Antrodia cinnamomea Exhibits a potent neuroprotective effect in the PC12 cell-A β model - Pharmacologically through adenosine receptors and mitochondrial pathway

A β Chemical analysis indicated that the ethanolic extract of Antrodia cinnamomea contained a huge amount (mg/g ethanolic extract of Antrodia cinnamomea) of polyphenolics (133±7), flavonoids (114±6), triterpenoids (175±26), and adenosine (370±17). When tested with Aβ(15M), the cell viability was suppressed in a dose-dependent fashion with an ICvalue of 10M. The biochemical parameters upregulated by Aβ(15M) involved TNF-α, ROS, MDA, NO, and the intracellular calcium ions. These adverse effects were effectively ameliorated by the ethanolic extract of Antrodia cinnamomea (1g/mL). The Western blot analysis revealed that Aβdownregulated BcL-2/Bax and upregulated cleaved caspases-9 and 3 without affecting cleaved caspase-8. The GM arrest elicited by Aβwas ameliorated by the ethanolic extract of Antrodia cinnamomea. TUNEL assay confirmed the apoptosis, and the ethanolic extract of Antrodia cinnamomea downregulated adenosine A1 and adenosine A2A receptors. Taken together, Aβtends to induce neurotoxicity on PC12 cells. The ethanolic extract of Antrodia cinnamomea is capable of suppressing its neurotoxicity by rescuing the mitochondrial apoptosis pathway and simultaneously by downregulating adenosine A1 and adenosine A2A receptors to retard neurodegeneration and memory dysfunction.