| Literature DB >> 25622068 |
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Abstract
Entities:
Year: 2015 PMID: 25622068 PMCID: PMC4306513 DOI: 10.1371/journal.pone.0117635
Source DB: PubMed Journal: PLoS One ISSN: 1932-6203 Impact factor: 3.240
Figure 3BE selectively induces apoptosis of Con A-activated CD3+ T cells through mitochondrial pathway.
CD3+ T cells were isolated from murine splenocytes using Miltenyi MACS Purification and incubated with indicated concentrations of BE for 24 h in the absence or presence of 5 µg/ml of Con A. (A–E) the percentages of Annexin V+, Fas+, and FasL+ cells were analyzed using PE-anti-Fas mAb/annexin V-FITC or PE-anti-FasL mAb/annexin V-FITC staining. A is a representative of three independent assays with PE-anti-Fas mAb/annexin V-FITC staining. B is a representative of three independent assays with PE-anti-FasL mAb/annexin V-FITC staining. C–E represents mean ± SEM of three independent experiments. (F, G) Loss of ΔΨm in T cells was analyzed using JC-1 staining. F is a representative of three independent assays, and G represents mean ± SEM of three independent experiments. (H) The release of cytochrome c (Cyto-c) from mitochondria in T cells after BE treatment in the presence of Con A was examined by Western blotting. (I) Protein levels of Bcl-2 and Bax in T cells after BE treatment in the presence of Con A were examined by Western blotting. The results shown in H and I are representative of three experiments. (J) The activities of caspase-3, 8, 9 in T cells after BE treatment in the presence of Con A was measured using colorimetric assay. Each column represents the mean ± SEM of 3 experimental values. *P<0.05 versus untreated controls.