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ObjectiveTo observe the effect of ethyl acetate extract of Acanthopanacis Senticosi Radix et Rhizoma seu Caulis on high-fat diet-induced apolipoprotein E gene knockout （ApoE-/-） mice， and explore its mechanism of treating atherosclerosis by regulating intestinal flora. MethodThirty-two 8-week-old male ApoE-/- mice were randomly divided into model group， rosuvastatin group （10 mg·kg-1）， high-， low-dose groups of ethyl acetate extract of Acanthopanacis Senticosi Radix et Rhizoma seu Caulis （75， 25 mg·kg-1）， with 8 mice in each group. Eight C57BL/6 mice were used as blank group. After 8 weeks of continuous administration， blood was taken to determine the blood lipid level. Enzyme-linked immunosorbent assay （ELISA） was used to detect the contents of related indexes in serum of mice. Hematoxylin-eosin （HE） staining was used to observe the formation of aortic plaque in mice. Cecal contents were collected and 16S rRNA amplicon sequencing was used to detect intestinal flora. ResultCompared with the blank group， the plaque area of the model group was significantly increased with inflammatory infiltration， the contents of triglyceride （TG）， total cholesterol （TC）， low-density lipoprotein cholesterol （LDL-C）， inflammatory factors and inducible nitric oxide synthase （iNOS） were increased， while the content of high-density lipoprotein cholesterol （HDL-C） was decreased. Compared with the model group， rosuvastatin group and high- and low-dose groups of ethyl acetate extract of Acanthopanacis Senticosi Radix et Rhizoma seu Caulis could improve the deposition of aortic plaque， reduce the contents of TG， TC， LDL-C， inflammatory factors and iNOS， and increase the content of HDL-C. Compared with the blank group， the relative abundances of Firmicutes and Proteobacteria in the model group increased， while the relative abundance of Bacteroidetes decreased. Alpha and Beta diversity analysis showed that samples of each group could be significantly isolated， and the total number and abundance of intestinal flora species in the model group were low. Compared with the model group， ethyl acetate extract of Acanthopanacis Senticosi Radix et Rhizoma seu Caulis could increase the relative abundance of beneficial bacteria and decrease the relative abundance of pathogenic bacteria. ConclusionEthyl acetate extract of Acanthopanacis Senticosi Radix et Rhizoma seu Caulis was mainly composed of flavonoids， which can treat atherosclerosis by regulating the intestinal flora and improve the pathological changes in the aorta of ApoE-/- mice induced by high-fat diet. The mechanism may be related to its ability to reduce the level of inflammatory factors， improve antioxidant capacity and repair the disorder of intestinal flora structure.
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AIM:To explore the relationship between the different stages of diabetic retinopathy and the related factors of vascular endothelial function,and to provide a theoretical basis for improving the function of vascular endothelium to find a way to delay or even inhibit the occurrence or progression of DR.METHODS:We collected during March 2015 to December 2015 in Department of Ophthalmology and endocrinology in our hospital,178 cases of type 2 diabetes mellitus patients and 62 cases of blood specimen in health control group.According to the results of fundus fluorescence angiography (FFA),they were divided into four groups,diabetes patients without retinopathy,diabetes patients with non proliferative diabetic retinopathy (NPDR),diabetes patients with proliferative diabetic retinopathy (PDR) and healthy control group.We detected blood samples of antithrombin Ⅲ (AT-Ⅲ),fibrinolytic enzyme activation inhibitor (PAI),the original organization type fibrinolytic enzyme activator (t-PA) index and the correlation of diabetic retinopathy in installment.RESULTS:This study showed that AT-Ⅲ was significantly different among the four groups (F=5.986,P＜ 0.01);PAI was significantly different among the patients without DR,patients with NPDR and patients with PDR (F=7.434,P＜0.01);t-PA was not significantly different among the four groups (F=2.556,P＞ 0.05);there were relations between the different stages of diabetic retinopathy and AT-Ⅲ,PAI.CONCLUSION:The degree of diabetic retinopathy has a close relationship with the content of antithrombin Ⅲ and plasminogen activator inhibitor,and it is closely related to the function of vascular endothelium.
