仙鹤草降糖有效部位筛选研究

目的 筛选仙鹤草降糖作用的有效部位,并初步探讨其降糖机制.方法 分别选正常小鼠、四氧嘧啶糖尿病小鼠模型和由葡萄糖灌胃高血糖小鼠模型,观察比较仙鹤草的水、95%乙醇、石油醚和乙酸乙酯提取部位的降糖效果,灌胃剂量为2.0 g·kg-1·d-1,采用苯乙双胍为阳性对照,葡萄糖氧化酶法测定血糖.结果 仙鹤草乙醇提取部位连续给药7 d,可显著降低正常小鼠血糖值,与正常对照组比较,血糖降低水平有显著性差异(P＜0.05);仙鹤草乙醇提取物能显著降低四氧嘧啶糖尿病小鼠的血糖,与模型组比较,有极显著性差异(P＜0.01);仙鹤草乙醇提取物能显著降低葡萄糖灌胃高血糖小鼠模型血糖,与模型组比较,有显著性差异(P＜0.05).结论 仙鹤草乙醇提取部位为有效降糖部位.     

仙鹤草降糖有效部位筛选研究

目的筛选仙鹤草降糖作用的有效部位,并初步探讨其降糖机制。方法分别选正常小鼠、四氧嘧啶糖尿病小鼠模型和由葡萄糖灌胃高血糖小鼠模型,观察比较仙鹤草的水、95%乙醇、石油醚和乙酸乙酯提取部位的降糖效果,灌胃剂量为2.0 g.kg-1.d-1,采用苯乙双胍为阳性对照,葡萄糖氧化酶法测定血糖。结果仙鹤草乙醇提取部位连续给药7 d,可显著降低正常小鼠血糖值,与正常对照组比较,血糖降低水平有显著性差异(P<0.05);仙鹤草乙醇提取物能显著降低四氧嘧啶糖尿病小鼠的血糖,与模型组比较,有极显著性差异(P<0.01);仙鹤草乙醇提取物能显著降低葡萄糖灌胃高血糖小鼠模型血糖,与模型组比较,有显著性差异(P<0.05)。结论仙鹤草乙醇提取部位为有效降糖部位。     

复方地黄醇提物对糖尿病大鼠早期视网膜病及肾病并发症的干预作用*

目的:研究复方地黄2种醇提取物对链脲佐菌素(STZ)诱导糖尿病大鼠的早期视网膜病变及糖尿病肾病的干预作用。方法:腹腔注射STZ 60 mg.kg-1建立糖尿病大鼠模型,4周后随机分组,5~8周3个治疗组分别每日给予氨基胍(100 mg.kg-1),复方地黄70%乙醇提取物(10 g.kg-1)及复方地黄95%乙醇提取物(10 g.kg-1)。8周后测定各组动物血清中血糖(G lu)、肌酐(Cr)和尿素氮(BUN)的含量,并测定肾组织中过氧化氢酶(CAT)活性、诱导型一氧化氮合成酶(iNOS)活性、一氧化氮(NO)和羟脯氨酸(HYP)含量;用RT-PCR测定视网膜PreproET-1和MMP-9 mRNA的表达。结果:与正常对照组比较,模型组大鼠血清Cr及BUN的含量以及肾脏组织iNOS活性、NO和HYP含量均显著升高,肾脏组织CAT活性显著降低,视网膜Prepro ET-1 mRNA表达量显著升高,MMP-9 mR-NA表达量显著降低。复方地黄70%和95%乙醇提取物组的血糖虽然无明显降低,但上述异常指标均明显逆转,与阳性对照组氨基胍接近。结论:复方地黄70%和95%乙醇提取物均能改善STZ诱导的糖尿病大鼠早期视网膜病变及糖尿病肾病发生,药效与AGEs受体拮抗剂氨基胍相当。     

玉米须提取物的小鼠急性毒性实验及降血糖作用观察

目的:研究玉米须乙醇及水提取物灌胃给药对小鼠的急性毒性作用,并观察其降血糖作用.方法:改良寇氏法计算玉米须提取物半数致死量(LD50)及其95％可信区间(CI).观察玉米须提取物对正常小鼠、葡萄糖致高血糖模型小鼠、肾上腺素致血糖升高小鼠的降血糖作用.结果:玉米须乙醇提取物LD50=203.106 g/kg(95％ CI 188.665～218.652 g/kg);水提取物LD50=105.203 g/kg(95％ CI 95.249～116.197 g/kg).玉米须水提取物和乙醇提取物对正常小鼠血糖无影响;乙醇提取物30 g/kg可明显降低葡萄糖导致的小鼠血糖升高(P＜0.01);水提取物与乙醇提取物30 g/kg可明显降低肾上腺素致小鼠升高的血糖值(P＜0.05或P＜0.01),且乙醇提取物可明显升高高血糖小鼠的肝糖原含量(P＜0.01).结论:玉米须水和乙醇提取物为无毒级中药提取物.两种提取物对正常小鼠无降低血糖作用,对高糖和肾上腺素所致的小鼠高血糖有降低作用,同时具有促进糖异生,调节糖代谢的作用.     

