OBJECTIVE:To establish a method for simultaneous determination of α-pinene,β-pinene and linalool in volatile oil of Hedychium flavum. METHODS:The volatile oil was extracted from H. flavum according to steam distillation stated in Chinese Pharmacopoeia(2015 edition volume Ⅳ). GC method was adopted to determine the content. The determination was performed on HP-5 capillary chromatographic column(30 m×0.032 mm×0.25 μm)with hydrogen flame ion detector(FID),nitrogen gas as carrier gas,with injector temperature of 200 ℃,and detector temperature of 250 ℃,column flow rate of 0.8 mL/min, samples size of 1 μL and split ratio of 40:1 by programmed temperature. RESULTS:The linear range of α-pinene,β-pinene and linalool were 0.090 5-2.413 3 mg/mL(r=0.999 9),0.098 3-2.620 0 mg/mL(r=0.999 9),0.169 1-4.510 0 mg/mL(r=0.999 8), respectively. RSDs of precision,stability(12 h),reproducibility tests were no more than 2.0%(n=6). The average recoveries were 99.84%(RSD=0.49%,n=6),100.24%(RSD=1.38%,n=6),99.41%(RSD=1.67%,n=6),respectively.The contents of α-pinene,β-pinene and linalool ranged 0.214 4-1.325 0,0.766 2-3.172 1,0.357 4-1.518 7 mg/g in volatile oil from 23 batches of H. flavum produced in Guizhou province. CONCLUSIONS:The method established in this experiment is rapid,simple and accurate.It can be used for the content determination of α-pinene,β-pinene and linalool in volatile oil from H.flavum.

Inflammation-driven endothelial dysfunction is the major initiating factor in atherosclerosis, while the underlying mechanism remains elusive. Here, we report that the non-canonical stimulator of interferon genes (STING)-PKR-like ER kinase (PERK) pathway was significantly activated in both human and mice atherosclerotic arteries. Typically, STING activation leads to the activation of interferon regulatory factor 3 (IRF3) and nuclear factor-kappa B (NF-κB)/p65, thereby facilitating IFN signals and inflammation. In contrast, our study reveals the activated non-canonical STING-PERK pathway increases scaffold protein bromodomain protein 4 (BRD4) expression, which encourages the formation of super-enhancers on the proximal promoter regions of the proinflammatory cytokines, thereby enabling the transactivation of these cytokines by integrating activated IRF3 and NF-κB via a condensation process. Endothelium-specific STING and BRD4 deficiency significantly decreased the plaque area and inflammation. Mechanistically, this pathway is triggered by leaked mitochondrial DNA (mtDNA) via mitochondrial permeability transition pore (mPTP), formed by voltage-dependent anion channel 1 (VDAC1) oligomer interaction with oxidized mtDNA upon cholesterol oxidation stimulation. Especially, compared to macrophages, endothelial STING activation plays a more pronounced role in atherosclerosis. We propose a non-canonical STING-PERK pathway-dependent epigenetic paradigm in atherosclerosis that integrates IRF3, NF-κB and BRD4 in inflammatory responses, which provides emerging therapeutic modalities for vascular endothelial dysfunction.