芒黄颗粒对糖尿病肾病大鼠的保护作用

目的：探讨芒黄颗粒（MHG）对Ⅱ型糖尿病肾病大鼠动物模型的保护作用。方法以腹腔注射链脲佐菌素（STZ）并长期高脂饮食制备大鼠糖尿病肾病模型。对大鼠血清空腹血糖（FBG）、空腹胰岛素（FINS）、血脂、肌酐（SCr）、尿素氮（BUN）、24 h 尿微量蛋白的含量等进行测定。结果 MHG 可显著降低造模大鼠空腹血糖、空腹胰岛素含量以及胰岛素抵抗指数,可显著降低造模大鼠血清三酰甘油、胆固醇、高密度脂蛋白及游离脂肪酸含量,能够显著降低模型大鼠 SCr、BUN 及尿微量蛋白含量。结论芒黄颗粒对糖尿病肾病大鼠具有较好的保护作用。     

Mangiferin, a natural xanthone, accelerates gastrointestinal transit in mice involving cholinergic mechanism

AIM: To investigate the effects of mangiferin on gastrointestinal transit (GIT) in normal and constipated mice, together with the possible mechanism.METHODS: Intragastrically-administered charcoal meal was used to measure GIT in overnight starved Swiss mice. In the first experiments, mangiferin (3 mg/kg, 10 mg/kg, 30 mg/kg, and 100 mg/kg, po) or tegaserod (1 mg/kg, ip) were administered 30 min before the charcoal meal to study their effects on normal transit. In the second series, mangiferin (30 mg/kg) was tested on delayed GIT induced by several different pharmacological agonists (morphine, clonidine, capsaicin) or antagonists (ondansetron, verapamil, and atropine) whereas in the third series, mangiferin (30 mg/kg, 100 mg/kg and 300 mg/kg) or tegaserod (1 mg/kg) were tested on 6 h fecal pellets outputted by freely fed mice. The ratio of wet to dry weight was calculated and used as a marker of fecal water content.RESULTS: Mangiferin administered orally significantly (P < 0.05) accelerated GIT at 30 mg/kg and 100 mg/kg (89% and 93%, respectively), similarly to 5-hydroxytryptamine₄ (5-HT₄) agonist tegaserod (81%) when compared to vehicle-treated control (63%). Co-administered mangiferin (30 mg/kg) totally reversed the inhibitory effect of opioid agonist morphine, 5-HT₃-receptor antagonist ondansetron and transient receptor potential vanilloid-1 receptor agonist capsaicin on GIT, but only to a partial extent with the GIT-delay induced by α₂-adrenoceptor agonist clonidine, and calcium antagonist verapamil. However, co-administered atropine completely blocked the stimulant effect of mangiferin on GIT, suggesting the involvement of muscarinic acetylcholine receptor activation. Although mangiferin significantly enhanced the 6 h fecal output at higher doses (245.5 ± 10.43 mg vs 161.9 ± 10.82 mg and 227.1 ± 20.11 mg vs 161.9 ± 10.82 mg of vehicle-treated control, at 30 and 100 mg/kg, P < 0.05, respectively), the effect of tegaserod was more potent (297.4 ± 7.42 mg vs 161.9 ± 10.82 mg of vehicle-treated control, P < 0.05). Unlike tegaserod, which showed an enhanced water content in fecal pellets (59.20% ± 1.09% vs 51.44% ± 1.19% of control, P < 0.05), mangiferin evidenced no such effect, indicating that it has only a motor and not a secretomotor effect.CONCLUSION: Our data indicate the prokinetic action of mangiferin. It can stimulate the normal GIT and also overcome the drug-induced transit delay, via a cholinergic physiological mechanism.     

HPLC法同时测定镇惊泻火颗粒中4种成分的含量

目的:建立同时测定镇惊泻火颗粒中芒果苷、芦荟大黄素、大黄素和大黄酚含量的方法。方法:采用高效液相色谱法。色谱柱为Capcell Pak C18(250 mm×4.6 mm,5μm),流动相为乙腈-0.1%甲酸水溶液(梯度洗脱),流速为1.0 ml/min,检测波长为254nm,柱温为20△。结果:芒果苷、芦荟大黄素、大黄素和大黄酚的质量浓度分别在10.180¹01.800、2.016101.800、2.016²0.160、1.07220.160、1.072¹0.720、1.02410.720、1.024¹0.240μg/ml范围内与各自峰面积积分值呈良好的线性关系(r分别为0.999 8、0.999 6、0.999 5、0.999 6);精密度、稳定性、重复性试验的RSD≤1.4%(n均为6);平均加样回收率分别为98.05%、97.39%、97.91%和98.93%,RSD分别为1.3%、1.5%、1.2%和1.4%(n均为6)。结论:该方法准确、稳定、重复性好,可用于镇惊泻火颗粒的质量控制。     

