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灵芝多糖降血糖作用的研究 总被引：6，自引：0，他引：6
目的：研究灵芝多糖对四氧嘧啶致高血糖小鼠、去甲肾上腺素致高血糖小鼠及正常小鼠血糖水平的影响。方法：制备四氧嘧啶致糖尿病小鼠模型及去甲肾上腺素致高血糖小鼠模型,给药2周后取血测定血糖水平。结果：灵芝多糖能明显降低四氧嘧啶所致糖尿病小鼠及去甲肾上腺索所致高血糖小鼠的血糖水平,其中高剂量组与模型对照组相比均有显著意义（P〈0．05）,而对正常小鼠血糖水平影响较小,低、中、高剂量组与正常对照组相比均无显著意义（P〉0．05）。结论：灵芝多糖对四氧嘧啶致高血糖小鼠及去甲肾上腺素致高血糖小鼠具有明显降血糖作用,而对正常小鼠血糖水平影响较小。 相似文献
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黑木耳多糖对糖尿病小鼠降血糖作用 总被引：7，自引：0，他引：7
目的：研究黑木耳多糖对正常小鼠及四氧嘧啶小鼠的降血糖作用。方法：黑木耳多糖灌胃30d，观察其对正常小鼠血糖的影响、对四氧嘧啶糖尿病小鼠血糖的影响。结果：黑木耳多糖对正常小鼠血糖有降低作用；糖尿病小鼠血糖显著降低。结论：黑木耳多糖具有显著降血糖作用。 相似文献
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粗毛黄褐孔菌多糖降血糖试验研究 总被引：2，自引：0，他引：2
通过研究粗毛黄褐孔菌多糖降血糖的作用,分别用不同剂量野生粗毛黄褐孔菌多糖,灌胃正常小鼠与四氧嘧啶致糖尿病小鼠,结果显示,野生粗毛黄褐孔菌多糖对正常小鼠无明显影响,对糖尿病小鼠在给药21 d后,中剂量组和高剂量组与阴性对照组间差异极显著,与阳性对照组之间差异不显著;用野生粗毛黄褐孔菌与人工栽培、液体发酵菌丝体多糖相同剂量灌胃糖尿病小鼠21 d后,三者降血糖作用无显著差异,均能一定程度降低糖尿病小鼠血糖。 相似文献
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桦褐孔菌人工培养菌丝体、菌核与野生菌核多糖的降血糖比较试验研究 总被引：6，自引：1，他引：6
目的是探讨桦褐孔苗人工培养菌丝体、菌核与野生菌核多糖的降血糖作用。方法：采用四氧嘧啶（200mg／kg体重）腹腔注射复制小鼠高血糖模型。分别给予小鼠应用桦褐孔菌人工培养菌丝体、菌核与野生菌核多糖提取物按不同剂量灌胃，葡萄糖氧化酶法测定各组的血糖水平。结果：桦褐孔菌菌丝体多糖提取物不同剂量组对四氧嘧啶型高血糖模型小鼠的血糖均有抑制作用，对正常小鼠无明显降血糖作用。桦褐孔菌人工培养菌丝体、菌核与野生菌核多糖三者的降血糖作用无显著性差异。结论：桦褐孔菌人工培养菌丝体、菌核与野生菌核多糖提取物对四氧嘧啶型高血糖模型小鼠均有降血糖作用。对正常小鼠无明显降血糖作用。 相似文献
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《中国食用菌》2017,(2)
以糖尿病小鼠代谢指标和肌肉Glut4、PI3K、Akt1和Akt2基因表达为观测点,探讨巴氏蘑菇多糖(Agaricus blazei Murill polysaccharides,ABMP)的降血糖作用。体重(30±2)g的健康雄性小鼠随机分为:正常对照组(NC组)、高血糖模型组(HM组)、低剂量组(LD组)、中剂量组(MD组)、高剂量组(HD组)、药物治疗组(DT组),每组8只。HM组、LD组、MD组、HD组和DT组腹腔注射2%四氧嘧啶3 d(200 mg·kg~(-1)体重),禁食12 h后,血糖值高于11 mmol·L~(-1)说明建模成功。NC组和HM组每天给予0.9%生理盐水,LD组、MD组、HD组每天分别给予50 mg/kg·体重、100 mg/kg·体重、200 mg/kg·体重的ABMP,DT组每天给予200 mg/kg·体重的阿卡波糖。每周测1次体重,7周后,检测血糖、胰岛素、肝糖原含量和肌肉组织中Glut4、PI3K、Akt1和Akt2基因的表达量。结果表明,与NC组相比,HM组空腹血糖升高,差异显著(P0.01),血清胰岛素和肝糖原水平明显降低(P0.01),肌肉中Glut4、PI3K、Akt1和Akt2基因的表达量下降,差异具有统计学意义(P0.05)。与HM组相比,LD组、MD组、HD组和DT组空腹血糖值均下降,差异显著(P0.05),血清胰岛素和肝糖原含量均上升,差异达显著水平(P0.05);肌肉中Glut4、PI3K、Akt1和Akt2基因的表达量升高。ABMP能够调节糖尿病小鼠体内糖代谢,降低血糖。 相似文献
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超高效液相色谱-串联质谱法分析啶氧菌酯在葡萄果实和园地土壤中的消解动态 总被引：3，自引：0，他引：3
《果树学报》2016,(5)
【目的】评价啶氧菌酯在葡萄上使用的安全性。【方法】采用超高效液相色谱-串联质谱法建立了葡萄果实和园地土壤中啶氧菌酯的残留检测方法,研究了啶氧菌酯在葡萄果实和园地土壤中的消解动态。样品中啶氧菌酯经乙腈提取,HLB小柱净化,超高效液相色谱-串联质谱(UPLC-MS/MS)检测。【结果】啶氧菌酯在葡萄果实和园地土壤中的最低检测质量分数均为0.01 mg·kg~(-1),最小检出量均为4.0×10-13g。当添加质量分数为0.01~5.0 mg·kg-1时,添加回收率为85%~100%,相对标准偏差为2.1%~4.4%。啶氧菌酯在葡萄果实和园地土壤中的降解动态曲线符合一级动力学方程,半衰期分别为5.9~12.6 d和2.2~10.7 d。【结论】该方法能用于检测啶氧菌酯在葡萄果实和园地土壤中的残留。啶氧菌酯在葡萄果实和园地土壤中降解较快。 相似文献
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培养方式对蜜环菌胞内多糖合成与抗眩晕症活性影响的研究 总被引：2，自引：1，他引：2
对蜜环菌在不同液态培养方式下胞内多糖的合成、组成以及抗眩晕症活性进行比较。结果显示,蜜环菌在摇床培养条件下形成菌丝球,菌丝多糖(AMP)和生物量在第8d达到最高产量,分别为124.32mg/L和10.85g/L,蜜环菌在静置培养条件下形成菌索,菌索多糖(ARP)与生物量在20d时达到最高,分别为588.40mg/L和37.17g/L,静置培养对蜜环菌胞内多糖的合成有利;两种多糖在多糖含量、蛋白质含量、糖醛酸含量以及皂苷含量等组成成分上基本一致;AKTA-purifier快速层析纯化系统(FPLC)检测显示,AMP与ARP有四个相同的多糖组分,ARP另多出一个组分;抗机械旋转所致小鼠眩晕症试验表明AMP与ARP活性相似,均能显著缩短眩晕小鼠逃避电击所用的时间(P<0.01),增加小鼠眩晕后的进食量,因而对机械旋转所致眩晕症具有一定疗效。 相似文献
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培养大鼠胰岛素瘤细胞(INS-1),以四氧嘧啶损伤细胞,培养液中加入不同浓度的AMP-1,MTT法测定细胞存活率,PI荧光染色观测凋亡细胞密度,流式细胞术法检测细胞凋亡率,Western blot法检测蛋白bcl-2和bax的表达。结果表明,AMP-1浓度在50 mg·L~(-1)至500 mg·L~(-1)之间,均可提高受四氧嘧啶损伤的INS-1细胞的存活率,其中浓度为400 mg·L~(-1)时存活率最高;凋亡细胞密度,随AMP-1浓度的增大而降低;AXN+AMP-1组INS-1细胞凋亡率均低于四氧嘧啶组;Western blot法检测显示bcl-2蛋白表达量升高,bax蛋白表达量降低。AMP-1对四氧嘧啶诱导大鼠INS-1细胞凋亡具有明显的拮抗作用,其作用机制可能是通过对线粒体途径中bcl-2和bax蛋白表达的调控而抑制了细胞的凋亡。 相似文献
