仙人掌粉对糖尿病大鼠血糖的影响

目的　研究仙人掌对糖尿病血糖的影响。方法　采用四氧嘧啶造成大鼠实验性糖尿病模型 ,然后将高、中、低 3种剂量的仙人掌粉加入到基础饲料中进行实验观察。结果　仙人掌粉高 (10g kg·d)、中 (5 .0g kg·d)剂量组均可显著降低糖尿病大鼠空腹血糖 ,并且高剂量组具有显著改善糖尿病大鼠尿量增加的作用。各剂量组对正常大鼠血糖无明显影响。结论　仙人掌粉能有效降低四氧嘧啶所导致的糖尿病大鼠的血糖、尿量     

四氧嘧啶诱发糖尿病大鼠血管紧张素的变化

实验观察了四氧嘧啶诱发糖尿病大鼠连续饲养１１０ｄ后体内肾素一血管紧张素系统的变化。结果表明，血浆和心脏的血管紧张素Ⅱ含量无明显变化，而肾脏的ＡｎｇⅡ含量却明显低于正常对照组。另外，心脏的心钠素（ＡＮＰ）含量在糖尿病大鼠与正常对照组之间无差别，血中的糖化血红蛋白含量基本无变化。上述结果表明，糖尿病大鼠早期心脏可能无明显损伤，而肾脏的肾素一血管紧张素系统活性降低。     

灵芝多糖对小鼠糖耐量的影响

目的 :探讨灵芝多糖对正常和糖尿病小鼠糖耐量的影响。方法 :采用腹腔注射四氧嘧啶 (2 0 0 mg· kg- 1 )诱导小鼠造成糖尿病模型 ,分别观察单次给予 0 .5 g·kg- 1、1.5 g· kg- 1灵芝多糖后 ,正常和糖尿病小鼠糖耐量的改变。结果 :灵芝多糖 0 .5 g· kg- 1仅能显著降低糖尿病小鼠餐后 1h和 2 h血糖 ,而灵芝多糖 1.5 g·kg- 1对正常和糖尿病小鼠餐后 1h和 2 h血糖均有显著降低作用。结论 :灵芝多糖能改善正常和四氧嘧啶糖尿病小鼠糖耐量。     

Changes in somatotrophic and lactotrophic functions of the adenohypophysis in rats with acute alloxan diabetes

By electrophoresis followed by colorimetric study of the stained gels an increased content of growth hormone and prolactin was found in the pituitary of rats during the development of alloxan diabetes. The STH and prolactin levels 4–5 days after injection of alloxan were higher by 45–58 and 38–43% respectively than in intact animals. Experiments on primary cell cultures using [¹⁴C]-L-leucine as labeled precursor revealed increased secretory activity of the somatotrophs and lactotrophs of rats with alloxan diabetes.Laboratory of Biological Standardization of Hormones, Institute of Experimental Endocrinology and Hormone Chemistry, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Yudaev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 11, pp. 536–538, November, 1979.     

四氧嘧啶致大鼠高血糖模型的实验研究

目的：探讨四氧嘧啶至Wistar大鼠高血糖模型的最佳实验条件。方法：根据不同条件对实验动物进行分组,使用四氧嘧啶腹腔注射导致动物产生高血糖,计算成模率和死亡率。结果：采用两次给药法,在给药剂量分别为120mg/kg(第1天）和100mg/kg（第2天）的条件下,随着体重的增高其成模率呈下降趋势。两次给药法的两组剂量（120mg/kg第1天,100mg/kg第2天;120mg/kg第1天,80mg/kg第2天）对成模率没有影响,剂量降低可减少死亡率。日照时间短,强度低,成模率明显降低,而且死亡率明显增高。结论：用四氧嘧啶制备糖尿病模型是一种经济可靠的实验方法。但实验条件要求较为苛刻。实验选取雄性Wistar大鼠,体重190-240g,在日照时间10h以上且阳光充足的条件下饲养。给药方式采取两步给药法,剂量为120mg/kg第1天,100mg/kg第2天,其成模率最高。     

泽泻水提物对正常及高血糖小鼠血糖的影响

泽泻水提物１０ｇ／ｋｇ及２０ｇ／ｋｇｉｇ２天，可使正常小鼠血糖明显降低。２０ｇ／ｋｇ治疗７天或预防给药３天均可使四氧嘧啶小鼠血糖明显降低     

金耳菌丝体多糖降血糖作用研究

目的:研究金耳菌丝体多糖(TMP)的降血糖作用,并对降糖机制进行初步探讨。方法:采用正常小鼠和四氧嘧啶诱导的高血糖大鼠模型,灌胃给药,监测血糖,测定肝糖原、乳酸及脂代谢相应指标。结果:腹腔注射75 mg/(kg·d)剂量的TMP 12 d可降低正常小鼠的血糖水平。以50、100、200 mg/(kg·d)三种剂量灌胃给药7 d,均可显著降低四氧嘧啶致高血糖大鼠的血糖水平,各剂量间无明显差异。连续给予100 mg/(kg·d)TMP 23 d,大鼠血糖得到控制,血糖和血清甘油三酯比对照组显著降低;肝糖原含量、血乳酸水平均与对照无明显差异。结论:TMP可有效降低糖尿病模型鼠的高血糖水平,对高血糖引发的高血脂有一定防护作用。     