芒果苷减轻缺氧复氧所致人心肌细胞损伤

目的:探讨芒果苷减轻缺氧复氧所致人心肌细胞损伤的效应及机制。方法:将人心肌AC16细胞分为正常对照组、缺氧复氧组及芒果苷(50、100和200μmol/L)+缺氧复氧组。分别采用RT-qPCR及Western blot法检测Kelch样环氧氯丙烷相关蛋白1(Keap-1)、Bax、Bcl-2、caspase-3、caspase-9和超氧化物歧化酶2(SOD2)的mRNA及蛋白表达;Western blot法检测细胞核中核因子E2相关因子2(Nrf-2)的表达水平;RT-qPCR法检测miR-432-3p的表达;DCFH-DA探针检测细胞内活性氧簇(ROS)的生成;CCK-8法检测细胞活力;流式细胞术检测细胞凋亡。结果:相对于正常对照组,缺氧复氧处理AC16细胞后,miR-432-3p和Keap-1的mRNA及蛋白表达无明显变化,Nrf-2核转位和ROS生成增多(P<0.05),Bax、caspase-3和caspase-9的mRNA及蛋白水平显著升高(P<0.05),SOD2和Bcl-2的mRNA及蛋白水平以及细胞活力显著降低(P<0.05),细胞凋亡显著增多(P<0.05);相对于缺氧复氧组,芒果苷处理组miR-432-3p表达显著上调(P<0.05),ROS生成减少(P<0.05),Keap-1、Bax、caspase-3和caspase-9的mRNA及蛋白水平显著下降(P<0.05),Nrf-2核转位进一步增多(P<0.05),SOD2和Bcl-2的mRNA及蛋白水平以及细胞活力显著升高(P<0.05),细胞凋亡显著减少(P<0.05),中、高剂量组的效应明显优于低剂量组,中、高剂量组间的差异无统计学显著性。结论:芒果苷可抑制缺氧复氧损伤所造成的心肌细胞活力下降及细胞凋亡,其机制可能与其促进miR-432-3p表达,进而上调Nrf-2抗氧化应激效应有关。     

芒果苷对金黄色葡萄球菌诱导肺炎的作用研究

目的 探究芒果苷对金黄色葡萄球菌诱导的肺炎的影响及对NF-KB信号通路的作用.方法 将50只Balb/c雄性小鼠采用随机数字法分为5组,每组10只:分别为对照组、金黄色葡萄球菌组、芒果苷(15、30、60 mg/kg)组.金黄色葡萄球菌诱导造模1 h后,芒果苷组给予腹腔注射芒果苷.12 h后,收集各组肺泡灌洗液、小鼠肺...     

芒果苷对小鼠抗应激作用的实验研究

目的　观察芒果苷对小鼠的抗应激作用。方法　予不同浓度、剂量的芒果苷和淀粉蒸馏水分别给小鼠灌胃 1h后 ,分组进行负重游泳、耐缺氧、耐低温的应激实验 ,实验过程中测定小鼠血清超氧化物歧化酶 (SOD )活力、丙二醛(MDA)含量的变化。结果　予芒果苷的小鼠在不同的抗应激实验中的生存时间均比对照组延长 (P均 <0 .0 1) ,血清中SOD活力上升、MDA含量下降 (P <0 .0 1或 0 .0 5 )。结论　芒果苷具有一定的抗应激作用。     

川东獐牙菜不同部位芒果苷的含量测定研究

目的建立高效液相色谱法测定川东獐牙菜不同部位芒果苷的含量。方法采用Hypersil C18柱(150 mm×4.6mm,5μm),流动相为甲醇-0.04%磷酸溶液在0-15 min内由22∶78到32∶68,流速1.0 ml.min-1,检测波长254 nm,柱温室温,用外标法定量,测定川东獐牙菜中芒果苷的含量。结果芒果苷的线性范围0.27-2.70μg,r=0.999 7,回收率100.90%,RSD为2.19%。结论该方法简便,快速,线性关系良好,可用于川东獐牙菜芒果苷的含量测定。     

芒果苷片薄膜包衣工艺的研究

目的：探讨芒果苷片薄膜包衣工艺的最佳工艺参数。方法：采用比较法和正交试验设计法，以包衣片外观合格率、硬度、增重、耐湿度、溶出度等作为考核指标，确定薄膜包衣的最佳工艺参数。结果：最佳包衣工艺参数为：包衣液浓度为13％，主机转速为12r&#183;min^-1，片床温度45℃。结论：此工艺稳定可行。     

芒果苷对花生四烯酸代谢产物的影响

目的:研究芒果苷对花生四烯酸(AA)代谢产物的影响,以阐明其抗炎机理。方法:分别以反相高效液相法和放射性免疫法测定大鼠胸腔渗出液中性白细胞中白三烯B4(LTB4)、LTC4S水平和6-酮-前列腺素1a(6-keto-PGFla)含量。结果:高、中剂量的芒果苷可明显降低6-keto-PGFla的含量;而高、中、低剂量的芒果苷对LTB4、LTC4的水平则无影响。结论:芒果苷的抗炎机制可能与其抑制花生四烯酸代谢通路中6-keto-PGFla的释放有关。     

Vascular effects of the Mangifera indica L. extract (Vimang)

The effects of the Mangiferia indica L. (Vimang) extract, and mangiferin (a C-glucosylxanthone of Vimang) on the inducible isoforms of cyclooxygenase (cyclooxygenase-2) and nitric oxide synthase (iNOS) expression and on vasoconstrictor responses were investigated in vascular smooth muscle cells and mesenteric resistance arteries, respectively, from Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Vimang (0.5-0.1 mg/ml) and mangiferin (0.025 mg/ml) inhibited the interleukin-1beta (1 ng/ml)-induced iNOS expression more in SHR than in WKY, and cyclooxygenase-2 expression more in WKY than in SHR. Vimang (0.25-1 mg/ml) reduced noradrenaline (0.1-30 microM)- and U46619 (1 nM-30 microM)- but not KCl (15-70 mM)-induced contractions. Mangiferin (0.05 mg/ml) did not affect noradrenaline-induced contraction. In conclusion, the antiinflammatory action of Vimang would be related with the inhibition of iNOS and cyclooxygenase-2 expression, but not with its effect on vasoconstrictor responses. Alterations in the regulation of both enzymes in hypertension would explain the differences observed in the Vimang effect.