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WU Chao-ming ZHENG Ju-jia PAN Ying-ying YE Yan-na PAN Xue-bo LIN Zhuo-feng 《园艺学报》2017,33(12):2212-2221
AIM: To investigate whether inactivation of extracellular signal-regulated kinase 1/2 (Erk1/2) will affect the function of fibroblast growth factor 21 (FGF21) to regulate glucose and lipid metabolism. METHODS: Male db/db mice (8 weeks old) were treated with U0126 (an inhibitor of Erk1/2 kinase) for 1 week, and then treated with recombinant human FGF21 protein and adenovirus-mediated FGF21 (Ad-FGF21). The profile changes of blood glucose and blood lipid were evaluated at 120 min or 4 weeks after FGF21 administration. Meanwhile, the molecular mechanism was explored by in vitro study. RESULTS: Treatment of db/db mice with recombinant human FGF21 protein significantly reduced blood glucose and triglyceride levels at 120 min after FGF21 administration, but these changes were comparable in U0126-treated mice. Furthermore, abnormal glucose and triglyceride levels, and glucose and insulin tolerance were strongly improved in db/db mice as accompanied with decreasing body fat content after 4 weeks of ad-FGF21 administration. Interestingly, treatment with or without U0126 did not influence these effects of FGF21. Mechanically, treatment with Ad-FGF21 significantly upregulated the protein levels of p-Erk1/2 and peroxisome proliferator-activated receptor γ (PPARγ) as well as the expression of adiponectin at mRNA and protein levels in adipose tissues. However, treatment with or without U0126 did not change the profiles. On the other hand, in vitro experiments also indicated that treatment of adipocytes with recombinant human FGF21 protein significantly activated Erk1/2 phosphorylation, and upregulated the expression levels of PPARγ and adiponectin (P<0.05). However, pre-administration of U0126 did not affect the profiles. CONCLUSION: Pharmaceutical inactivation of Erk1/2 by U0216 does not affect the biological function of FGF21 to regulate blood glucose balance and improve abnormal blood lipids in vivo. 相似文献
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AIM：To establish the animal model of insulinoma and to analyze the properties of insulinoma for further study. METHODS：The hormone-releasing ability of rat insulinoma cell line INS-1 was detected in vitro. INS-1 cells were transplanted into the left kidney capsule of nude mice. The islets of the animals were destroyed by intraperitoneal injection of streptozocin (STZ) 3 d before transplantation or 2 weeks after transplantation. The venous blood was sampled, and the level of blood glucose less than 2.8 mmol/L was defined as successful establishment of insulinoma model. Different irritants were given to the model animals, and the changes of blood glucose and insulin content in serum were observed. The pancreatic tissues and the renal tissues in the injecting sites were taken from all mice for detecting insulin and glucagon by immunohistochemical staining. RESULTS：Insulinoma cells expressed insulin and glucagon at the same time. The blood glucose was less than 2.8 mmol/L 3 