Studies on Paeoniflorin

Paeoniflorin is a white fine powder chemical compound with Molecular Formula:C23H28O11 and Molecular Weight: 480.47 . It is one of the major constituents of a herbal medicine derived from Paeonia lactiflora. It can also be isolated from the fresh water fern Salvinia molesta.In Paeonia, it can form new compounds with addition of phenolic substituents. Paeoniflorin has antiandrogenic propertie, the CAS Registry Number is 23180-57-6.

Paeoniflorin, the principal component of Paeoniae Radix prescribed in traditional Chinese medicine, has been reported to exhibit many pharmacological effects including protection against ischemic injury. 

However, the mechanisms underlying the protective effects of Paeoniflorin(CAS NO:23180-57-6) on cerebral ischemia are still under investigation. The present study showed that Paeoniflorin treatment for 14 days could significantly inhibit transient middle cerebral artery occlusion (MCAO)-induced over-activation of astrocytes and microglia, and prevented up-regulations of pro-inflamamtory mediators in plasma and brain. 

Further study demonstrated that chronic treatment with Paeoniflorin suppressed the activations of JNK and p38 MAPK, but enhanced ERK activation. And PF could reverse ischemia-induced activation of NF-κB signaling pathway. Moreover, our in vitro study revealed that PF treatment protected against TNFα-induced cell apoptosis and neuronal loss.

Taken together, the present study demonstrates that Paeoniflorin produces a delayed protection in the ischemia-injured rats via inhibiting MAPKs/NF-κB mediated peripheral and cerebral inflammatory response. Our study reveals that PF might be a potential neuroprotective agent for stroke.

We demonstrated that Paeoniflorin is an effective compound in the modulation of autophagic activity. Treatment with MPP+ significantly inhibited autophagy and induced apoptosis in PC12 cells. However, co-treatment with Paeoniflorin upregulated the autophagy and clearly showed neuroprotective effects. 

In addition, the CMA pathway was activated as a compensatory mechanism, while Paeoniflorin efficiently maintained the CMA activity near the normal range. We also exposed PC12 cells to an acidic medium, since acidosis is a common cause of mitochondrial dysfunction and neuron degeneration. 

Similarly, the deficiency of autophagy and the overactivity of CMA were both attenuated by Paeoniflorin. Thus, the key finding of the present study was that Paeoniflorin potently protected PC12 cells against MPP+ or acidosis-induced injury by upregulating the autophagic pathway.

In summary, the main findings of this study are: (1) Paeoniflorin and Ami both potently protected PC12 cells against MPP+ or acidosis induced injury by upregulating the autophagic pathway; (2) Paeoniflorin reduced calcium in flux by inhibiting ASIC1a channels; (3) the activity of ASICs altered the function of ALP.

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