Paeoniflorin (PF) is an active ingredient of Radix Paeoniae, which is known to exert neuroprotective effects. However, the mechanims behind the neuroprotective effects of PF are not yet fully understood. The apoptosis of neurons plays an important role in the cerebral ischemia-induced cascade response. This study aimed to investigate neuroprotective effects of PF against glutamate-induced PC12 cellular cytotoxicity and to determine whether these effects are mediated via the inhibition of apoptosis in vitro and the activity of mitochondrial apoptosis-associated proteins in PC12 cells. Exposure of the PC12 cells to glutamate induced cell morphological changes, significantly decreased cell viability and induced apoptosis, with similar results being observed from the Hoechst 33342 staining and Annexin V/PI staining experiments. Glutamate also increased the lactate dehydrogenase release by the PC12 cells. However, treatment with PF prevented these effects. Furthermore, PF inhibited Bax and Bad expression and increased Bcl-2 and Bcl-xL expression; it also decreased the levels of downstream protein (caspase-3 and caspase-9). Collectively, our results indicate that PF protects PC12 cells against glutamate-induced neurotoxicity possibly through the inhibition of the expression of mitochondrial apoptosis-associated proteins.

A new indole alkaloid, nauclofficine (1), together with three known alkaloids, naucleamide A (2), naucleamide D (3) and latifoliamide A (4), were isolated from the stems and leaves of Nauclea officinalis. Their structures were established on the basis of extensive spectral analyses. All known compounds were isolated from N. officinalis for the first time. The cytotoxicities of compounds 1～4 were evaluated against five cancer cell lines (HL-60, A549, SMMC-7721, MCF-7 and SW480).Research results showed that compounds 1～4 exhibited significant inhibitory effects with IC 50 values comparable to those of cisplatin.