to 4 weeks after inoculation of INS-1 cells. Apparent tumor formed in the left kidneys where INS-1 cells were transplanted and the tumor diameters were more than 1 cm. The level of blood glucose transiently increased to higher than the normal level in the mice with tumor cell transplantation after intraperitoneal injection of STZ, and then decreased gradually and returned to less than 2.8 mmol/L after 2 weeks. The level of blood glucose in the normal nude mice after administration of STZ increased significantly. After transplantation of INS-1 cells, the level of blood glucose decreased gradually, and returned to less than 2.8 mmol/L after 4 weeks. After stimulated with high glucose, the blood glucose levels in the mice with 3 methods to establish the insulinoma models showed lower glucose peaks than that in the normal control mice. After stimulated with high glucose plus arginine or acetylcholine in the normal animals, the blood glucose peak was lower than that in the normal animals only stimulated with high glucose, and rapidly recovered to the normal level. However, the levels of blood glucose in the mice with 3 methods to establish the insulinoma models under the same stimulations were significantly higher than that in the mice only stimulated with high glucose. After stimulated with high glucose plus norepinephrine, the blood glucose peak time in the normal animals delayed, and the blood glucose level declined slowly. After stimulated with high glucose plus norepinephrine, the levels of blood glucose in the mice with 3 methods to establish the insulinoma models increased as compared with that in the mice only stimulated with high glucose. Compared with normal control group, serum insulin in insulinoma mice increased significantly. CONCLUSION：The insulinoma animal model is successfully established by transplantation of INS-1 cells into the renal capsule of nude mice. The insulinoma cells express both insulin and glucagon, and are not easily damaged by STZ. 相似文献
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AIM: To explore the effects of chlorogenic acid (CGA) on endothelial dysfunction in db/db mice and the possible mechanism. METHODS: Male db/db mice (n=12) were divided into control group and CGA group, with 6 mice in each group. The mice in CGA group were treated with diet containing 0.02% CGA, while the mice in control group were given normal diet only. The observation period was 12 weeks. Fasting blood glucose level, tail blood pressure and the body weight were analyzed each week. At the end of the 12th week, the mice were anesthetized and blood was taken from carotid artery. The plasma levels of heme oxygenase-1 (HO-1), catalase (CAT), NAD(P)H dehydrogenase quinone 1 (NQO1) and glutathione peroxidase-1 (GPx-1) were measured by ELISA. The mouse aortas were isolated, and the superoxide anion and nitric oxide (NO) levels were measured by DHE and DAF-2 DA staining, respectively. Wire Myograph System was used to detect the vasorelaxation of db/db mouse aorta. The protein levels of peroxisome proliferator-activated receptor α (PPARα), nuclear factor E2-related factor 2 (Nrf2), phosphorylated AMP-activated protein kinase (p-AMPK), phosphorylated endothelial NO synthase (p-eNOS), P22phox and P47phox