Journal Of Advanced Pharmacy Education And Research, Journal Year: 2024, Volume and Issue: 14(1), P. 84 - 90
Published: Jan. 1, 2024
Language: Английский
Journal Of Advanced Pharmacy Education And Research, Journal Year: 2024, Volume and Issue: 14(1), P. 84 - 90
Published: Jan. 1, 2024
Language: Английский
Antioxidants, Journal Year: 2023, Volume and Issue: 12(12), P. 2077 - 2077
Published: Dec. 5, 2023
Selenium (Se) deficiency disrupts intracellular REDOX homeostasis and severely deteriorates immune anti-inflammatory function in high-yielding periparturient dairy cattle. To investigate the damage of extracellular vesicles derived from Se-deficient MAC-T cells (SeD-EV) on normal mammary epithelial cells, an vitro model Se was established. produced many ROS, promoting apoptosis release inflammatory factors. Extracellular were successfully isolated by ultrahigh-speed centrifugation identified transmission electron microscopy, particle size analysis, surface markers (CD63, CD81, HSP70, TSG101). RNA sequencing performed exosomal RNA. A total 9393 lncRNAs 63,155 mRNAs transcripts SeC SeD groups, respectively, which 126 955 differentially expressed. Furthermore, SeD-EV promoted TUNEL analysis. significantly inhibited Bcl-2, while Bax Cleaved Caspase3 greatly increased. Antioxidant capacity (CAT, T-AOC, SOD, GSH-Px) SeD-EV-treated cells. Additionally, p-PERK, p-eIF2α, ATF4, CHOP, XBP1 all elevated supplemented with SeD-EV. In addition, p-PI3K, p-Akt, p-mTOR decreased strikingly conclusion, caused oxidative stress, thus triggering inflammation through endoplasmic reticulum stress PI3K-Akt-mTOR signaling pathway, contributed to explaining mechanism causing mastitis.
Language: Английский
Citations
12Journal of Nutrition, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
Language: Английский
Citations
0Antioxidants, Journal Year: 2025, Volume and Issue: 14(2), P. 190 - 190
Published: Feb. 7, 2025
This study was designed to evaluate the protective effects of eleutheroside B (EB) in high-altitude-induced myocardial injury (HAMI) and unravel underlying molecular mechanisms. SD rats were used for vivo experiments. Following pretreatment with EB, exposed a hypobaric environment within chamber 48 h. Electrocardiograms, H&E staining, serum biochemical indices measured EB on HAMI. Immunofluorescence Western blotting utilized detect expression associated proteins. In parallel, hypoxic cell incubator establish an vitro model hypoxia-induced injury. The anti-necroptotic effect its potential mechanisms investigated verified vitro. Exposure hypoxia led electrocardiogram disorders, pathological changes tissue, increased concentrations BNP CK-MB, elevated levels oxidative stress indicators inflammatory factors. Additionally, necroptosis-related proteins upregulated. Pretreatment effectively ameliorated caused by hypoxia, mitigated inflammation, suppressed necroptosis. Furthermore, facilitated translocation Nrf2 into nucleus. conclusion, this provides evidence suggesting that may exert against HAMI inhibiting cardiomyocyte necroptosis via Nrf2/HO-1 signaling pathway.
Language: Английский
Citations
0Journal Of Advanced Pharmacy Education And Research, Journal Year: 2024, Volume and Issue: 14(1), P. 84 - 90
Published: Jan. 1, 2024
Language: Английский
Citations
0