硝苯吡啶与格列本脲相互作用对正常大鼠和高血糖大鼠血糖水平的影响

目的:研究硝苯吡啶以及硝苯吡啶与格列本脲合用对空腹大鼠和肾上腺素诱发高血糖大鼠血糖水平的影响。方法:本实验采用葡萄糖氧化酶法测定血糖含量。结果:硝苯吡啶2 .5mg/kgig使空腹大鼠血糖水平显著升高(P<0 .0 1 ) ,并加重肾上腺素诱发的高血糖反应。而硝苯吡啶与降糖药格列本脲0 .9mg/kg合用时不影响空腹大鼠的血糖水平,硝苯吡啶对肾上腺素诱发高血糖大鼠灌胃格列本脲后的降血糖作用亦无明显影响。结论:尽管硝苯吡啶对空腹大鼠以及肾上腺素诱发高血糖大鼠有显著升高血糖的作用,但对格列本脲的降血糖作用无明显不良影响     

乌拉坦诱导的高血糖反应(英文)

目的:观察麻醉剂量的乌拉坦对空腹大鼠、葡萄糖负荷大鼠,肾上腺素或四氧嘧啶诱发高血糖大鼠血糖水平的影响,并探讨其对外源性胰岛素降血糖作用的影响。方法:葡萄糖氧化酶法测定血糖含量。结果:麻醉剂量1.5g·kg~(-1)乌拉坦(sc,ip各半)显著升高空腹大鼠和葡萄糖负荷大鼠的血糖水平,但对肾上腺素(胰岛功能正常)或四氧嘧啶(胰岛功能受损)诱发的高血糖大鼠的血糖水平无明显影响。在四氧嘧啶诱发的高血糖大鼠,乌拉坦显著对抗外源性胰岛素的降血糖作用。结论:乌拉坦升高血糖的作用除与已知的释放肾上腺素有关外,抑制胰岛素的降血糖作用也是其升高血糖的机制之一。     

乌拉坦对大鼠胰岛素水平的影响(英文)

目的　观察麻醉剂量的乌拉坦对空腹大鼠、葡萄糖负荷大鼠和肾上腺素诱发高血糖大鼠血浆胰岛素水平的影响。方法　采用放射免疫测定法测定血浆胰岛素活性。结果　麻醉剂量的乌拉坦 (1 .5g·kg-1 ,sc ,ip各半 )给药后 2 0min显著升高空腹大鼠及葡萄糖负荷大鼠血浆胰岛素水平 ,给药后 50min血浆胰岛素水平分别从 (1 1± 4)及 (1 1± 4)mU·L-1 升至 (2 5±1 1 )及 (47± 6)mU·L-1 ;相同剂量的乌拉坦给药后 1 4 0min使肾上腺素诱发的高血糖大鼠血浆胰岛素水平从 (1 0± 3)升至 (51± 1 8)mU·L-1 。与血浆胰岛素水平的变化相比 ,乌拉坦给药后 50min显著升高空腹大鼠和葡萄糖负荷大鼠的血糖水平 ,但对肾上腺素诱发的高血糖大鼠的血糖水平无明显影响。结论　乌拉坦显著升高空腹大鼠、葡萄糖负荷大鼠及肾上腺素诱发的高血糖大鼠血浆胰岛素水平。乌拉坦促进胰岛素分泌的机制包括高血糖依赖性促分泌和非血糖依赖性促分泌两种     

格列本脲乳胶剂的制备及初步药效学

目的制备格列本脲乳胶剂,并观察其对正常大鼠的降血糖作用。方法采用改进的Franz扩散池,考察不同浓度二乙胺、不同有机胺和促进剂对格列本脲透皮吸收的影响,并评价优选处方对正常大鼠的降血糖作用。结果当二乙胺和氮酮的质量分数分别为0.70%和3%时,格列本脲乳胶剂的稳态渗透速率最高,并且能显著降低正常大鼠空腹血糖(P<0.01)。结论格列本脲乳胶剂的降血糖作用显著,有望成为一种治疗糖尿病的新型制剂。     