were determined by Western blot. RESULTS: Dietary CGA decreased fasting blood glucose and body weight in db/db mice as compared with control group (P<0.01 or P<0.05). The plasma levels of HO-1, CAT, NQO1 and GPx-1 in CGA group were higher than those in control group (P<0.01 or P<0.05). Administration of CGA for 12 weeks attenuated superoxide anion level, increased NO level in the mouse endothelium and improved endothelium-dependent relaxation of the db/db mouse aorta. CGA also increased the protein levels of PPARα, Nrf2, p-AMPK and p-eNOS, and decreased P22phox and P47phox levels (P<0.01). CONCLUSION: Dietary CGA improves db/db mouse endothelium-dependent relaxation. This effect may be related to the increases in the levels of antioxidant molecules PPARα, Nrf2 and p-AMPK, and the up-regulation of antioxidant capacity, thus decreasing the oxidative stress, promoting eNOS phosphorylation, and increasing NO level. 相似文献
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AIM: To differentiate bone marrow mesenchymal stem cells (BMSCs) into functional insulin-producing cells to produce sufficient pancreatic islet cells for transplantation. METHODS: Recombinant adenovirus vectors carrying PDX1 and NKX6.1 genes were constructed and the bone marrow mesenchymal stem cells were infected by the recombinant adenovirus combined with several cytokines for differentiation. The expressions of PDX1, NKX6.1 and insulin and C-peptide in the differentiated bone marrow mesenchymal stem cells were detected by RT-PCR and Western blotting. After the differentiated bone marrow mesenchymal stem cells were transplanted into subrenal capsule of diabetic mice, cell morphology of the grafts as well as their secretion of insulin and C-peptide were detected. Besides, regulating capacities of grafts on the blood glucose level of the diabetic mice were also detected. RESULTS: BMSCs induced by recombinant adenovirus (pAdxsi-CMV-PDX1/CMV-NKX6.1) and several cytokines showed positive dithizone staining and the expressions of β-cell related molecule such as insulin and glucose transporter 2 were detected by RT-PCR, which showed a sustaining and stable expression. The similar results were showed by Western blotting, immunohistochemical staining and indirect immunofluorescence. The insulin secretions in the cells stimulated with glucose at concentrations of 5.5 and 25 mmol/L in the experimental group were (1 240.4±109.3) mU/L and (3 539.8±245.1) mU/L, respectively, and were significantly higher than those in control group. Moreover, transplantation of the cells to STZ mice in treatment group made serum glucose recover to normal level. CONCLUSION: PDX1 and NKX6.1 gene-modified bone marrow mesenchymal stem cells differentiate into insulin-producing cells in vitro. When these cells transplanted into STZ induced diabetic mice, their serum glucose could return to the normal level and they could live well. Thus this is a promising method for diabetes treatment. 相似文献
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选择健康雄性昆明小鼠随机分组,建立糖尿病小鼠模型后分别灌胃不同剂量的巴氏蘑菇(Agaricus blazei)多糖(低、中和高剂量组分别灌胃50、100和200mg/kg/d),阳性对照组灌胃200mg/kg/d阿卡波糖,正常对照和模型组灌胃生理盐水,7周后考察巴氏蘑菇多糖对糖尿病小鼠脂代谢的影响。结果表明:与糖尿病模型组相比,多糖各剂量组和阳性对照组空腹血糖值和血清总胆固醇含量均显著下降;多糖中、高剂量组和阳性对照组的血清甘油三酯含量也显著下降;与模型组相比,附睾脂肪中阳性对照组的glut4、pi3k、akt1和akt2mRNA的表达量均显著升高,多糖组中glut4(低、中和高剂量组)、akt1(低、中和高剂量组)、akt2(中和高剂量组)和pi3k(高剂量组)mRNA的表达量显著升高。 相似文献