新疆昆仑雪菊提取物对糖尿病小鼠血糖的影响

目的:观察新疆昆仑雪菊提取物对糖尿病小鼠血糖的影响,初步探讨其可能的作用机理。方法:采用高糖高脂饲料喂养联合小剂量链脲佐菌素(STZ)腹腔注射诱导糖尿病小鼠模型,将成模小鼠按血糖均衡随机分为模型组、新疆昆仑雪菊提取物低(2 g·kg-1)、中(4 g·kg-1)、高(8 g·kg-1)剂量组和二甲双胍(0.16 g·kg-1)组,取同批次健康小鼠作为空白组。对血糖、C肽、糖化血红蛋白(Hb A1c)、IRI和ISI等指标进行观察分析。结果:干预4周后,与模型组比较,新疆昆仑雪菊提取物中、高剂量组可降低糖尿病小鼠的血糖和糖化血红蛋白值(P<0.05),提取物三个剂量组都可提高血清的C肽水平和ISI值(P<0.01),提取物高剂量组可降低IRI值(P<0.01)。结论:新疆昆仑雪菊提取物可能通过增加胰岛素分泌,减轻胰岛素抵抗以及恢复胰岛β细胞功能来发挥降血糖作用。     

复方地黄提取物对链脲佐菌素诱导的糖尿病大鼠肠系膜动脉舒张功能的改善作用

目的:观察复方地黄三种不同提取物对链脲佐菌素(STZ)诱导的糖尿病(DM)大鼠肠系膜动脉舒张功能的影响。方法:以STZ(60mg·kg-1,i.p)诱导糖尿病大鼠模型,30d后分别用复方地黄95%乙醇提取物(107.8mg·kg-1),70%乙醇提取物(154.7mg·kg-1),水提取物(56.8mg·kg-1)i.g治疗,每天1次,连续30d,60d后分别记录在L-精氨酸(L-Arg),L-硝基精氨酸(L-NOArg,NLA)及吲哚美辛(indomethacin,Ind)存在或不存在时大鼠肠系膜血管舒张功能。结果:与正常组相比,模型组大鼠肠系膜动脉舒张反应减弱;NO基础释放较正常组的36.2%,NO诱导释放为正常组的22.3%,NO在内皮依赖性舒张中的比例为正常组的32.9%;95%、70%乙醇提取物组NO基础释放为正常组的62.0%、79.7%;NO诱导释放为正常组的51.4%、72.4%;NO在内皮依赖性舒张的比例为正常组的59.4%、79.2%。水提取物效果不明显。结论:糖尿病模型大鼠肠系膜动脉舒张功能异常,主要由NO介导;复方地黄提取物能够保护内皮细胞损伤,改善血管内皮细胞功能。     

香椿乙醇提取物对糖尿病模型小鼠降血糖作用的初步研究

目的:研究香椿乙醇提取物对糖尿病模型小鼠的降血糖作用及机制。方法:将四氧嘧啶用0.9%NS配成0.02g.mL-1溶液,按200mg·kg-1腹腔注射小鼠,5d后测血糖,空腹血糖>10.00mmol.L-1为高血糖模型小鼠。将模型小鼠随机分为4组,即模型(0.9%NS)、二甲双胍(70mg·kg-1)和香椿乙醇提取物高、低剂量组(剂量分别为1、0.5g·kg-1);另设正常组(蒸馏水),5组均每天灌胃1次,连续7d,末次给药后禁食24h,空腹眼眶静脉取血,测血糖和血清胰岛素水平。结果:与模型组比较,香椿乙醇提取物高、低剂量组血糖水平显著降低(P<0.05或P<0.01);血清胰岛素水平显著增高(P<0.05或P<0.01)。结论:香椿乙醇提取物对四氧嘧啶所致的高血糖模型小鼠有显著的降血糖作用,其作用机制可能与升高血清胰岛素水平有关。     