国产格列美脲对家兔和大鼠降血糖作用研究

目的 :研究国产格列美脲 (Gli)对家兔、大鼠血糖及糖耐量水平和胰岛素释放的影响。方法 :以正常Wister大鼠和家兔为实验对象 ,以给药前、后血糖和胰岛素水平的变化为指标 ,观察Gli的降血糖作用。结果 :Gli呈剂量依赖性降低大鼠血糖 ,平均降低23 % ,其效价强度与格列本脲相当 ;糖耐量实验表明 ,Gli呈剂量依赖性地阻遏家兔灌服葡萄糖所致30min和60min血糖的升高 ;时效关系研究显示 ,大鼠给予Gli后30min血糖开始下降 ,3h时已降至坪值 ,大约为给药前的60 % ;该药能明显促进大鼠和家兔的胰岛素释放 ,与给药前相比胰岛素水平平均上升40 %～70 % ,其效价强度约为格列本脲的2倍。结论 :Gli可以通过促进胰岛素的释放而降低血糖 ,其降血糖的效价强度与格列本脲等效 ,且起效更快、更为温和 ,但作用时间略短     

麦冬多糖降血糖作用的药效学观察

目的观察麦冬多糖对血糖的影响,为临床实验提供实验依据。方法选用正常小鼠,自发性高血糖小鼠.链脲霉素诱发高血糖大鼠,观察麦冬多糖对血糖、血清胰岛素及糖化血红蛋白的影响。结果麦冬多糖(75、150、300mg/kg)。对正常小鼠血糖无明显影响;但能降低自发性高血糖小鼠血糖及升高血清胰岛素;麦冬多糖(75、150、300mg/kg),能降低链脲霉素诱发高血糖大鼠的血糖及糖化血红蛋白,能推迟大鼠口服蔗糖后血糖升高时间及降低血糖峰浓度。结论麦冬多糖对糖尿病小鼠和大鼠都有降血糖作用。     

山药多糖对糖尿病小鼠降血糖作用的研究

目的 探讨山药多糖对糖尿病小鼠的降血糖作用.方法 将90只小鼠随机分成山药多糖组、 格列苯脲组和健康对照组,各30只.小鼠经腹腔注射200 mg/kg四氧嘧啶建立糖尿病小鼠模型,用山药多糖？ 连续给小鼠模型灌胃给药12 d,以格列苯脲作阳性对照.结果 山药多糖组对糖尿病小鼠的血糖有明显降低 作用,与格列苯脲组比较差异无统计学意义（P＞0.05）.结论 山药多糖具有显著的降血糖作用.     

木姜叶柯总黄酮对大小鼠血糖和糖耐量的影响

目的 探讨木姜叶柯总黄酮对大小鼠血糖和糖耐量的影响.方法 采用遗传性高血糖小鼠、四氧嘧啶诱发高血糖小鼠模型、链脲菌素诱发大鼠高血糖模型,观察木姜叶柯总黄酮对大小鼠血糖和糖耐量的影响.结果 与模型组比较,木姜叶柯总黄酮低、中、高剂量(50、100、200 mg/kg)给药,明显降低遗传性高血糖小鼠的空腹血糖(P＜0.05);显著降低四氧嘧啶诱发高血糖小鼠的空腹血糖(P＜0.05),同时能显著改善其糖耐量(P＜0.05).木姜叶柯总黄酮低、中、高剂量(30、60、120 mg/kg)给药明显降低链脲菌素诱发高血糖大鼠的空腹血糖(P＜0.05)并能显著改善高血糖大鼠糖耐量(P＜0.05).结论 木姜叶柯总黄酮能显著改善高血糖大小鼠的血糖水平和糖耐量,提示其可用于糖尿病的治疗.     

黄精多糖对小鼠血糖水平的影响及机理初探

目的:探讨黄精多糖对小鼠血糖水平的影响。方法:将正常小鼠及高血糖模型小鼠随机分为五组:黄精多糖大、中、小剂量组,阳性对照组及正常对照组,分别测定各组小鼠的血糖值及高血糖模型小鼠肝脏中cAMP的含量。结果:黄精多糖对正常小鼠血糖水平无明显影响;但可显著降低肾上腺素诱发的高血糖小鼠的血糖值,剂量500mg/kg降血糖作用最为显著;同时降低肾上腺素模型小鼠肝脏中cAMP的含量。结论:黄精多糖降血糖作用机理与降低肝脏中cAMP的含量密切相关。     

