Next Article in Journal
Sinigrin and Its Therapeutic Benefits
Next Article in Special Issue
Optimization of Betulinic Acid Extraction from Tecomella undulata Bark Using a Box-Behnken Design and Its Densitometric Validation
Previous Article in Journal
GC×GC-TOFMS Analysis of Essential Oils Composition from Leaves, Twigs and Seeds of Cinnamomum camphora L. Presl and Their Insecticidal and Repellent Activities
Previous Article in Special Issue
Two New Oleanane-Type Saponins with Anti-Proliferative Activity from Camellia oleifera Abel. Seed Cake
Article Menu
Issue 4 (April) cover image

Export Article

Open AccessArticle
Molecules 2016, 21(4), 418;

Bryonolic Acid, a Triterpenoid, Protect Against N-methyl-d-Aspartate-Induced Neurotoxicity in PC12 Cells

College of Pharmacy, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou 350122, Fujian, China
Author to whom correspondence should be addressed.
Academic Editors: Vassilios Roussis and Efstathia Ioannou
Received: 9 January 2016 / Revised: 10 March 2016 / Accepted: 23 March 2016 / Published: 28 March 2016
(This article belongs to the Collection Triterpenes and Triterpenoids)
Full-Text   |   PDF [3063 KB, uploaded 28 March 2016]   |  


Calcium overload is considered to be one of the mechanisms of cerebral ischemia. Ca2+ influx and Ca2+/calmodulin-dependent protein kinase II (CaMKII) and cAMP response element-binding protein (CREB) phosphorylation are considered to be involved in N-Methyl-d-aspartate (NMDA)-induced apoptosis process. This study investigated the neuroprotective effects of bryonolic acid (BA) in an NMDA-induced rat adrenal pheochromocytoma cell line (PC12) cells and the potential mechanism. PC12 was treated by NMDA to establish an excitotoxicity model. BA (110,100 and 1000 μM final concentration) was added to the medium 24 h prior to the addition of NMDA. Subsequently, a methyl thiazolyl tetrazolium (MTT) assay and a lactate dehydrogenase (LDH) release were performed. Ca2+ concentration was demonstrated using a scanning-dual wavelength fluorimetric method. In addition, protein and mRNA levels were determined via Western blot and real-time PCR. In the presence of BA, MTT assay and LDH assay showed that more cells were viable in comparison with the NMDA group. Moreover, the concentration of Ca2+ decreased with the addition of BA in culture. Furthermore, BA could upregulate protein expressions of Bcl-2, p-CREB, and p-CaMKII and downregulate protein expression of Bax. The mRNA results showed that the pattern of mRNA expression were similar to their respective protein levels. All these results indicate that BA protected PC12 cells against NMDA-induced apoptosis by inhibiting Ca2+ influx and regulating gene expression in the Ca2+-CaMKII-CREB signal pathway. Therefore, the present study supports the notion that BA may be a promising neuroprotective agent for the treatment of cerebral ischemia disease. View Full-Text
Keywords: bryonolic acid; PC12 cells; Ca2+; Bcl-2; Bax; p-CaMKII; p-CREB bryonolic acid; PC12 cells; Ca2+; Bcl-2; Bax; p-CaMKII; p-CREB

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Que, J.; Ye, M.; Zhang, Y.; Xu, W.; Li, H.; Xu, W.; Chu, K. Bryonolic Acid, a Triterpenoid, Protect Against N-methyl-d-Aspartate-Induced Neurotoxicity in PC12 Cells. Molecules 2016, 21, 418.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top