BACKGROUND Ulcerative colitis(UC)is a chronic and treatment-resistant disorder requiring potent therapeutics that are effective and safe.Cedrol(CE)is a bioactive natural product present in many traditional Chinese med...BACKGROUND Ulcerative colitis(UC)is a chronic and treatment-resistant disorder requiring potent therapeutics that are effective and safe.Cedrol(CE)is a bioactive natural product present in many traditional Chinese medicines.It is known for its suppression of inflammation and mitigation of oxidative stress.Its therapeutic efficacy and mechanistic underpinnings in UC remain uncharacterized.AIM To investigate the therapeutic potential and mechanisms of CE in UC.METHODS The anti-inflammatory activity and intestinal barrier-repairing effects of CE were assessed in a dextran sulfate sodium-induced murine colitis model.Network pharmacology was employed to predict potential targets and pathways.Then molecular docking and dynamics simulations were utilized to confirm a stable interaction between CE and the toll-like receptor 4(TLR4)/myeloid differentiation factor 2(MD2)complex.The anti-inflammatory mechanisms were further verified using in vitro assays.Additionally,the gut microbiota composition was analyzed via 16S rRNA gene sequencing.RESULTS CE significantly alleviated colitis symptoms,mitigated histopathological damage,and suppressed inflammation.Moreover,CE restored intestinal barrier integrity by enhancing mucus secretion and upregulating tight junction proteins(zonula occludens 1,occludin,claudin-1).Mechanistically,CE stably bound to MD2,inhibiting lipopolysaccharide-induced TLR4 signaling in RAW264.7 cells.This led to suppression of the downstream mitogen-activated protein kinase and nuclear factor kappa B signaling pathways,downregulating the expression of tumor necrosis factor-alpha,interleukin-1β,and interleukin-6.Gut microbiota analysis revealed that CE reversed dextran sulfate sodium-induced dysbiosis with significant enrichment of butyrogenic Christensenella minuta.CONCLUSION CE acted on MD2 to suppress proinflammatory cascades,promoting mucosal barrier reconstitution and microbiota remodeling and supporting its therapeutic use in UC.展开更多
Three steam distillation devices (D-1, D-2 and D-4) or one simultaneous distillation (D-3, water-diethyl ether) as well as the process of CO2-SFE (Supercritical fluid extraction) were adopted in extraction of essentia...Three steam distillation devices (D-1, D-2 and D-4) or one simultaneous distillation (D-3, water-diethyl ether) as well as the process of CO2-SFE (Supercritical fluid extraction) were adopted in extraction of essential oils from Chinese-fir (Cunninghamia lancedata (Lamb) Hook.) and the chemical components of the extracted essential oil were analyzed by Gas chromatograph-MS analyses. The results showed that the essential oil could be almost extracted out within 2 hours and the device-3 had the highest extraction efficiency. The major chemical component of the oil was cedrol. The yield of the extracted essential oils from Chinese fir decreased gradually with the increase of the distillation time. The best condition for extraction by means of CO2-SFE is 100 kg·cm?2 in pressure and 40°C in temperature for. Keywords Chinese fir - Essential oil - Cedrol - Supercritical fluid extraction CLC number S781.4 Document code A Foundation item: This paper was support by the Key Foundation Research Project (G1999016001) of China and the Japan International Cooperation AgencyBiography: HUANG Luo-hua (1957-), male, Research associate, Research Institute of Wood Industry, Chinese Academy of forestry, Beijing 100091, P. R. ChinaResponsible editor: Song Funan展开更多
用A lam ar b lue法对提取的侧柏叶、种皮及种子挥发油进行了抗人肺癌细胞实验,结果表明侧柏叶、种皮和种子挥发油对肺癌细胞NC I-H460有明显抑制率,分别为86.24%、47.80%和97.73%。其中以叶挥发油和种子挥发油最高。采用气-质联用法对...用A lam ar b lue法对提取的侧柏叶、种皮及种子挥发油进行了抗人肺癌细胞实验,结果表明侧柏叶、种皮和种子挥发油对肺癌细胞NC I-H460有明显抑制率,分别为86.24%、47.80%和97.73%。其中以叶挥发油和种子挥发油最高。采用气-质联用法对侧柏叶、种皮和种子挥发油的化学成分进行了研究,其含有的挥发物质种类侧柏叶、种皮和种子分别为8,31和21个成分,其挥发油成分也不尽相同,侧柏叶含量最高的是α,,α4,8-四甲基-3,7环癸二烯-1-甲醇和雪松醇分别占总挥发油的27.213%和26.193%,种皮和种子挥发油中含量最高的都是雪松醇,分别占总挥发油的28.277%和26.919%。其中,对侧柏叶挥发油4℃低温下重结晶得到的雪松醇进行了鉴定,纯度达97.06%,对雪松醇抗人肺癌细胞实验结果是雪松醇对人肺癌细胞NC I-H460半致死浓度为44.98μg.mL-1。展开更多
基金Supported by the Provincial Key Cultivation Laboratory for Digestive Disease Research,No.2021SYS13Shanxi Province’s“Si Ge Yi Pi”Science and Technology Driven Medical Innovation Project,No.2021MX03Shanxi Provincial Basic Research Program,No.202403021222423.