格列美脲与格列本脲治疗2型糖尿病比较

目的 :研究格列美脲治疗 2型糖尿病的疗效、不良反应及对胰岛素分泌的影响。方法 :6 7例 2型糖尿病分为 2组 ,格列美脲组 33例 ,初始剂量为1mg ,po ,qd ;格列本脲组 34例 ,初始剂量为2 .5mg ,po ,qd ;2组均根据血糖调整剂量 ,服药 12wk后测定血糖、胰岛素、糖化血红蛋白 (HbA1c)等变化。结果 :12wk治疗后格列美脲组空腹血糖、餐后 2h血糖和HbA1c值明显下降 [(2 .5±s 0 .4 )mmol·L- 1,(3.72± 0 .0 6 )mmol·L- 1和 (1.5 7±0 .0 5 ) % ,均P <0 .0 1];空腹胰岛素水平升高值无明显变化 [(0 .8± 0 .4 )mU·L- 1,P >0 .0 5 ];餐后 2h胰岛素水平明显升高 [(13.5± 2 .2 )mU·L- 1,P <0 .0 1],与格列本脲组比较差异均无显著意义 (P >0 .0 5 )。但格列本脲组餐后 2h胰岛素水平变化明显高于格列美脲组 [(37± 4 )mU·L- 1vs (34± 4 )mU·L- 1,P <0 .0 1) ]。结论 :格列美脲是一种安全有效的降糖药 ,较格列本脲有更强的胰外降糖作用     

地尔硫对大鼠胰岛素水平的影响

目的　观察钙拮抗剂地尔硫 (Dil)对空腹大鼠、葡萄糖负荷大鼠以及肾上腺素诱发高血糖大鼠血浆胰岛素水平的影响。方法　采用放射免疫测定法测定血浆胰岛素含量。结果　空腹大鼠灌胃给予 10mg·kg-1和 10 0mg·kg-1Dil后 ,胰岛素水平升高 ;与对照组相比 ,Dil 10 0mg·kg-1给药后 30min使胰岛素水平增加了 1 31倍。在糖耐量试验中 ,Dil两剂量均升高胰岛素水平。在肾上腺素诱发高血糖大鼠 ,Dil 10 0mg·kg-1仅在给药后 1h轻度升高血浆胰岛素水平。结论　Dil升高空腹大鼠和葡萄糖负荷大鼠血浆胰岛素水平 ,该作用除与药物诱发的血糖升高有关外 ,可能也与Dil的某些尚未发现的作用有关。     

Laboratory evaluation of the hypoglycemic effect of Anacardium occidentale Linn (Anacardiaceae) stem-bark extracts in rats

This study evaluated the hypoglycemic effect of stem-bark extracts of Anacardium occidentale Linn., of the Anacardiaceae family, in normal (normoglycemic) and in streptozotocin-treated diabetic rats. Young adult, male Wistar rats weighing 250-300 g were used. Diabetes mellitus was induced in the test rats by intraperitoneal injections of streptozotocin (STZ, 90 mg/kg). In one set of experiments, graded doses of the aqueous and methanolic stem-bark extracts of A. occidentale (100-800 mg/kg p.o.) were separately administered to groups of fasted normal and fasted diabetic rats. In another set of experiments, 800 mg/kg p.o. of the aqueous or methanolic extract of the plant, a dose which produced maximal hypoglycemic effects in both fasted normal and diabetic rats in the previous set of experiments, were used. The hypoglycemic effects of single doses (i.e., 800 mg/kg p.o.) of A. occidentale stem-bark aqueous and methanolic extracts were compared with those of insulin (5 microU/kg s.c.) and glibenclamide (0.2 mg/kg p.o.) in both fasted normal and fasted diabetic rats. Following acute treatment, relatively moderate-to-high doses of A. occidentale stem-bark extracts (100-800 mg/kg p.o.) produced dose-dependent, significant reductions (p< 0.05-0.001) in the blood glucose concentrations of both fasted normal and fasted diabetic rats. On their own, both insulin (5 microU/kg s.c.) and glibenclamide (0.2 mg/kg p.o.) produced significant reductions (p< 0.01-0.001) in the blood glucose concentrations of the fasted normal and fasted diabetic rats. At single doses of 800 mg/kg p.o., A. occidentale stem-bark aqueous and methanolic extracts significantly reduced (p< 0.001) the mean basal blood glucose concentrations of fasted normal and fasted diabetic rats. The hypoglycemic effect of the methanolic plant extract was found to be slightly more pronounced than that of the aqueous plant extract in both the normal and diabetic rats examined. A. occidentale contains a diverse group of chemical compounds. Since methanol extractives of plants usually contain many chemical compounds, each of which is capable of producing definite biological activities via different mechanisms, it is difficult to draw any logical conclusion on the mechanism of the hypoglycemic effect of such a diverse mixture of chemical compounds contained in the plant extracts used in this study. While it is possible that the hypoglycemic effects of the plant extracts may be due, at least in part, to their terpenoid and/or coumarin contents, the mechanism of their hypoglycemic action remains largely speculative. However, this is unlikely to be due to the stimulation of pancreatic beta-cells and subsequent secretion of insulin. Although A. occidentale stem-bark aqueous or methanolic extract is less potent than insulin as an antidiabetic agent, the results of this experimental animal study indicate that it possesses hypoglycemic activity, and thus lends credence to the folkloric use of the plant in the management and/or control of adult-onset, type-2 diabetes mellitus among the Yoruba-speaking people of Western Nigeria.     