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AIM: To investigate the expression of survivin in pancreas in the streptozotocin-induced diabetic mice. METHODS: Low dose of streptozotocin was used to induce diabetes mellitus in BALB/c mice. Body weight and blood glucose concentrations were examined at 1, 2, 3 and 4 weeks after the streptozotocin injection. Expression of survivin mRNA was detected by real-time FQ-PCR. RESULTS: Survivin was expressed in the pancreas of normal BALB/c mice. Low dose of streptozotocin provoked hyperglycaemia with increased survivin expression in the pancreas, but blood glucose concentration and expression of survivin was not significantly changed in control group. CONCLUSION: Survivin is expressed in the pancreas of normal BALB/c mice. Streptozotocin increases survivin expression in the pancreas, which may be related with islets regeneration. 相似文献
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AIM：To explore the effect of retinoid X receptor (RXR) agonist bexarotene (Bex) and vitamin D receptor (VDR) agonist calcitriol (Cal) on the expression of nuclear factor-kappa B (NF-κB) and the development of atherosclerosis in streptozotocin-induced diabetic apolipoprotein E knockout (STZ-ApoE-/-) mice. METHODS：Male mice were treated for 12 weeks as follows: (1) C57+vehicle; (2) ApoE-/-+vehicle; (3) STZ-ApoE-/-+vehicle; (4) STZ-ApoE-/-+Bex (10 mg·kg-1·d-1); (5) STZ-ApoE-/-+Cal (10 μg/kg, twice a week); (6) STZ-ApoE-/-+Bex (10 mg·kg-1·d-1)+Cal (10 μg/kg, twice a week). Intraperitoneal injection of STZ was performed to establish the diabetic animal model. Western blotting and immunohistochemical method was used to detect NF-κB level in the thoracic aorta. Plaque area in the thoracic aorta was measured using HE staining. RESULTS：Compared with the C57 mice, the fasting blood glucose in the ApoE-/- mice was not remarkably changed. The levels of total cholesterol (TC) and low-density lipoprotein (LDL) were greatly increased. The fasting blood glucose and lipid levels in STZ-ApoE-/-group were much higher than those in ApoE-/- group. Compared with STZ-ApoE-/- group, the fasting blood glucose and lipid levels in Bex group and Cal group were not significantly changed. Compared with the C57 mice, the protein expression of NF-κB in the ApoE-/- mice and the STZ-ApoE-/- mice was remarkably increased. Compared with STZ-ApoE-/- group, the levels of NF-κB in Bex group, Cal group and combination group were greatly decreased.Compared with STZ-ApoE-/- group, the thoracic artery plaque areas in Bex group and Cal group were inhibited (both P<005). Compared with Bex group, the plaque area of the thoracic artery in combination group was significantly decreased (P<005). CONCLUSION：Bexarotene or calcitriol decreases the development of atherosclerosis in streptozotocin-induced diabetic ApoE-/- mice. Bexarotene combined with calcitriol affords greater protection than monotherapy. The mechanism may be involved in down-regulating the expression of NF-κB. 相似文献
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LIN Xiao-yan LIN Qiu-ping XU Chang-sheng NING Ruo-bing ZHU Jiang LIN Jin-xiu CHAI Da-jun 《园艺学报》2014,30(9):1537-1545