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To observe the efficacy of compound Dendrobium on Sprague Dawley rats (SD) hypertension model induced by "dietary disorders" and its relevant mechanism, totally 50 SD rats were fed with high-sugar, high-fat diet and alcohol for four weeks. According to the blood pressure after modeling, the rats were divided into model group, valsartan group (8 mg·kg⁻¹), low, medium and high-dose Dendrobium candidum compound groups (1.65, 3.30, 5.00 g·kg⁻¹), with 10 rats in each group, and the other 10 SD rats were also taken as the normal group. After four weeks of treatment, blood pressure was measured. Orbital blood was collected for the determination of serum cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL), calculation of atherosclerosis index (AI). Nitric acid reductase method was used to detect serum nitric oxide (NO); the levels of serum endothelin-1 (ET-1) and intercellular adhesion molecule-1 (ICAM-1) were measured by ELISA. The rats were put to death after the last administration, and the protein expressions of PI3K/AKT/eNOS in thoracic aorta of rats in each group were detected by Western blot. The aorta was separated and stained with hematoxylin-eosin (HE) to observe the changes in the endothelium and blood vessels in the thoracic aorta. Masson staining was used to observe the formation of aortic collagen. The expressions of nitric oxide synthase (eNOS) and ICAM-1 in aortic endothelial cells were observed by immunohistochemistry. In contrast, the results show D. candidum compound can significantly reduce the blood pressure in hypertensive rats, increase HDL-c, and reduce AI, while increasing serum NO content, decreasing ET-1 and ICAM-1 levels and promoting PI3K/AKT/NOS protein expressions. The lesion degree of the D. candidum compound group was reduced, and the collagen deposition was significantly reduced. Meanwhile, D. candidum compound can significantly increase the expression of eNOS, and reduce the formation of ICAM-1.Therefore, D. candidum compound has an obvious antihypertensive effect on hypertensive rats, which may be related to the increase in PI3K/AKT/eNOS signaling pathways and NO generation, the inhibition of the secretion of ICAM-1 and ET-1, the protection of the vascular endothelium and the improvement of aortic disease.
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Objective To investigate the expression of vascular endothelial factor C(VEGF-C) and E-cadherin in gastric cancer and explore the relationship between expression of VEGF-C and E-cadherin and the pathogenesis of gastric cancer.Methods Real-time quantitative reverse ranscriptase-polymerase chain rection was applied on 40 cases of gastric cancer and corresponding adjacent noncancerous tissues,in order to detect mRNA expression of VEGF-C and E-cadherin gene.VEGF-C and E-cadherin protein expression in gastric cancer and adjacent normal gastric mucosa were detected by immunohistochemistry.Statistical analysis was carried out to analyze the correlation among VEGF-C,E-cadherin and protein expression with various clinical parameters in these gastric cancer patients.Results The expression of VEGF-C protein in 40 cases of gastric cancer's cancer tissues was 0.461±0.012,significantly higher than that in the adjacent normal tissues(0.036+0.023;t=1.101,P＜0.05),but E-cadherin expression was significantly lower than that of the adjacent normal tissues (0.079±0.002 vs.0.321±0.005;t=1.844,P＜0.05).There was correlation between VEGF-C mRNA expression with histological grading,TNM staging,lymph node and distant metastasis (t=-1.621,-1.474,-2.378,-1.966,P＜0.05).There was correlation between E-cadherin mRNA expression with tumor size,histological grading,TNM stage,there was a significant difference (t=1.875,1.673,1.544,P＜0.05).VEGF-C and E-cadherin protein expression was negatively correlated(r=-0.688,P＜0.05).Conclusion Up-regulated of VEGF-C gene and decreased expression of E-cadherin may play an important role in the carcinogenesis of gastric cancer
