ABSTRACT
We explored the mechanism of patchouli oil in the treatment of inflammatory bowel disease (IBD) based on network pharmacology and differentially expressed genes in macrophages. The chemical composition of patchouli oil was detected by GC-MS, targets for active components were collected through TCMSP and Swiss Target Prediction platform, and targets for treatment of IBD were retrieved from DrugBank, GeneCards, OMIM, PharmGkb, and TTD databases. The intersection targets were merged, Cytoscape software was used to construct the "component-to-intersection target" network, and protein-protein interaction (PPI) network was drawn with String platform. The intersection targets were enriched for GO and KEGG enrichment analysis on Metascape platform, and the molecular docking of AutoDock Vina was used to verify the analysis results. The macrophage chip data was downloaded, and the differential genes were obtained by using R software. KEGG signaling pathway analysis of differentially expressed genes were performed by DAVID platform. Real-time fluorescence quantitative PCR was used to verify the screened components in the cell model in vitro. The 14 main components of patchouli oil corresponded to 112 targets, and the intersection obtained 97 common targets of patchouli oil for IBD treatment. GO enrichment analysis yielded 53 items. Eighteen items were obtained by KEGG enrichment analysis, involving cAMP signaling pathway, Notch signaling pathway, adhesion connection, Th17 cell differentiation and other signaling pathways. Molecular docking showed that the selected active components of patchouli oil had good binding activity with the targets. Differentially expressed genes were enriched in inflammatory pathways such as Toll-like receptors, JAK-STAT and NF-κB signaling pathways. q-PCR showed that patchouli oil, patchouli alcohol, pogostone can reduce the mRNA levels of cytokines (TNF-α, IL-1β, IL-6, and IL-23) and up-regulate the mRNA levels of tight junction proteins (occludin and claudin-1) in the inflammatory model of NCM460 normal colon epithelial cells. Patchouli alcohol can significantly reduce the levels of TNF-α, IL-6, and IL-1β inflammatory factors in RAW264.7 macrophages induced by LPS. This study revealed the multi-component, multi-target and multi-pathway of patchouli oil, and confirms the anti-inflammatory effect of patchouli oil and its main components in the inflammatory cell model in vitro and the protection of intestinal epithelial barrier integrity function, which provides a theoretical basis for further elucidating the mechanism of patchouli oil in the treatment of IBD.
ABSTRACT
Objective To obtain a clear and qualified oral liquid preparation of Huoxiangzhengqi by improving the addition methods of patchouli oil and perilla leaf oil. Methods Palvis Talci was used to improve the solubility of patchouli oil and perilla leaf oil. Firstly, the two kinds of oil were mixed with Palvis Talci and triturated sufficiently. Then, the mixture was mixed with the physic liquor and agitated sufficiently. At last, the clear preparation was obtained after filtration. Results The preparation was clear, well-tasted and qualified. Conclusion The improved method is feasible, simple, stabilized and economical.
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[ ABSTRACT] AIM:To investigate the antipyretic effect of patchouli oil on lipopolysaccharide ( LPS)-induced fe-ver in rabbits.METHODS:Male rabbits (n=42) were randomly divided into 7 groups according to their body weight and basal body temperature, including control group, model group, western medical positive group, traditional Chinese medical positive group, and high, middle and low doses (2%, 1%and 0.5%) of patchouli oil groups.Subsequently, except the controls, the rabbits were injected with LPS at a dose of 1 mL/kg (2 mg/L) through marginal ear vein to establish rabbit fever model and the rabbits in control group received the same volume of NS.The rabbits in control group and model group were injected with 0.5%Tween-80 0.5 h late, and the rabbits in the other groups were treated with correspoonding drugs. The effect of patchouli oil on the body temperature was observed, and the levels of interleukin-1β( IL-1β) and tumor nec-rosis factor-α(TNF-α) in the serum, and prostaglandin E2(PGE2) and cyclic adenosine monophosphate (cAMP) in the hypothalamus were measured by radioimmunoassay.RESULTS: The body temperature and the levels of IL-1β, TNF-α, cAMP and PGE2 in model group were significant higher than those in control group.Patchouli oil notably inhibited the body temperature in the febrile rabbits.From 1.5 h to 5.5 h after administration, the body temperatures were increased by (1.06 ±1.55), (1.62 ±1.36), (1.38 ±1.22), (0.98 ±0.98) and (0.48 ±0.95) ℃in high patchouli oil group, re-spectively.From 3.5 to 5.5 h after administration, the body temperatures were elevated by ( 1.47 ±0.73 ) , ( 1.15 ± 0.68) and (0.63 ±0.54) ℃ in middle patchouli oil group, respectively.A tendency of downregulation of the elevated body temperatures was observed at every time point after administration in low patchouli oil group.Patchouli oil significantly decreased the levels of TNF-αin the serum and cAMP content in the hypothalamus, and attenuated the elevated tendency of the IL-1βlevel in the serum and PGE2 level in the hypothalamus.CONCLUSION:Patchouli oil evidently has antipyretic effect on LPS-induced fever in the rabbits.The antipyretic mechanism might be related to the inhibition of TNF-αlevel in serum and cAMP content in the hypothalamus.
ABSTRACT
Objective To obtain a clear and qualified oral liquid preparation of Huoxiangzhengqi by improving the addition methods of patchouli oil and perilla leaf oil. Methods Pulvis Talci was used to improve the solubility of patchouli oil and perilla leaf oil. Firstly, the two kinds of oil were mixed with Pulvis Talci and triturated sufficiently. Then, the mixture was mixed with the physic liquor and agitated sufficiently. At last, the clear preparation was obtained after filtration. Results The preparation was clear, well-tasted and qualified. Conclusion The improved method is feasible, simple, stabilized and economical.