Ahmed Marwa A, Hassanein Khaled M A
Department of Physiology Faculty of Medicine, Assiut University Assiut 71526, Egypt.
Int J Physiol Pathophysiol Pharmacol. 2012;4(3):156-66. Epub 2012 Sep 20.
To study the possible beneficial effect of estrogen (17β-estradiol E(2)) on hyperglycemia, oxidative stress and liver dysfunctions in STZ-induced diabetic rats. A total of 40 albino male rats were randomly divided into four groups: a control group (I), a diabetic group (II), a group given 17β estradiol (E(2)) for 15 days (III), and a diabetic group given E(2) for 30 days (IV). Diabetes was induced in the rats by 65 mg/kg streptozosin (STZ) via an intraperitoneal (i.p.) injection. E(2) was given in a dose of 500ug/kg/day by oral gavage.
E(2) administration significantly lowered plasma glucose levels, increased plasma insulin levels, and improved glucose tolerance of groups III and IV. In addition, E(2) enhanced glutathione peroxidase (GPX) and reduced lipid peroxidation in the hepatic tissues (as compared to diabetic rats). E(2) caused significant decrease of plasmatic phosphatase alkaline (PAL), lactate dehydrogenase (LDH), aspartate and lactate transaminases (AST and ALT) activities of group III and IV compared to group II. Moreover, E(2) restored the histological structure of the liver and pancreas of treated groups and increased the insulin receptors expression in the liver of groups III and IV compared to diabetic rats. Notably, these beneficial effects of E(2) on diabetic rats were more prominent in group IV compared to those of group III.
E(2) has a beneficial effect on hyperglycemia, oxidative stress and ameliorates the liver dysfunction in diabetic rats and these effects may be mediated through stimulating β-cell proliferation in pancreas and increased the insulin receptor expression in the liver tissues.
研究雌激素(17β-雌二醇E₂)对链脲佐菌素诱导的糖尿病大鼠高血糖、氧化应激和肝功能障碍可能产生的有益作用。总共40只白化雄性大鼠被随机分为四组:对照组(I)、糖尿病组(II)、给予17β-雌二醇(E₂)15天的组(III)以及给予E₂ 30天的糖尿病组(IV)。通过腹腔注射65mg/kg链脲佐菌素(STZ)诱导大鼠患糖尿病。通过口服灌胃给予E₂,剂量为500μg/kg/天。
给予E₂显著降低了III组和IV组的血糖水平,提高了血浆胰岛素水平,并改善了葡萄糖耐量。此外,与糖尿病大鼠相比,E₂增强了肝组织中的谷胱甘肽过氧化物酶(GPX)并减少了脂质过氧化。与II组相比,E₂使III组和IV组的血浆碱性磷酸酶(PAL)、乳酸脱氢酶(LDH)、天冬氨酸和乳酸转氨酶(AST和ALT)活性显著降低。此外,与糖尿病大鼠相比,E₂恢复了治疗组肝脏和胰腺的组织结构,并增加了III组和IV组肝脏中胰岛素受体的表达。值得注意的是,与III组相比,E₂对糖尿病大鼠的这些有益作用在IV组中更为显著。
E₂对糖尿病大鼠的高血糖、氧化应激具有有益作用,并改善肝功能障碍,这些作用可能通过刺激胰腺β细胞增殖和增加肝组织中胰岛素受体表达来介导。