FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1848407029> ?p ?o ?g. }

• W1848407029 endingPage "95" @default.
• W1848407029 startingPage "84" @default.
• W1848407029 abstract "Triptolide is the major active ingredient of Tripterygium Glycosides (TG), a traditional Chinese medicine with very potent anti-inflammatory effects and has been used in China for the treatment of rheumatoid arthritis and many other inflammatory diseases. However, clinical application of triptolide is restricted due to its multiple side effects, especially male infertility. The mechanism of triptolide on reproduction toxicity remains unclear. In the present study, a GC–MS based metabolomic approach was employed to evaluate the mechanism of triptolide-induced reproductive toxicity as well as identify potential novel biomarkers for the early detection of spermatogenesis dysfunction. In brief, male mice were divided into two groups with or without triptolide intraperitoneal injection at 60 μg/kg/day for 2 weeks and toxic effect of triptolide on testicular tissues were examined by biochemical indicator analysis, testis histopathologic analysis, and sperm quantity analysis. Metabolomics technology was then performed to evaluate systematically the endogenous metabolites profiling. Our results demonstrated that triptolide suppressed the marker-enzymes of spermatogenesis and testosterone levels, decreased sperm counts, reduced the gonad index and destroyed the microstructure of testis. Multivariate data analysis revealed that mice with triptolide induced testicular toxicity could be distinctively differentiated from normal animals and 35 and 39 small molecule metabolites were changed significantly in testis and serum, respectively (Fold-changes >1.5, P < 0.05), in triptolide-treated mice. Abnormal level of fatty acids, an important energy source of sertoli cells with critical role in maintaining normal function of the testis tissue, was observed in triptolide-treated mice. Additionally, the protein expressions of PPAR, a transcription factor known to play a pivotal role in lipid and energy metabolism was significantly decreased in the testis tissue of triptolide-treated mice. In summary, our study represents the first comprehensive GC–MS based metabolomics analysis of triptolide-induced testicular toxicity. We reported for the first time that exposure to triptolide led to marked changes of a panel of endogenous metabolites in both testis and serum. The impairment of spermatogenesis may be caused by abnormal lipid and energy metabolism in testis via the down-regulation of PPARs mediated by triptolide. The presence of research suggested that PPARs and its related fatty acids metabolism may serve as potential targets for intervention or treatment of male infertility induced by triptolide." @default.
• W1848407029 created "2016-06-24" @default.
• W1848407029 creator A5011078484 @default.
• W1848407029 creator A5011844099 @default.
• W1848407029 creator A5026984704 @default.
• W1848407029 creator A5033933325 @default.
• W1848407029 creator A5035315901 @default.
• W1848407029 creator A5051945295 @default.
• W1848407029 creator A5065493202 @default.
• W1848407029 creator A5066934433 @default.
• W1848407029 creator A5083801181 @default.
• W1848407029 date "2015-10-01" @default.
• W1848407029 modified "2023-09-27" @default.
• W1848407029 title "Triptolide disrupts fatty acids and peroxisome proliferator-activated receptor (PPAR) levels in male mice testes followed by testicular injury: A GC–MS based metabolomics study" @default.
• W1848407029 cites W1978449362 @default.
• W1848407029 cites W1983228926 @default.
• W1848407029 cites W1984967504 @default.
• W1848407029 cites W1988472694 @default.
• W1848407029 cites W1989059608 @default.
• W1848407029 cites W1997062226 @default.
• W1848407029 cites W2006270384 @default.
• W1848407029 cites W2010381561 @default.
• W1848407029 cites W2015428927 @default.
• W1848407029 cites W2015690892 @default.
• W1848407029 cites W2020215730 @default.
• W1848407029 cites W2022336568 @default.
• W1848407029 cites W2022702812 @default.
• W1848407029 cites W2024732892 @default.
• W1848407029 cites W2030295813 @default.
• W1848407029 cites W2035350812 @default.
• W1848407029 cites W2043708267 @default.
• W1848407029 cites W2043771612 @default.
• W1848407029 cites W2046284605 @default.
• W1848407029 cites W2052802169 @default.
• W1848407029 cites W2055041208 @default.
• W1848407029 cites W2066351227 @default.
• W1848407029 cites W2067984761 @default.
• W1848407029 cites W2077399334 @default.
• W1848407029 cites W2079594443 @default.
• W1848407029 cites W2081491337 @default.
• W1848407029 cites W2085280452 @default.
• W1848407029 cites W2085693656 @default.
• W1848407029 cites W2089747726 @default.
• W1848407029 cites W2096612144 @default.
• W1848407029 cites W2103788846 @default.
• W1848407029 cites W2108373171 @default.
• W1848407029 cites W2111705682 @default.
• W1848407029 cites W2126218858 @default.
• W1848407029 cites W2129074344 @default.
• W1848407029 cites W2134032476 @default.
• W1848407029 cites W2135607659 @default.
• W1848407029 cites W2136693483 @default.
• W1848407029 cites W2139019393 @default.
• W1848407029 cites W2140269135 @default.
• W1848407029 cites W2141939741 @default.
• W1848407029 cites W807109299 @default.
• W1848407029 cites W3150450440 @default.
• W1848407029 doi "https://doi.org/10.1016/j.tox.2015.07.008" @default.
• W1848407029 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26219505" @default.
• W1848407029 hasPublicationYear "2015" @default.
• W1848407029 type Work @default.
• W1848407029 sameAs 1848407029 @default.
• W1848407029 citedByCount "65" @default.
• W1848407029 countsByYear W18484070292016 @default.
• W1848407029 countsByYear W18484070292017 @default.
• W1848407029 countsByYear W18484070292018 @default.
• W1848407029 countsByYear W18484070292019 @default.
• W1848407029 countsByYear W18484070292020 @default.
• W1848407029 countsByYear W18484070292021 @default.
• W1848407029 countsByYear W18484070292022 @default.
• W1848407029 countsByYear W18484070292023 @default.
• W1848407029 crossrefType "journal-article" @default.
• W1848407029 hasAuthorship W1848407029A5011078484 @default.
• W1848407029 hasAuthorship W1848407029A5011844099 @default.
• W1848407029 hasAuthorship W1848407029A5026984704 @default.
• W1848407029 hasAuthorship W1848407029A5033933325 @default.
• W1848407029 hasAuthorship W1848407029A5035315901 @default.
• W1848407029 hasAuthorship W1848407029A5051945295 @default.
• W1848407029 hasAuthorship W1848407029A5065493202 @default.
• W1848407029 hasAuthorship W1848407029A5066934433 @default.
• W1848407029 hasAuthorship W1848407029A5083801181 @default.
• W1848407029 hasConcept C123765429 @default.
• W1848407029 hasConcept C126322002 @default.
• W1848407029 hasConcept C134018914 @default.
• W1848407029 hasConcept C142724271 @default.
• W1848407029 hasConcept C16685009 @default.
• W1848407029 hasConcept C190283241 @default.
• W1848407029 hasConcept C194671627 @default.
• W1848407029 hasConcept C204787440 @default.
• W1848407029 hasConcept C21565614 @default.
• W1848407029 hasConcept C2780695664 @default.
• W1848407029 hasConcept C2781079059 @default.
• W1848407029 hasConcept C2781087480 @default.
• W1848407029 hasConcept C2781164371 @default.
• W1848407029 hasConcept C29730261 @default.
• W1848407029 hasConcept C55493867 @default.
• W1848407029 hasConcept C59822182 @default.
• W1848407029 hasConcept C60644358 @default.

• next