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Tomatidine inhibits tumor necrosis factor-α-induced apoptosis in C2C12 myoblasts via ameliorating endoplasmic reticulum stress

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Author(s)
Seung‑Eun SongSu‑Kyung ShinHyun‑Woo ChoSeung‑Soon ImJae‑Hoon BaeSeon Min WooTaeg‑Kyu KwonDae‑Kyu Song
Keimyung Author(s)
Im, Seung SoonBae, Jae HoonKwon, Taeg KyuSong, Dae Kyu
Department
Dept. of Physiology (생리학)
Dept. of Immunology (면역학)
Journal Title
Mol Cell Biochem.
Issued Date
2018
Volume
444
Issue
1-2
Keyword
TomatidineTNF-αC2C12 myoblastER stressApoptosis
Abstract
In this study, we examined the effect of tomatidine on tumor necrosis factor (TNF)-α-induced apoptosis in C2C12 myoblasts. TNF-α treatment increased cleaved caspase 3 and cleaved poly (ADP-ribose) polymerase (PARP) protein levels in a doseand time-dependent manner. Pretreatment of cells with 10 μM tomatidine prevented TNF-α-induced apoptosis, caspase 3 cleavage, and PARP cleavage. Cells were treated with 100 ng/mL TNF-α for 24 h, and flow cytometry was utilized to assess apoptosis using annexin-V and 7-aminoactinomycin D. TNF-α up-regulated activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP) expression. This effect was suppressed by pretreatment with tomatidine. Pretreatment with 4-phenylbutyric acid (a chemical chaperone) also inhibited TNF-α-induced cleavage of caspase 3 and PARP and upregulation of ATF4 and CHOP expression. In addition, tomatidine-mediated inhibition of phosphorylation of c-Jun amino terminal kinase (JNK) attenuated TNF-α-induced cleavage of PARP and caspase 3. However, tomatidine did not affect NF-κB activation in TNF-α-treated C2C12 myoblast cells. Taken together, the present study demonstrates that tomatidine attenuates TNF-α-induced apoptosis through down-regulation of CHOP expression and inhibition of JNK activation.
Keimyung Author(s)(Kor)
임승순
배재훈
권택규
송대규
Publisher
School of Medicine (의과대학)
Citation
Seung‑Eun Song et al. (2018). Tomatidine inhibits tumor necrosis factor-α-induced apoptosis in C2C12 myoblasts via ameliorating endoplasmic reticulum stress. Mol Cell Biochem., 444(1–2), 17–25. doi: 10.1007/s11010-017-3226-3
Type
Article
ISSN
1573-4919
Source
https://link.springer.com/article/10.1007%2Fs11010-017-3226-3
DOI
10.1007/s11010-017-3226-3
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/41688
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
1. School of Medicine (의과대학) > Dept. of Physiology (생리학)
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