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The commercial sesame oil was selected as the research subject and its volatile flavor components was extracted through solvent-assisted flavor evaporation (SAFE). Then, the aroma substances of the sesame oil were semi-quantitatively analyzed based on triple quadrupole gas chromatography-mass spectrometry. Finally, the relative odor activity values (ROAV) were combined to analyze the terms of volatile flavor contributions. The results showed that a total of 107 volatile flavor components were identified in sesame oil, of which 35 substances were seem as contributed flavor (ROAV≥0. 01), including 4 sulfides, 5 phenols, 10 pyrazines, 4 furans, 3 aldehydes, 4 thiazoles, 2 pyrroles, 2 thiophenes, and 1 indole. They provided "cabbage" "fishy" "sulfur" "smoky" "popcorn" "oil" and "roasted sesame". In particular, compounds 14 flavor components with ROAV≥0. 10 were determined as key flavor components, such as acetyl pyrazine, 2-furanmethanol, 2,3-dimethyl-pyrazine, 2,3,5-trimethylpyrazine, dimethyl disulfide, dimethyl trisulphide, methyl furfuryl disulfide, methyl thiolacetate, 4-vinyl-2- methoxyphenol, 2-methoxyphenol, hexanal, 2-ethyl-6-methyl-pyrazine, 2-methyl-3-furanothiol and 3-ethyl-2,5- dimethyl-pyrazine. Using this method to determine the key volatile flavor components of sesame oil, not only could expand the flavor database of sesame oil, but also could provide an important material basis for evaluating and regulating the flavor quality of sesame oil. [ABSTRACT FROM AUTHOR]

Ethnopharmacological Relevance: Duodenal motility disorder is a contributing factor to dyspepsia. The traditional Chinese medicine (TCM) formula Wei-Tong-Xin (WTX), originated from the famous ancient Chinese formula "Wan Ying Yuan", has been demonstrated efficacy in alleviating dyspepsia., Aim of the Study: The current study aims to elucidate the chemical composition of WTX to establish the pharmacodynamic material basis. On the basis of component, in depth to illuminate the mechanism by which WTX treats dyspepsia via constructing the comprehensive analysis of multi-platform., Materials and Methods: The chemical constituents of WTX were systematically analyzed by UHPLC-Q-TOF-MS/MS data processing methods. Based on this, network pharmacology was employed to predict the mechanism by which WTX improved dyspepsia. The dyspepsia mouse model was constructed, and histopathology as well as intestinal permeability were assessed using H&E staining, PAS staining and FITC-dextran assay. Protein expression was detected using Western blot, immunofluorescence, immunohistochemistry and ELISA kits., Results: A total of 100 chemical components of WTX were preliminarily identified. Network pharmacological analysis indicated that the therapeutic mechanism of WTX in treating dyspepsia may be related to the regulation of inflammation and oxidative stress-related signaling pathways. In vivo studies showed that WTX mitigated duodenal inflammation and oxidative stress responses, repairing the intestinal mucosal barrier damaged by cisplatin (CIS). Additionally, WTX restored the number of glial cells diminished by inflammatory damage, and ameliorated the serotoninergic neuronal dysfunction caused by insufficient secretion of glia-derived neurotrophic factor (GDNF), and enhanced intestinal transit., Conclusions: In this study, a total of 100 components of the WTX extract were identified through literature review and mass spectrometry database search. Utilizing computer technology, in conjunction with pharmacodynamic and mechanistic studies, WTX has been found to restore serotoninergic neuronal function by reducing intestinal mucosal inflammatory and oxidative damage, ultimately promoting intestinal transport and treating dyspepsia., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Microcirculatory problems in the intestinal mucosa are the primary cause of ulcerative colitis (UC). Although UC is commonly treated with paeoniae radix alba (PRA), its exact mechanism of action is unclear., Purpose: To examine how PRA affects UC induced by dextran sulfate sodium (DSS) and the mechanism of its effects., Methods: The primary active components of PRA were identified using high-performance liquid chromatography (HPLC), and network pharmacology techniques were used to predict the possible targets of action and signaling pathways in treatment for UC. A model of UC was established in vivo using rats, and a PRA intervention was performed. The amounts of cytokines in the colonic tissues and serum were measured using enzyme-linked immunosorbent assay (ELISA). The permeability of the intestinal mucosa was measured using a fluorescein isothiocyanate (FITC)-dextran assay and western blot. A PeriCam PSI system was used to view the microcirculation of the intestinal mucosa, and immunohistochemistry and immunofluorescence stains were used to detect angiogenesis. An electron microscope was used to observe the damage to the endothelium of the colon. Western blot and immunohistochemistry analyses were used to evaluate the protein expression of hypoxia-inducible factor-1 alpha (HIF-1α) in colon tissues, and qRT-PCR was used to assess the lncRNA expression of MALAT1., Results: HPLC identified 10 main active components of PRA, and the network pharmacology results showed that the treatment of UC with PRA was associated with the HIF-1 signaling pathway. The results of animal experiments revealed that PRA significantly improved the pathological damage to the colon and the microcirculatory issues in the intestinal mucosa. PRA also inhibited colonic endothelial cell damage and angiogenesis, which may be related to the inhibition of the increased expression of lncRNA MALAT1 and HIF-1α in colon tissues., Conclusions: The anti-UC effect of PRA by improving intestinal mucosal microcirculatory disorders was first reported in this study. PRA deactivated the lncRNA MALAT1/HIF-1α pathway, inhibited endothelial angiogenesis, restored intestinal mucosal microvascular homeostasis, improved microcirculatory disorders, and alleviated the symptoms of DSS-induced UC in rats., Competing Interests: Declaration of competing interest The authors declare that they have no competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier GmbH. All rights reserved.)