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- Title
Baicalin Protects the Cardiomyocytes from ER Stress-Induced Apoptosis: Inhibition of CHOP through Induction of Endothelial Nitric Oxide Synthase.
- Authors
Shen, Mingzhi; Wang, Lin; Yang, Guodong; Gao, Lei; Wang, Bo; Guo, Xiaowang; Zeng, Chao; Xu, Yong; Shen, Liangliang; Cheng, Ke; Xia, Yuesheng; Li, Xiumin; Wang, Haichang; Fan, Li; Wang, Xiaoming
- Abstract
Baicalin, the main active ingredient of the Scutellaria root, exerts anti-oxidant and anti-apoptotic effects in cardiovascular diseases. However, the therapeutic mechanism of baicalin remains unknown. Cultured neonatal rat cardiomyocytes were pre-treated with baicalin (0–50 µM) for 24 h, and subsequently treated with tunicamycin (100 ng/ml). Cell viability was detected by MTT assay, and cell damage was determined by LDH release and TUNEL assay. The expression of CHOP, JNK, caspase-3, eNOS was analyzed by western blot. NO was measured by DAF-FM staining. As a result, treatment with baicalin significantly reduced apoptosis induced by ER stress inducer tunicamycin in cardiomyocytes. Molecularly, baicalin ameliorated tunicamycin-induced ER stress by downregulation of CHOP. In addition, baicalin inverted tunicamycin-induced decreases of eNOS mRNA and protein levels, phospho eNOS and NO production through CHOP pathway. However, the protective effects of baicalin were significantly decreased in cardiomyocytes treated with L-NAME, which suppressed activation of nitric oxide synthase. In conclusion, our results implicate that baicalin could protect cardiomyocytes from ER stress-induced apoptosis via CHOP/eNOS/NO pathway, and suggest the therapeutic values of baicalin against ER stress-associated cardiomyocyte apoptosis.
- Subjects
CARDIOVASCULAR disease treatment; HEART cells; ANTIOXIDANTS; APOPTOSIS; ENZYME inhibitors; LABORATORY rats; ENDOTHELIAL cells; NITRIC-oxide synthases; ENDOPLASMIC reticulum
- Publication
PLoS ONE, 2014, Vol 9, Issue 2, p1
- ISSN
1932-6203
- Publication type
Article
- DOI
10.1371/journal.pone.0088389