文摘BACKGROUND Ulcerative colitis(UC)is a chronic and treatment-resistant disorder requiring potent therapeutics that are effective and safe.Cedrol(CE)is a bioactive natural product present in many traditional Chinese medicines.It is known for its suppression of inflammation and mitigation of oxidative stress.Its therapeutic efficacy and mechanistic underpinnings in UC remain uncharacterized.AIM To investigate the therapeutic potential and mechanisms of CE in UC.METHODS The anti-inflammatory activity and intestinal barrier-repairing effects of CE were assessed in a dextran sulfate sodium-induced murine colitis model.Network pharmacology was employed to predict potential targets and pathways.Then molecular docking and dynamics simulations were utilized to confirm a stable interaction between CE and the toll-like receptor 4(TLR4)/myeloid differentiation factor 2(MD2)complex.The anti-inflammatory mechanisms were further verified using in vitro assays.Additionally,the gut microbiota composition was analyzed via 16S rRNA gene sequencing.RESULTS CE significantly alleviated colitis symptoms,mitigated histopathological damage,and suppressed inflammation.Moreover,CE restored intestinal barrier integrity by enhancing mucus secretion and upregulating tight junction proteins(zonula occludens 1,occludin,claudin-1).Mechanistically,CE stably bound to MD2,inhibiting lipopolysaccharide-induced TLR4 signaling in RAW264.7 cells.This led to suppression of the downstream mitogen-activated protein kinase and nuclear factor kappa B signaling pathways,downregulating the expression of tumor necrosis factor-alpha,interleukin-1β,and interleukin-6.Gut microbiota analysis revealed that CE reversed dextran sulfate sodium-induced dysbiosis with significant enrichment of butyrogenic Christensenella minuta.CONCLUSION CE acted on MD2 to suppress proinflammatory cascades,promoting mucosal barrier reconstitution and microbiota remodeling and supporting its therapeutic use in UC.
基金The Key Foundation Research Project (G1999016001) of China and the Japan International Cooperation Agency
文摘Three steam distillation devices (D-1, D-2 and D-4) or one simultaneous distillation (D-3, water-diethyl ether) as well as the process of CO2-SFE (Supercritical fluid extraction) were adopted in extraction of essential oils from Chinese-fir (Cunninghamia lancedata (Lamb) Hook.) and the chemical components of the extracted essential oil were analyzed by Gas chromatograph-MS analyses. The results showed that the essential oil could be almost extracted out within 2 hours and the device-3 had the highest extraction efficiency. The major chemical component of the oil was cedrol. The yield of the extracted essential oils from Chinese fir decreased gradually with the increase of the distillation time. The best condition for extraction by means of CO2-SFE is 100 kg·cm?2 in pressure and 40°C in temperature for. Keywords Chinese fir - Essential oil - Cedrol - Supercritical fluid extraction CLC number S781.4 Document code A Foundation item: This paper was support by the Key Foundation Research Project (G1999016001) of China and the Japan International Cooperation AgencyBiography: HUANG Luo-hua (1957-), male, Research associate, Research Institute of Wood Industry, Chinese Academy of forestry, Beijing 100091, P. R. ChinaResponsible editor: Song Funan
文摘用A lam ar b lue法对提取的侧柏叶、种皮及种子挥发油进行了抗人肺癌细胞实验,结果表明侧柏叶、种皮和种子挥发油对肺癌细胞NC I-H460有明显抑制率,分别为86.24%、47.80%和97.73%。其中以叶挥发油和种子挥发油最高。采用气-质联用法对侧柏叶、种皮和种子挥发油的化学成分进行了研究,其含有的挥发物质种类侧柏叶、种皮和种子分别为8,31和21个成分,其挥发油成分也不尽相同,侧柏叶含量最高的是α,,α4,8-四甲基-3,7环癸二烯-1-甲醇和雪松醇分别占总挥发油的27.213%和26.193%,种皮和种子挥发油中含量最高的都是雪松醇,分别占总挥发油的28.277%和26.919%。其中,对侧柏叶挥发油4℃低温下重结晶得到的雪松醇进行了鉴定,纯度达97.06%,对雪松醇抗人肺癌细胞实验结果是雪松醇对人肺癌细胞NC I-H460半致死浓度为44.98μg.mL-1。
