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Antrodia camphorata (A. camphorata) is an edible fungus containing various bioactive compounds generally used for health benefits. This study aimed to explore the potential neuroprotective activities of solid‐state‐cultured mycelium of A. camphorata (SCMAC) against Parkinson's disease (PD), as well as the underlying mechanism using an in vitro 6‐hydroxydopamine (6‐OHDA)‐induced PC12 cell model. The results showed that SCMAC extracts alleviated cell toxicity induced by 6‐OHDA and the loss of dopaminergic neurons, which was confirmed by the increase of cell viabilities, inhibition of cell apoptosis, the upregulation of tyrosine hydroxylase (TH) and dopamine transporter (DAT) levels and the downregulation of α‐Synuclein level. After purification, 11 compounds were identified by the NMR technique, including a quinone, four phenolic acid derivatives, three ubiquinone derivatives, two alkaloids, and a triterpenoid. The present study suggests that SCMAC could be an attractive candidate for the prevention or treatment of PD. Practical applications: Parkinson's disease seriously affects the lifetime and quality of the elder population for a long history. Long‐term consumption of L‐DOPA will result in side effects, such as developing abnormal involuntary movements called dyskinesia. This study showed that natural SCMAC extracts could be a potential therapeutic agent for the treatment of neurodegenerative disorder. [ABSTRACT FROM AUTHOR]

Biochanin A (Bio‐A), an isoflavone abundant in chickpeas, possesses hypoglycemic, hypolipidemic, and anti‐inflammatory effects. However, whether Bio‐A has antihepatosteatosis effect remains unclear. This study aimed to evaluate the antihepatosteatosis effect of Bio‐A on oleate (OA)‐treated hepatocytes, and explore the underlying mechanism. When incubated with OA for 24 h, HepG2 cells were treated with various concentrations of Bio‐A for 24 h to obtain an optimal antihepatosteatosis dose. HepG2 cells were treated with the AMP‐activated protein kinase (AMPK) inhibitor Compound C, or the sirtuin‐3 (SIRT3) inhibitor 3‐TYP, and incubated with 50 μM Bio‐A. The results indicated that 12.6% of lipid content, particularly 11.0% of triglyceride content, and the expression of adipocyte differentiation‐related protein were significantly decreased in Bio‐A‐treated hepatosteatosis cells, followed by an increase in the expression of Beclin 1, phosphorylation of Unc‐51‐like kinase 1 (ULK‐1), the microtubule‐associated protein 1 light chain 3 (LC3)‐II/LC3‐I ratio, and a decrease in expression of p62. The results indicated that Bio‐A upregulated autophagosome formation and autophagy flux. In addition, Bio‐A increased SIRT3 expression and AMPK phosphorylation in OA‐treated HepG2 cells. Blockade of AMPK and SIRT3 blocked the antihepatosteatosis effect and ULK‐1 activation by Bio‐A. AMPK inhibition did not eliminate the activation of SIRT3 by Bio‐A. AutoDock analysis demonstrated that interaction might exist between Bio‐A and SIRT3. In conclusion, Bio‐A reduced fat accumulation in OA‐treated HepG2 cells by activating SIRT3/AMPK/ULK‐1‐mediated autophagy. The findings provide a theoretical basis for the effect of Bio‐A on hepatic steatosis‐related diseases. Practical applications: This study highlights the antihepatosteatosis effects of biochanin A (Bio‐A) on oleate (OA)‐treated hepatocytes. Bio‐A, one of the isoflavones in Cicer arietinum Linn., possesses multiple bioactivities such as antiobesity, anti‐inflammation, and hypoglycemic and hypolipidemic effects. This study provides a new application of Bio‐A to treat hepatic steatosis, and revealed the underlying mechanism of Bio‐A involved in the activation of the SIRT3/AMPK/ULK‐1‐mediated autophagy. The findings provide a theoretical basis for the application of Bio‐A to hepatic steatosis‐related diseases. [ABSTRACT FROM AUTHOR]