| Toxicol In Vitro. 2013 Mar;27(2):908-14. |
| The neuroprotective effect of praeruptorin C against NMDA-induced apoptosis through down-regulating of GluN2B-containing NMDA receptors.[Pubmed: 23313464] |
Praeruptorin C (Pra-C), one of the principal bioactive components derived from the root of Peucedanum praeruptorum Dunn, has been widely used as an antioxidant and a calcium antagonist to treat diseases. The present study investigated the protective effect of Pra-C on cultured cortical neuron injury induced by glutamate.
METHODS AND RESULTS:
After challenge with 200μM N-methyl-d-aspartate (NMDA) for 30min, loss of cell viability and excessive apoptotic cell death were observed in cultured cortical neurons. Pra-C conferred protective effects against loss of cellular viability in a concentration-dependent manner. Pra-C also significantly inhibited neuronal apoptosis induced by NMDA exposure by reversing intracellular Ca(2+) overload and balancing Bcl-2 and Bax expression. Furthermore, Pra-C significantly reversed the upregulation of GluN2B-containing NMDA receptors by exposure to NMDA but did not affect the expression of GluN2A-containing NMDA receptors.
CONCLUSIONS:
These findings suggest that Pra-C partially protects cortical neurons by inhibiting the expression of GluN2B-containing NMDA receptors and regulating the Bcl-2 family. |
| Acta Pharmacol Sin. 2002 Feb;23(2):129-32. |
| Inhibitory effects of praeruptorin C on cattle aortic smooth muscle cell proliferation.[Pubmed: 11866872] |
To study the effects of praeruptorin C (pra-C) on proliferation of cattle aortic smooth muscle cells (SMC).
METHODS AND RESULTS:
The DNA synthesis of SMC was measured using the incorporation of [3H]thymidine([3H]TdR). Cell cycle phase was evaluated by flow cytometry and cytotoxicity was evaluated by measuring lactic dehydrogenase (LDH) activity.
Whether or not treated with angiotensin II (Ang-II), SMC proliferation was suppressed by pra-C in a concentration-dependent manner at range from 0.001 micromol/L to 10 micromol/L. The inhibitory effects appeared to be related to G1-S block in cell cycle traverse while the LDH activities did not change dramatically.
CONCLUSIONS:
Pra-C can completely inhibit SMC proliferation induced by Ang II and partly inhibit the growth of SMC- induced by bovine serum, which is important in prevention and treatment of vascular hyperplastic disease. |
| Chinese Heart Journal, 2008(5):513-6. |
| Effects of praeruptorin C on myocardial plasma membrane calcium handling proteins during ischemia/reperfusion[Reference: WebLink] |
To explore the cardioprotective mechanism of praeruptorin C(Pra-C)during ischemia/reperfusion.METHODS Cultured rat neonatal cardiomyocytes were randomly divided into 3 groups: ischemia/reperfusion group(9 h ischemia followed by 1 h reperfusion,I/R),Pra-C pretreatment group(pretreated with Pra-C for 1 h before I/R) and control group.The leakage of intracellular lactate dehydrogenase(LDH) in various groups was determined by biochemical autoanalyzer.Activity of natrium-calcium exchanger(NCX) was indicated by Na+-dependent 45Ca2+ uptake tested by liquid scintillation counting.Semi-quantitative RT-PCR was employed to detect the mRNA level of NCX.Activity of plasma membrane calcium ATPase(PMCA) was determined by microcolorimetrg of inorganic phosphorus. Compared with that in I/R group,the LDH leakage in Pra-C pretreatment group was significantly reduced(P0.01).The Na+-dependent 45Ca2+ uptake was significantly increased in I/R group(P0.01) compared with that in control group.This increase could be significantly attenuated in Pra-C pretreatment group.The level of NCX mRNA in I/R group was also significantly increased(P0.01) compared with that in control group and this increase could be significantly attenuated in Pra-C pretreatment group(P0.01).No significant change of PMCA activity was observed between various groups.
CONCLUSIONS:
NCX mediates the cardioprotective effect of Pra-C during ischemia/reperfusion in the neonatal rat cardiomyocytes I/R model. |
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