Qingke (highland barley) Baijiu is a special Chinese Baijiu which is mainly produced from Qinghai-Tibet Plateau. Since the pine board is used as the bottom of the fermentation pit, we deduced that the terpenoids and norisoprenoids in pine board might be introduced into Qingke Baijiu. Thus, the terpenoids and norisoprenoids in Qingke Baijiu were investigated by headspace solid phase microextraction (HS-SPME) combined with comprehensive two-dimensional gas chromatography coupled to time-of-flight mass spectrometry (GC × GC-TOFMS). The results showed that γ-terpinene (0.70–530.72 μg/L), α-phellandrene (0.34–256.66 μg/L), longicyclene (0–38.55 μg/L), α-pinene (1.21–35.54 μg/L) and limonene (0.93–23.69 μg/L) were the top 5 terpenoids/norisoprenoids in Qingke Baijiu. Pulegone was detected and reported for the first time in Baijiu, and the concentrations in Qingke Baijiu were 0.78 μg/L (fresh) and 3.90 μg/L (7 years old). According to the principal component analysis (PCA) plot, young, aged, and retail Qingke Baijiu could be differentiated clearly. Fold change (FC) and t-tests analysis indicated that β-pinene, γ-terpinene, and α-selinene were the most different terpenoids/norisoprenoids between young and aged Qingke Baijiu, and longifolene was the most different terpenoids/norisoprenoids between base and retail Qingke Baijiu. The terpenoids and norisoprenoids, such as (E)-β-ionone, isoborneol and β-cyclocitral, could be potential markers indicating the ageing process of Qingke Baijiu.

The increased vascular inflammation is a key event in the development of atherosclerotic lesions. Antrodia cinnamomea has been shown to promote anticancerogenic activity through decreasing inflammation. However, the potential role of A. cinnamomea in cardiovascular diseases remains unexplored. Herein, using carotid arterial ligation models, we found that ethanol extract from A. cinnamomea (EEAC) significantly inhibited neointimal hyperplasia in a dose-dependent manner, accompanied with the reduced expression of activated p65 and inflammatory cytokines. We also show that EEAC ameliorated TNF-α-induced phosphorylation of p65 and pro-inflammatory cytokine expression in both vascular smooth muscle cells (VSMCs) and macrophages in vitro. Mechanistically, EEAC suppressed expression levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM-1) in VSMCs, which attenuates the ability of monocytes/macrophages adhesion to VSMCs. Furthermore, the expression level of these adhesion molecules and infiltration of monocytes/macrophages were also decreased in neointimal VSMCs of arteries pretreated with EEAC. Altogether, our results reveal a novel function of A. cinnamomea in suppressing vascular inflammation upon ligation injury during neointimal formation, likely through inhibition of inflammatory cell infiltration via downregulating the adhesion molecules in VSMCs. Thus, A. cinnamomea may offer a pharmacological therapy to slow down disease progression in patients with vascular injury.