AIM: To explore the effects of atorvastatin (Atorv) on atherosclerosis in streptozotocin (STZ)-induced diabetic apolipoprotein E knockout (ApoE-/-) mice with fat-rich diet and the possible mechanism. METHODS：C57 mice served as control. ApoE-/- mice (n=34) fed with high-fat diet were randomly divided into ApoE-/- group, STZ-ApoE-/- group and STZ-ApoE-/-+Atorv group. Intraperitoneal injection of streptozotocin was performed to create diabetic animal model. Blood glucose was determined by glucose oxidase method. Blood lipid levels were detected by enzymic method or selective homogeneous method. The plaque area in the thoracic aorta was measured by HE staining. The protein level of nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase subunit gp91phox in the thoracic aorta was determined by Western blotting. The levels of reactive oxygen species (ROS) in blood and thoracic aorta homogenates were detected by Fenton reaction and Griess reagent. Human umbilical vein endothelial cells (HUVECs) were isolated from healthy umbilical cords by collagenase I and cultured. ROS production was detected by flow cytometry. NADPH oxidase activity was measured using lucigenin assay.Effects of retinoid X receptor α (RXRα) on inhibition of oxidative stress by atorvastatin were evaluated by RNA interference and plasmid transfection. RESULTS：(1) Compared with C57 group, the plaque areas of the thoracic aorta in ApoE-/- group were increased. No difference of the fasting glucose between the 2 groups was observed. The levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), thoracic aorta gp91phox protein and ROS in blood and thoracic aorta homogenates were higher in ApoE-/- group than those in C57 group. (2) Compared with ApoE-/- group, the plaque areas of the thoracic aorta in STZ-ApoE-/- group were further enlarged ［(314.13±35.72) μm2 vs (215.88±34.19) μm2, P<0.05］. The levels of blood glucose, TG, TC and LDL-C, thoracic aorta gp91phox protein and ROS in blood and thoracic aorta homogenates were higher in STZ-ApoE-/- group than those in ApoE-/- group (P<0.05). (3) Compared with STZ-ApoE-/- group, the plaque areas of the thoracic aorta in STZ-ApoE-/- +Atorv group were reduced ［(217.47±24.56） μm2 vs （314.13±35.72） μm2, P<0.05］. The levels of blood glucose, LDL-C, TC, HDL-C and TG showed no significant difference between the 2 groups. Thoracic aorta gp91phox protein level and ROS production in blood and thoracic aorta homogenates were lower in STZ-ApoE-/- +Atorv group than those in STZ-ApoE-/- group (P<0.05). (4) High glucose-induced increases in NADPH oxidase activity and gp91phox expression were significantly inhibited by atorvastatin (10-6 mol/L) in HUVECs. The inhibitory effects of atorvastatin on high glucose-induced ROS production and NADPH oxidase activation were largely impaired when the cells were transfected with RXRα siRNA. However, the effect of atorvastatin was significantly strengthened when RXRα was over-expressed in the HUVECs transfected with RXRα plasmid. CONCLUSION：Atorvastatin inhibits atherogenesis by depressing high glucose-induced oxidative stress in diabetic ApoE-/- mice with fat-rich diet. The anti-oxidative stress effect of atorvastatin is mediated by RXRα. 相似文献