Taurochenodeoxycholic acid induces NR8383 cells apoptosis via PKC/JNK-dependent pathway.
Our former studies have suggested that taurochenodeoxycholic acid (TCDCA) as a signaling molecule shows obvious anti-inflammatory and immune regulation properties. In this research, we tentatively explored the potential effects and the possible mechanism that involve in the apoptotic process in NR8383 cells induced by TCDCA. Using flow cytometry analysis, we evaluated the apoptosis rate. Gene expression levels were determined by qPCR. The expressions of protein kinase C (PKC), Jun N-terminal kinase (JNK) and their phosphorylation were measured by Western Blot. We observed the activities of caspase-3 and caspase-8 with Caspase-Glo® regent. The results demonstrated that TCDCA dramatically improved the apoptosis rate of NR8383 cells in a concentration-dependent manner. In the meantime, PKC mRNA levels and activities were significantly augmented by TCDCA treatments. In addition, JNK, caspase-3 and caspase-8 mRNA expression levels and activities were increased by TCDCA, while they were markedly decreased by specific inhibitors. We conclude that TCDCA contributes to the apoptosis through the activation of the caspase cascade in NR8383 cells, and the PKC/JNK signaling pathway may be involved in this process. These results indicate that TCDCA may be a latent effective pharmaceutical product for apoptosis-related diseases.
College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, China; Key Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture, Hohhot, China.
Xu
X
Wang
College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, China; Key Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture, Hohhot, China; College of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Ziying
Z
Zhang
College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, China; Key Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture, Hohhot, China.
Xiuling
X
He
College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, China; Key Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture, Hohhot, China.
Wei
W
Mao
College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, China; Key Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture, Hohhot, China.
Lei
L
Zhou
College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, China; Key Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture, Hohhot, China. Electronic address: lpfnmg@126.com.
Peifeng
P
Li
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D002460:Cell Line; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D011493:Protein Kinase C / Q000235:genetics / Q000378:metabolism*; D013655:Taurochenodeoxycholic Acid / Q000494:pharmacology*
D013655:Taurochenodeoxycholic Acid; D011493:Protein Kinase C; D048031:JNK Mitogen-Activated Protein Kinases; D053148:Caspase 3; D053181:Caspase 8
Apoptosis; Caspase; JNK; Macrophage; PKC; TCDCA