43 ± 7.53% vs. 37.85 ± 6.47%; P < 0.01), whereas it was not significantly different to the control group (60.34 ± 9.86%). Icariin treatment significantly increased the blastocyst cell numbers (47.02 ± 4.93 vs. 37.70 ± 5.80; P < 0.01), and reduced the rates of apoptosis (5.51 ± 2.35% vs. 10.11 ± 4.21%; P < 0.01), whereas the blastocyst cell numbers and apoptotic rates revealed no significant differences between the vivo (46.06 ± 6.50, 5.95 ± 2.56%) and control groups (45.77 ± 4.09, 6.18 ± 2.41%). Icariin treatment significantly improved miR-21 expression in all embryo stages, reduced the transcriptional levels of caspase 3 and PTEN, and increased the levels of Bcl-2. The protein expression levels of caspase 3 and PTEN were decreased in blastocysts and the level of Bcl-2 was increased (P < 0.01). These had no significant differences with the vivo and control groups, and the protein levels revealed no significant differences between two- and four-cell embryos. Thus, miR-21 was necessary for preimplantation embryonic development, and embryo quality was closely associated with the apoptosis-related protein expression levels regulated by miR-21. Icariin upregulated miR-21 expression and reduced apoptosis in embryos with reduced miR-21. It also improved embryonic developmental quality in vitro, indicating an important regulatory role for miR-21 in blastocyst development in vitro." @default.
• W2005901598 created "2016-06-24" @default.
• W2005901598 creator A5002374127 @default.
• W2005901598 creator A5004690387 @default.
• W2005901598 creator A5029857128 @default.
• W2005901598 creator A5030790932 @default.
• W2005901598 creator A5034567696 @default.
• W2005901598 creator A5035946181 @default.
• W2005901598 creator A5065460631 @default.
• W2005901598 creator A5077439743 @default.
• W2005901598 creator A5089966579 @default.
• W2005901598 date "2014-08-01" @default.
• W2005901598 modified "2023-10-03" @default.
• W2005901598 title "The regulatory role of icariin on apoptosis in mouse preimplantation embryos with reduced microRNA-21" @default.
• W2005901598 cites W1966913788 @default.
• W2005901598 cites W1968163453 @default.
• W2005901598 cites W1970089531 @default.
• W2005901598 cites W1977170922 @default.
• W2005901598 cites W1979413046 @default.
• W2005901598 cites W1980181091 @default.
• W2005901598 cites W1982314799 @default.
• W2005901598 cites W1989125392 @default.
• W2005901598 cites W1990079648 @default.
• W2005901598 cites W1991966840 @default.
• W2005901598 cites W1995199345 @default.
• W2005901598 cites W2003232219 @default.
• W2005901598 cites W2011193885 @default.
• W2005901598 cites W2021132772 @default.
• W2005901598 cites W2030038054 @default.
• W2005901598 cites W2044123448 @default.
• W2005901598 cites W2051584801 @default.
• W2005901598 cites W2054606782 @default.
• W2005901598 cites W2058904686 @default.
• W2005901598 cites W2059934269 @default.
• W2005901598 cites W2062575747 @default.
• W2005901598 cites W2063695505 @default.
• W2005901598 cites W2065651660 @default.
• W2005901598 cites W2075750528 @default.
• W2005901598 cites W2081297751 @default.
• W2005901598 cites W2087400084 @default.
• W2005901598 cites W2087582557 @default.
• W2005901598 cites W2088206141 @default.
• W2005901598 cites W2091108445 @default.
• W2005901598 cites W2111316275 @default.
• W2005901598 cites W2112079154 @default.
• W2005901598 cites W2116405910 @default.
• W2005901598 cites W2116475621 @default.
• W2005901598 cites W2117900553 @default.
• W2005901598 cites W2126374067 @default.
• W2005901598 cites W2128982949 @default.
• W2005901598 cites W2148574613 @default.
• W2005901598 cites W2150309926 @default.
• W2005901598 cites W2153180469 @default.
• W2005901598 cites W2315994376 @default.
• W2005901598 cites W2327415429 @default.
• W2005901598 cites W2418321058 @default.
• W2005901598 doi "https://doi.org/10.1016/j.theriogenology.2014.05.006" @default.
• W2005901598 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24948525" @default.
• W2005901598 hasPublicationYear "2014" @default.
• W2005901598 type Work @default.
• W2005901598 sameAs 2005901598 @default.
• W2005901598 citedByCount "10" @default.
• W2005901598 countsByYear W20059015982015 @default.
• W2005901598 countsByYear W20059015982016 @default.
• W2005901598 countsByYear W20059015982017 @default.
• W2005901598 countsByYear W20059015982018 @default.
• W2005901598 countsByYear W20059015982019 @default.
• W2005901598 countsByYear W20059015982022 @default.
• W2005901598 countsByYear W20059015982023 @default.
• W2005901598 crossrefType "journal-article" @default.
• W2005901598 hasAuthorship W2005901598A5002374127 @default.
• W2005901598 hasAuthorship W2005901598A5004690387 @default.
• W2005901598 hasAuthorship W2005901598A5029857128 @default.
• W2005901598 hasAuthorship W2005901598A5030790932 @default.
• W2005901598 hasAuthorship W2005901598A5034567696 @default.
• W2005901598 hasAuthorship W2005901598A5035946181 @default.
• W2005901598 hasAuthorship W2005901598A5065460631 @default.
• W2005901598 hasAuthorship W2005901598A5077439743 @default.
• W2005901598 hasAuthorship W2005901598A5089966579 @default.
• W2005901598 hasConcept C142724271 @default.
• W2005901598 hasConcept C153911025 @default.
• W2005901598 hasConcept C154113507 @default.
• W2005901598 hasConcept C16685009 @default.
• W2005901598 hasConcept C190283241 @default.
• W2005901598 hasConcept C196795494 @default.
• W2005901598 hasConcept C196843134 @default.
• W2005901598 hasConcept C204787440 @default.
• W2005901598 hasConcept C207001950 @default.
• W2005901598 hasConcept C2777609662 @default.
• W2005901598 hasConcept C2778177303 @default.
• W2005901598 hasConcept C2779549131 @default.
• W2005901598 hasConcept C2780685212 @default.
• W2005901598 hasConcept C54355233 @default.
• W2005901598 hasConcept C55493867 @default.
• W2005901598 hasConcept C71924100 @default.
• W2005901598 hasConcept C86554907 @default.
• W2005901598 hasConcept C86803240 @default.
• W2005901598 hasConcept C87073359 @default.

• next