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Objective To analyze the effects of miR-181a-5p overexpression on metabolites in the small intestines of mice with subcutaneous oral cancer by detecting changes in metabolites and metabolic pathways.Methods Three groups were included in study:Control group,negative control and miR-181a-5p overexpression group.To establish a subcutaneous oral cancer model in mice,variously treated cell suspensions were subcutaneously injected into the upper right of the groin in female M-NSG severely immunodeficient mice.Changes in pathology and small intestinal tissues were assessed by HE staining.Changes in mouse body weight were also assessed.Tandem orbitrap mass spectrometry and ultra-high performance liquid chromatography-tandem time-of-flight mass spectrometry,were used to examine metabolites in the small intestines.By pre-analyzing the original data and quality rating sample data,XCMS was able to assess which metabolites were different among the groups.To identify unique metabolic pathways,KEGG enrichment analysis was used.Results A total of 170 distinct metabolites were found in the small intestinal tissues of Control and NC groups.Choline metabolism,alanine,aspartate,and glutamate metabolism,GABA synaptic metabolism,glycerophospholipid metabolism,cAMP signaling route,cancer center carbon metabolism,and niacin and niacin amine metabolic pathways were important signaling pathways for metabolite enrichment.In the NC group,16 distinct metabolites with VIP values larger than 2 were found in the small intestines compared with the OE group overexpressing miR-181a-5p.Glycerin phosphorylcholine,palmitic acid,3-hydroxybutyl carnitine,and β-hydroxybutyric acid were among the metabolites that significantly varied.The primary enhanced metabolic pathway was the choline pathway.Conclusions Mouse small intestines underwent slight changes from subcutaneous oral cancer with the greatest effect on metabolites critical for energy metabolism.The choline metabolic pathway was the pathway that selected absolutely metabolites in mouse small intestines with subcutaneous grafts of oral cancer.
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Aim To investigate the effect of ginsenoside Rg1 on gut injury following intestinal ischemia reperfusion in rats and the possible mechanism.Methods By using rat model of intestinal I/R injury, 30 male SD rats were randomly divided into 3 groups(n =10 in each group):sham-operation group, I/R group(control group)and ginsenoside Rg1 group(treatment group).The contents of tumor necrosis factor α(TNF-α), interleukin-6(IL-6), malondialdehyde(MDA), the activity of superoxide dismutase(SOD)in intestinal mucosa were measured respectively.Chiu's count was used to assess the changes in intestinal pathological morphology.Results TNF-α, IL-6, MDA contents and the intestinal injury score in control group were significantly increased compared to those in sham-operation group, while SOD contents in control group were significantly decreased compared to sham-operation group.Inversely, TNF-α, IL-6, MDA contents and the intestinal injury score in treatment group were significantly decreased compared to those in control group, while SOD contents in treatment group were significantly increased compared to control group.Conclusion Pretreatment with ginsenoside Rg1 has protective effect on intestinal ischemia-reperfusion injury in rats, which may be attributed to decreased contents of TNF-α, IL-6, MDA and increased levels of SOD.
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Aim To observe the influences of ginsenoside Rg1 on the spontaneous contraction of small intestine smooth muscle of rabbits in vitro and explore the mechanism.Methods With the isothermal perfusion of small intestine in vitro,the influences of ginsenoside Rg1 on the spontaneous contraction of small intestine was observed and the mechanism of ginsenoside Rg1 was studied.Results Ginsenoside Rg1 reduced the amplitude of contraction of small intestine smooth muscle in rabbits in a dose-depended manner.Bay K8644 and nitro-L-arginine methylester(L-NAME)could completely block the inhibition of ginsenoside Rg1 on the contraction of small intestine smooth muscle.Ginsenoside Rg1 inhibited the intracellular calcium-depended contraction induced by rynodine in the Ca2+ free Tyrode's solution.Conclusions Ginsenoside Rg1 inhibits the contraction of small intestine smooth muscle of rabbits in vitro.The mechanism may be related to increase NO concentration in small intestine smooth muscle so that it inhibits extracellular Ca2+ inflowing via cell membrane and intracellular Ca2+ releasing via sarcoplasmic reticulum.