Comparison of the effects of efaroxan and glibenclamide on plasma glucose and insulin levels in rats.

The effect of efaroxan (1 and 5 mg/kg p.o.; a selective alpha 2-adrenoceptor antagonist) was compared to glibenclamide (1 and 5 mg/kg p.o.; a standard sulphonylurea) on basal plasma glucose levels of fed and fasted rats. In addition, the effect of efaroxan (5 mg/kg p.o.) and glibenclamide (2 or 5 mg/kg p.o.), alone and in combination, on the hyperglycaemia and hyperinsulinaemia induced by glucose challenges, were investigated. An intra-arterial (250 mg/kg i.a.) and a subcutaneous (1 g/kg s.c.) glucose challenge were used to stimulate the fast and slow release phases of insulin secretion. Efaroxan increased plasma insulin levels in both conscious fed and fasted rats without greatly affecting plasma glucose levels. Glibenclamide also elevated insulin levels, but was associated with marked hypoglycaemia. Efaroxan and glibenclamide potentiated the slow and fast release of insulin secretion, but glibenclamide had a tendency to produce hypoglycaemia in these test situations, a property not shared by efaroxan. A combination of efaroxan and glibenclamide produced a greater elevation in the slow and fast insulin release phases than either compound alone, but did not enhance the hypoglycaemia seen with glibenclamide alone. These results provide further evidence that pancreatic alpha 2-adrenoceptors are involved in the regulation of insulin secretion.     

Hypoglycemic effect of Hypoxis hemerocallidea corm (African potato) aqueous extract in rats

Diabetes mellitus has been recognized as a clinical syndrome since ancient times, and remains a crippling global health problem today. It is a group of heterogeneous, autoimmune, hormonal and metabolic disorders, often accompanied by hypertension, hyperlipidemia and obesity. Current estimates suggest that approximately 150 million people worldwide suffer from diabetes mellitus. The present study was undertaken to examine the hypoglycemic effect of aqueous extract of Hypoxis hemerocallidea (family: Hypoxidaceae) corm (locally known as "African Potato") in normal (normoglycemic) and in streptozotocin (STZ)-treated, diabetic rats. Young adult, male Wistar rats weighing 250-300 g were used. Diabetes mellitus was induced in the group of diabetic test rats by intraperitoneal injections of STZ (90 mg/kg). In one set of experiments, graded doses of the aqueous extract of African Potato (100-800 mg/kg p.o.) were administered to 12-h fasted normal and diabetic rats. In another set of experiments, 800 mg/kg of African potato extract, a dose of the plant extract that produced maximal hypoglycemic effects in fasted normal and diabetic rats in our pilot experiments, was used. The hypoglycemic effect of this single dose was compared with those of insulin (5 micro U/kg s.c.) and glibenclamide (5 mg/kg p.o.) in 12-h fasted normal and diabetic rats. Following acute treatment, relatively moderate to high doses of African potato extract (100-800 mg/kg p.o.) produced dose-dependent, significant reductions (p < 0.05-0.001) in the blood glucose concentrations of fasted normal and diabetic rats. Similarly, insulin (5 micro U/kg s. c.) and glibenclamide (5 mg/kg p.o.) produced significant reductions (p < 0.01-0.001) in the blood glucose concentrations of the fasted normal and diabetic rats. At a dose of 800 mg/kg, the plant extract caused 30.20% and 48.54% reductions in the blood glucose concentrations of fasted normal and STZ-treated diabetic rats, respectively. While it is likely that the hypoglycemic effect of the plant extract is largely due to its phytosterols and/or sterolin content, the exact mechanism of its hypoglycemic action is still obscure and will have to await further studies. However, the results of this experimental animal study indicate that African potato possesses hypoglycemic activity; and thus lends credence to the suggested folkloric use of the herb in the control and/or management of adult-onset, type 2 diabetes mellitus in some communities of South Africa.     

