Polyporenic acid C Inhibitor

Solid. Powder

98.00%

Store at -20 degree C for 3 years powder
-80 degree C for 2 years in solvent

482.69

<1mg/ml refers to the product slightly soluble or insoluble

C31H46O4

[H][C@@]12CC=C3C(=CC[C@]4(C)[C@@H]([C@@H](CCC(=C)C(C)C)C(O)=O)[C@H](O)C[C@@]34C)[C@@]1(C)CCC(=O)C2(C)C

465-18-9

PARP
Caspase
PI3K

In this study, we investigated the effect of Polyporenic acid C (PPAC), a lanostane-type triterpenoid from P. cocos, on the growth of A549 nonsmall cell lung cancer cells (NSCLC). The results demonstrate that PPAC significantly reduced cell proliferation via induction of apoptosis as evidenced by sub-G1 analysis, annexin V-FITC staining, and increase in cleavage of procaspase-8, -3, and poly(ADP-ribose)-polymerase (PARP). However, unlike our previously reported lanostane-type triterpenoid, pachymic acid, treatment of cells with PPAC was not accompanied by disruption of mitochondrial membrane potential and increase in cleavage of procaspase-9. Further, PPC-induced apoptosis was inhibited by caspase-8 and pan caspase inhibitors but not by a caspase-9 inhibitor. Taken together, the results suggest that PPAC induces apoptosis through the death receptor-mediated apoptotic pathway where the activation of caspase-8 leads to the direct cleavage of execution caspases without the involvement of the mitochondria. Furthermore, suppressed PI3-kinase/Akt signal pathway and enhanced p53 activation after PPAC treatment,suggests this to be an additional mechanism for apoptosis induction.

Chromatin/Epigenetic; PARP; Apoptosis; PI3K/Akt/mTOR signaling