中药仙鹤复方提取物急性毒性试验及对小鼠移植性肿瘤H22的抗肿瘤作用研究

目的 研究中药仙鹤复方乙醇提取物的急性毒性,以及中药仙鹤复方乙醇提取物和水提取多糖对小鼠移植性肿瘤H22的抑瘤作用,进而对中药仙鹤复方进行抗肿瘤活性研究.方法 测定中药仙鹤复方乙醇提取物的LD50,建立荷实体型肝癌H22小鼠模型,观察中药仙鹤复方乙醇提取物和水提取多糖的抑瘤作用.结果 中药仙鹤复方乙醇提取物的LD50为26.95g·kg-1,95%可信区间为21.99～33.01g·kg-1;中药仙鹤复方乙醇提取物9.25g·kg-1·d-1剂量组与中药仙鹤复方水提取多糖8.05g·kg-1·d-1剂量组时小鼠移植性肿瘤H22均有明显的抑制作用,其抑瘤率分别为49.2%(P＜0.01)和33.7%(P＜0.01).结论 中药鹤复方乙醇提取物和水提取多糖对小鼠移植性肿瘤H22有抑制作用.     

两色金鸡菊乙酸乙酯提取物对STZ诱导的糖尿病SD大鼠的影响

目的观察两色金鸡菊乙酸乙酯提取物对糖尿病大鼠糖脂代谢及肝脏、肾脏功能的影响。方法高糖高脂喂养联合腹腔注射链脲佐菌素(streptozotocin,STZ)建立2型糖尿病SD大鼠模型,成模大鼠随机分6组(正常组、模型组、两色金鸡菊乙酸乙酯提取物高、中、低3个剂量组0.15、0.3、0.6 g·kg-1、阳性药二甲双胍0.16 g·kg-1组)。正常组和模型组灌胃生理盐水,其余组每天灌胃给药两色金鸡菊提取物,每周测体重及随机血糖,给药4周后处死,收集大鼠血清,检测血脂四项、肝功肾功指标、血清胰岛素及糖化血红蛋白水平。结果两色金鸡菊乙酸乙酯提取物可有效降低糖尿病大鼠的随机血糖和糖化血红蛋白及血清甘油三酯、低密度脂蛋白、血清总蛋白、血肌酐及血尿酸水平,同时能升高糖尿病大鼠血清白蛋白的含量。结论两色金鸡菊乙酸乙酯提取物能降低糖尿病SD大鼠的血糖血脂,保护其肝肾功能。     

桦褐孔菌不同提取物小鼠急性毒性实验研究

目的研究桦褐孔菌不同提取物对小鼠急性毒性作用,为临床安全用药提供依据。方法采用经典的急性毒性实验方法,测定桦褐孔菌水提物和70%乙醇提取物的半数致死量(LD50),并观察其毒性反应。结果随着给药量的增大,桦褐孔菌水提物和醇提取物对小鼠毒性作用逐渐增强,死亡率逐渐升高,空白组没有异常变化。按生药量计算水提物的LD50是17.49g·kg-1,95%可信区间为16.36～18.70g·kg-1;醇提取物LD50是61.97g·kg-1,95%可信区间为53.73～71.46g·kg-1。结论桦褐孔菌水提物和70%乙醇提取物均有一定的毒性,且水提物毒性起效量比70%乙醇提取物的起效量小。     

Self-monitoring of blood glucose in diabetes

A key aim of management in people with diabetes mellitus is to control blood glucose concentrations, in order to avoid the complications of persistently raised levels (with their attendant healthcare costs) and improve quality of life. However, such control is associated with an increased likelihood of hypoglycaemia, particularly among patients on insulin therapy. In pursuit of good glycaemic control while avoiding hypoglycaemia, self-monitoring of blood glucose is widely acknowledged as a routine part of management in patients with type 1 diabetes. However, the cost of monitoring products has now become a major issue for healthcare providers. This has led to some restrictions being placed on self-monitoring, especially for patients with type 2 diabetes, where the evidence for a benefit is less clear-cut. With this in mind, we review the data relating to the benefits of self-monitoring in adults with diabetes, particularly those with type 2 disease.     