Effects of new hypoglycemic agent 2-piperazinyl-4-methyl-amino-5-methylthieno [2,3-d]pyrimidine dihydrochloride hydrate

The antidiabetic effects of 2-piperazinyl-4-methylamino-5-methylthieno [2,3-d]pyrimidine dihydrochloride hydrate (Compound-(I] were investigated in various animals and in various conditions. Compound-(I) is a new hypoglycemic agent structurally unrelated to sulfonylurea and biguanide. It produced dose dependent hypoglycemic effects (10-100 mg/kg) in rats and mice under fed, fasted and glucose tolerated states. However, it was ineffective in fasted guinea pigs even when given at 100 mg/kg. In normal fed rats and mice, hypoglycemic effects of Compound-(I) were estimated to be 3-19 times and 12-70 times more potent than tolbutamide and phenformin, respectively. Compound-(I) also produced hypoglycemic action in streptozocin diabetic rats and genetically diabetic KK mice. Especially, its hypoglycemic effect was observed at the dose as low as 3 mg/kg p.o. in KK mice. However, elevation of blood lactate was accompanied by lowering of blood glucose after oral administration of Compound-(I) in normal rats and mice and in streptozocin diabetic rats, while these effects were not observed in guinea pigs. In addition, plasma insulin significantly increased after administration of Compound-(I) in both normal and KK mice, while this increase in plasma insulin was not so prominent in fed rats. This elevation in plasma insulin might be produced by alpha 2-adrenergic antagonism at pancreatic B cell as Compound-(I) suppressed epinephrine induced hyperglycemia by elevating plasma insulin. In conclusion, Compound-(I) seems mainly to produce hypoglycemic action through extrapancreatic mechanism which increases blood lactate associated with anaerobic glycolysis or inhibition of gluconeogenesis. In addition, elevation of plasma insulin also might be responsible for hypoglycemic effects.     

Stachyose extract from Rehmannia glutinosa Libosch. to lower plasma glucose in normal and diabetic rats by oral administration

The hypoglycemic effects of water extract and stachyose extract (Part III) from Rehmannia glutinosa Libosch. were investigated in this paper by oral administration to normal, glucose- and adrenaline-induced hyperglycemic and alloxan-induced diabetic rats. The results showed that Part III had the effect of lowering fasted plasma glucose level and partially preventing hyperglycemia induced by glucose (2.5 g x kg(-1), i.p.) and adrenaline (300 microg x kg(-1), i.p.), respectively, but no obvious dose-dependent effect was found when it was administered at the doses of 100, 200 and 400 mg x kg(-1) for 6 days, i.g. In alloxan-induced diabetic rats, Part III (200 mg x kg(-1) for 15 days, i.g.) gave a significant decrease in blood glucose level. The results suggested that Part III, which is mainly composed of stachyose from Rehmannia glutinosa Libosch., had a significant hypoglycemic effect in glucose- and adrenaline-induced hyperglycemic and alloxan-induced diabetic rats.     

Drug-drug interaction between voriconazole and oral hypoglycemic agents in diabetic rats

Objective:

The objective was to study the of drug-drug interaction between voriconazole and oral hypoglycemic agents in normal and alloxan induced diabetic rats.

Materials and Methods:

The study was designed in two phases. In the first phase, influence of glibenclamide (0.45 mg/kg, p.o.) and pioglitazone (2.7 mg/kg, p.o. once daily) on blood glucose levels in normoglycemic rats was studied and then influence of voriconazole (18 mg/kg, p.o. twice daily.) pre-treatment on the hypoglycemic activity studied. Simultaneously the influence of voriconazole treatment for seven consecutive days (per se effect) on blood glucose levels was also studied in normoglycemic rats. In the second phase of the study alloxan-induced diabetic rats were used to find out the influence of voriconazole pre-treatment on glibenclamide and pioglitazone induced hypoglycemic effect in pathophysiological condition. Blood samples were collected from retro orbital plexus at regular intervals of 0.0, 0.5, 1.0, 2.0, 4.0, 8.0, 12.0, 18.0 and 24.0 h after drug treatment. All the blood samples were analyzed for plasma glucose by glucose oxidase peroxidase method (GOD/POD).

Results:

The therapeutic dose of voriconazole potentiates the hypoglycemic activity of glibenclamide and pioglitazone both in normoglycemic and diabetic rats respectively.