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Objective To explore the effect of intrahepatic injection of liposome-mediated VEGF plasmid on ischemia-reper-fusion liver injury and its mechanism. Methods Rabbits were randomly divided into normal group, ischemia-reperfusion group and recombinant VEGF therapy group( liposome-mediated transfer of VEGF plasmid into liver via portal vein 20 min before ischemia of liver). The model of liver ischemia-reperfusion injury was established. Liver function and the activity of SOD.XO in blood were determined at the 0,2nd,6th,12th,and 24th h after operation. RT-PCR technique was applied to detect the expression level of Fas mRNA in liver tissues of every group,and flow cytometry was used to measure cell apoptosis rate at the 6th h after operation. At the 24th h after operation,all rabbits were killed and liver tissues of ischemia were taken to make pathological sections for observing the morphology and microstructure under the light microscopy and electron microscopy. ResuJts The level of ALT in recombinant VEGF therapy group was markedly reduced as compared with ischemia-reperfusion group at the 6th,12th,and 24th h after operation( P<0. 05). The activity of SOD in recombinant VEGF therapy group was significantly higher than in ischemia-reperfusion group at the 6th, 12th,and 24th h after operation. The activity of XO in recombinant VEGF therapy group was significantly lower than that in ischemia-reperfusion group at the 6th,12th,and 24th h after operation(P< 0. 05 or P<0. 01). In addition,there was significant difference in the expression of Fas mRNA and cell apoptosis rate between recombinant VEGF therapy group and ischemia-reperfusion group(P<0. 01). The injury of hepatocytes in recombinant VEGF therapy group was significantly alleviated as compared with that in ischemia-reperfusion group under the light microscopy and e-lectron microscopy. Conclusion Liposome-mediated transfer of VEGF plasmid into liver before ischemia of liver can obviously protect hepatocytes by increasing anti-oxidative ability, decreasing the expression of Fas mRNA, and finally inhibiting hepato-cyte apoptosis.
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Objective:To observe the expression of VEGF-C protein in human gastric cancer cells SGC-7901 those transfected by pCI-neo-antisense VEGF-C and investigate whether antisense VEGF-C gene could inhibit the growth of human gastric carcinoma cell line in vitro.Methods:By the liposome infection protocol,We transfected two different plasmids including pCI-neo and pCI-neo antisense VEGF-C into human gastric cancer cell line SGC-7901 cultured in vitro.Then those resistant clones were selected by G418 and expanded in DMEM culture medium.Then we used Immunohistochemical method and Western-blot to detect target genes and its expression.The cell viability was detected by MTT assay.We took the untransfected group as the control.Results:The immunohistochemical method and Western-blot showed that there were no expression of VEGF-C mRNA and its protein in the group that transfected by plasmid pCI-neo antisense VEGF-C.MTT assay showed that the group of transfected with antisense VEGF-C had a lower cell viability than other groups(P
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Objective To investigate the expressions of paxillin and vascular endothelial growth factor (VEGF) in lung carcinoma.Method SP immunohistological staining was used to detect the expression of paxillin and VEGF in 79 patients with lung carcinoma.Result 1.The expression rate of PAX and VEGF was 34.1% and 64.6%respectively.2.Significant positive correlation was found between the expression of PAX and lymphoid metastasis (P
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Objective To evaluate the expression of vascular endothelial factor ( VEGF) -D in predicting the prognosis of colorectal carcinoma (CRC). Methods Between Jan 1996 and Jan 1998, 69 patients with CRC undergoing curative surgery were included in this study. Postoperative follow-up included physical examination, serum CEA, and imaging every 3 months in the first and the second year, every 6 months in the third year and once a year thereafter. The expression of VEGF-D protein and microvessel density ( MVD ) in 69 tissues of CRC and 20 normal colorectal tissues was examined by immunohistochemistry (IHC). Results of IHC staining were quantified by Axioplan 2 imaging analysis system. Results VEGF-D protein expression in the cytoplasm was found in all of the CRC tissues and 25% (5/20 ) of normal tissues. The VEGF-D expression was much higher in tumor tissue than in the corresponding normal tissue (P