环孢素诱发血糖升高

1例27岁女性患者因白细胞减少症和血小板减少症给予口服司坦唑醇（2 mg,3次/d）、再造升血片（4片,3次/d ）,皮下注射非格司亭（150μg,1次/d ）、重组人白细胞介素11（2 mg,1次/d）、重组人促红素（10000 U,3次/周）,静脉滴注头孢美唑（2 g,2次/d）,以及成分输血等治疗。用药前空腹血糖5.3 mmol/L。18 d后诊断为再生障碍性贫血,加用环孢素125 mg,2次/d口服。加药第28天,患者空腹血糖升至9.8 mmol/L,予饮食控制。第36天,空腹血糖8.2 mmol/L。第45天,空腹血糖达10.7 mmol/L,餐后2 h血糖为18.7 mmol/L,将环孢素剂量改为100 mg,2次/d,并加用二甲双胍500 mg,2次/d口服,且严格执行糖尿病饮食。第47天,空腹血糖7.3 mmol/L;第55天,空腹血糖5.4 mmol/L,餐后2 h血糖11.3 mmol/L。     

Recent developments in blood glucose sensors

Diabetes has recently become a leading cause of death worldwide. To date, although there is no means to cure or prevent diabetes, appropriate medication and blood sugar monitoring can enhance treatment efficiency, alleviate the symptoms, and diminish the complications of the condition. This review article deals with current growth areas in the market for blood glucose sensors and possible future alternatives, which are generally considered to be the point sample test and the continuous glucose monitor (CGM). Most glucose sensors are enzyme-based, whereas others are enzyme-free. The former class is sensitive and some products are extensively employed for daily self-sensing and in hospital environments as reliable diagnostic tools. The latter class, particularly the boronic acid fluorescent sensor, is facile and extremely promising. Practicality demands that all types of sensors offer accuracy, specificity, and real-time detection.     

Self-monitoring of blood glucose in diabetic pregnancy

Admission to hospital is usually recommended to achieve the best possible diabetic control during pregnancy. We have used blood glucose monitoring at home to find out if patients can achieve equally good control outside hospital. Twenty-five consecutive diabetic patients were studied, of whom 20 had taken insulin before pregnancy. Six of their 14 previous pregnancies had ended in perinatal death. The 25 women performed 4247 blood glucose measurements during their pregnancies. Overall the mean blood glucose concentration was 7.1 mmol/l (128 mg/100 ml); before meals the mean was 6.5 mmol/l (117 mg/100 ml). Mean concentrations were lower in the third trimester, but at no stage was control in hospital significantly better than at home. The mean hospital stay before delivery was 22 days, and all patients had live babies. Monitoring blood glucose concentrations at home produces greater understanding and motivation among patients, improves control early in pregnancy, and shortens time spent in hospital.     

Increase of blood glucose concentrations in diabetic patients with glucagon eyedrops.

Hypoglycemic crisis is a common occurrence in diabetic patients. In order to reverse the hypoglycemia, glucagon eyedrops at concentrations of 2.5%, 5.0%, and 7.5% were instilled to the eyes of diabetic patients who were fasted overnight. The glucagon eyedrops raised the blood glucose efficiently in a dose-dependent manner and peaked at 30 min after drug instillation. At 2.5%, glucagon raised the blood glucose 0.83 mmol.L-1 which exceeded the minimal requirement of 0.56 mmol.L-1 increase in blood glucose level at hypoglycemic crisis. At 5.0% and 7.5%, glucagon eyedrops increased the blood glucose level further to 1.76 and 1.91 mmol.L-1, respectively. These results indicate that glucagon can be delivered effectively through ocular route to raise the systemic blood glucose for the treatment of hypoglycemic crisis.     

GABA agonists differentially modify blood glucose levels of diabetic rats.

This study described the effects of GABA agonists on glucose plasma concentrations of streptozotocin-induced diabetic rats. Low doses of an indirect GABA agonist, AOAA (aminooxyacetic acid); a GABA(A) and a GABA(B) agent, THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridone) and baclofen, respectively; and a benzodiazepine were administered to non-diabetic and to diabetic rats. Plasma glucose concentrations were estimated during fasting and after an oral glucose load. Diazepam (1 mg/kg), baclofen (1 mg/kg) and AOAA (30 mg/kg), significantly decreased glycemia after oral glucose overload of streptozotocin-induced diabetes. None of the GABA-acting agents tested changed fasting or glucose overload glycemia of normal rats. Diazepam was the only drug to increase the fasting blood glucose concentration of diabetic rats. Treatment with AOAA or diazepam was accompanied by increased insulin plasma concentrations in diabetic rats to levels similar to the ones of non-diabetic animals. These results demonstrate that benzodiazepines and other GABA drugs act the endocrine pancreas in vivo, ultimately increasing plasma insulin and decreasing high blood glucose levels of diabetic rats. The acute and prolonged effects of the multitude of drugs acting on the GABA(A)-benzodiazepine-chloride ionophore complex remain to be broadly investigated as a therapeutic tool in diabetes.