Phytopharmacological evaluation of Byesukar for hypoglycaemic activity and its effect on lipid profile and hepatic enzymes of glucose metabolism in diabetic rats: Original Article

Many anti-diabetic herbal preparations have been recommended in alternative systems of medicine for the treatment of diabetes. No systematic study has been done on the anti-diabetic efficacy of Byesukar, a polyherbal formulation to treat diabetes. The anti-diabetic efficacy of byesukar ethanol extract was evaluated in an animal model of diabetes induced by alloxan. Male Wistar rats were divided in to four groups. Group 1 was normal control group; group 2 and 3 received alloxan. After inducing experimental diabetes group 2 served as diabetic control; group 3 received byesukar (500 mg/kg body weight) orally for 30 consecutive days. Group 4 were normal rats which received byesukar extract alone. The effect of byesukar on glucose level in diabetic rats was studied and the level of glucose metabolizing enzymes (Hexokinase, glucose-6-phosphatase and fructose 1, 6-bisphosphatase) in the liver and kidney were estimated. The effect of byesukar on the serum and tissue lipid profile (Cholesterol, triglycerides, phospholipids and free fatty acids) were also estimated in diabetic rats. Our results indicate that treatment with byesukar resulted in significant reduction of blood glucose, tissue glucose-6-phosphatase and fructose 1, 6-bisphosphatase activity. The decreased tissue hexokinase activity in diabetes state was found to be significantly increased by byesukar treatment. Also the byesukar treated diabetic rats showed a significant decrease in the tissue lipid profile compared to the diabetic rats. In conclusion the decreased blood glucose accompanied with decreased lipid profile and changes in the activities of the glucose metabolizing enzymes shows the antidiabetic effect of byesukar.     

On the accumulation of alloxan in the pancreatic β-cells

Summary Autoradiographic studies revealed that the radioactivity in the pancreatic islets was higher than in any other mouse tissue after intravenous injections of tracer doses of ¹⁴C-2-alloxan. The concentration of radioactivity in the endocrine pancreas concerned a great majority of the cells indicating that at least cells were involved. The uptake of the radioisotope in the pancreatic islets was considerably reduced when the small amounts of ¹⁴C-2-alloxan were complemented with carrier to bring up the total dose to the diabetogenic level or were proceeded by higher doses of non-radioactive alloxan. There was no accumulation of radioactivity in the islets after injection of the non-diabetogenic conversion products of ¹⁴C-2-alloxan obtained in an alkaline medium and only insignificant uptake was noted after exposure of the radioactive alloxan to the reactive SH-groups of glutathione. The absence of significant radioactivity in the islets of growing animals after tracer doses of ¹⁴C-2-alloxan suggests that the ability of the cells to concentrate alloxan is confined to the adult age.This study was supported by grants from the Swedish Medical Research Council, the United States Public Health Service (AM-05759-05) and Knut and Alice Wallenbergs Stiftelse.     

Oxidative stress increased hepatotoxicity induced by nano‐titanium dioxide in BRL‐3A cells and Sprague–Dawley rats

Extensive studies have shown that titanium dioxide (TiO₂) nanomaterials (NMs) can cause toxicity in vitro and in vivo under normal conditions. However, an adverse effect induced by nano‐TiO₂ in many diseased conditions, typically characterized by oxidative stress (OS), remains unknown. We investigated the toxicity of nano‐TiO₂ in rat liver cells (BRL‐3A) and Sprague–Dawley (SD) rat livers under OS conditions, which were generated using hydrogen peroxide (H₂O₂) in vitro and alloxan in vivo, respectively. In vitro results showed that cell death ratios after nano‐TiO₂ exposure were significantly enhanced (up to 2.62‐fold) in BRL‐3A cells under OS conditions, compared with normal controls. Significant interactions between OS conditions and nano‐TiO₂ resulted in the rapid G0/G1 to S phase transition and G2/M arrest, which were opposite to G0/G1 phase arrest in cells after NMs exposure only. In vivo results showed that obvious pathological changes in rat livers and the increased activities of four enzymes (i.e. aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase and alkaline phosphatase) owing to liver damage after nano‐TiO₂ exposure under OS conditions, compared with their healthy controls. In addition, compared with increased hepatotoxicity after nano‐TiO₂ exposure, micro‐TiO₂ showed no adverse effects to cells and rat livers under OS conditions. Our results suggested that OS conditions synergistically increase nano‐TiO₂ induced toxicity in vitro and in vivo, indicating that the evaluation of nanotoxicity under OS conditions is essentially needed prior to various applications of NMs in foods, cosmetics and potential treatment of diseases. Copyright © 2013 John Wiley & Sons, Ltd.