Conclusion:

The results indicate that the dose of oral hypoglycemic agents needs to be adjusted if co-administered with voriconazole.KEY WORDS: Drug-drug interaction, glibenclamide, hypoglycemic, pioglitazone, voriconazole     

Effect of nifedipine on plasma catecholamines in man at rest and during exercise

Summary Blood pressure, heart rate, and plasma catecholamine concentrations were measured in 9 normotensive volunteers during a randomized cross-over study of oral nifedipine (10 mg×5) and placebo; measurements were made at rest and during maximal anaerobic exercise. At rest nifedipine reduced blood pressure and increased heart rate and plasma noradrenaline, whereas plasma adrenaline did not change. During exercise, the blood pressure response was similar in nifedipine and placebo treated subjects; however, heart rate was significantly higher with nifedipine. Plasma noradrenaline increased more during exercise in nifedipine-treated subjects. By contrast, nifedipine inhibited the increase in plasma adrenaline induced by exercise.The results suggest that peripheral vasodilatation induced by nifedipine is responsible for increased sympathetic nerve activity, both at rest and during exercise, and that nifedipine inhibits adrenaline secretion in man.The data were presented in part at the Symposium: Calcium entry blockers and tissue protection, Rome, 1984     

Hypoglycemic activity of aqueous seed extract of Hunteria umbellata in normal and streptozotocin-induced diabetic rats

The present study evaluated the aqueous seed extract of Hunteria umbellata K. Schum (Apocynaceae) for hypoglycemic activity in rats. Diabetes was induced by a single dose of streptozotocin (50?mg/kg i.p.). Daily doses of 400, 800, and 1000?mg/kg of extract were orally administered to fasted normal and diabetic rats. Blood glucose levels were monitored after 0, 2, 4, 8, 12?h and on day 14 post treatment. Liver glycogen levels were also estimated on day 14. In normal rats, only 400?mg/kg of the extract produced a significant reduction in blood glucose at the 4?h (P?<?0.05) which was 22.15?±?4.88%. In diabetic rats, the extract, 400, 800?mg/kg, caused significant reduction (P?<?0.01), 51.87% ± 5.79% and 43.47% ± 8.06% respectively, with maximum effect at 8?h. This reduction in blood glucose was greater than that of glibenclamide (31.03% ± 8.86%). Diabetic rats administered with 400?mg/kg extract produced a significant reduction (P?<?0.01) on day 14 (43.60% ± 8.10%). Liver glycogen levels were significantly increased (P?<?0.05) in diabetic rats administered with doses of 400 and 800?mg/kg extracts and these were comparable to glibenclamide. Acute toxicity data showed no mortality in mice up to 17.5?g/kg. We conclude that the extract possesses marked hypoglycemic effects in diabetic rats possibly through increased glycogenesis, thus justifying its use in herbal medicine for the treatment of diabetes.     

Effects of 18alpha-glycyrrhizin on the pharmacodynamics and pharmacokinetics of glibenclamide in alloxan-induced diabetic rats

This paper investigated the effects of 18alpha-glycyrrhizin (18alpha-GL) on the pharmacodynamics and pharmacokinetics of glibenclamide in experimental diabetic rats. 18alpha-GL (25 mg/kg) and/or glibenclamide (1 mg/kg) were given to alloxan-induced diabetic rats for consecutive 5 days. When the rats were co-treated with 18alpha-GL and glibenclamide, fasting plasma glucose concentration was further reduced, plasma insulin content and liver glycogen level were increased markedly as compared with glibenclamide-treated animals. Meanwhile, in co-treated group, elimination rate constant (Ke) of glibenclamide was reduced while peak plasma concentration (C(max)), area under the plasma concentration vs time curve (AUC(0-14 h)) and elimination half-life (T(1/2Ke)) were increased significantly vs glibenclamide alone administered rats. The activities of hepatic CYP3A and the markers of liver injury, plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST), were significantly decreased in rats treated with 18alpha-GL alone and in combination with glibenclamide. Results of immunohistochemistry showed that 18alpha-GL improved the effects of glibenclamide on the pathological morphology of pancreatic islet beta cells and the intensities of positive immunostaining for insulin. Our results revealed that 18alpha-GL led to the enhancement of the hypoglycemic effect of glibenclamide by inhibiting the activity of CYP3A; on the other hand, 18alpha-GL protected the pancreatic islet beta cells and liver from damage in diabetes which suggested that 18alpha-GL might be beneficial as an adjuvant drug of glibenclamide in a proper dose, especially to the diabetic patients associated with liver dysfunction.