Uzomba Chinedu Godwin, Ezemagu Uchenna Kenneth, Ofoegbu Mary-Sonia, Lydia Njoku, Goodness Essien, Emelike Chinedum, Obinna Uchewa, Nwafor Alo Joseph, Mbajiorgu Ejikeme Felix
Department of Anatomy, Faculty of Basic Medical Sciences, College of Medical Sciences, Alex Ekwueme Federal University Ndufu-Alike, Ebonyi State, Abakaliki, Nigeria.
Department of Physiology, Faculty of Basic Medical Sciences, College of Medical Sciences, Alex Ekwueme Federal University Ndufu-Alike, Ebonyi State, Abakaliki, Nigeria.
Anat Cell Biol. 2024 Sep 30;57(3):446-458. doi: 10.5115/acb.24.054. Epub 2024 Jul 5.
The study aims to compare the action of and glibenclamide on alloxan-induced diabetes and ascertain how an aqueous extract of the edible mushroom regulates the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), oxidative stress biomarkers and renal toxicity in a diabetic male Wistar rat model. Twenty-five adult male Wistar rats were randomly grouped into five groups with five rats per. Group 1 and those in the treatment groups received normal feed and water . Group 2 received intraperitoneal administration of alloxan monohydrate (150 mg/kg body weight). Group 3 received alloxan monohydrate and glibenclamide (5 mg/kg body weight bwt), group 4 received alloxan monohydrate plus the extract (250 mg/kg bwt) and group 5 received alloxan monohydrate plus the extract (500 mg/kg bwt). The administration of glibenclamide plus the extract was oral for 14 days. Glibenclamide and the extract lowered blood glucose level, catalase, and glutathione peroxidase activities, increased the superoxide dismutase (SOD) activity in rats with alloxan induced diabetes. The extract at 500 mg/kg bwt reduced the plasma urea and sodium concentration in the treated rats. The extract and glibenclamide could detoxify alloxan and restore its induced renal degeneration and glomeruli atrophy, intra renal hemorrhage and inflammation and oxidative biomarkers through activation of Nrf2 expression. The drug glibenclamide and have appreciable hypoglycemic activity and potential to restore the normal renal architecture in the rats, hence they offer similar curative effects. Additionally, the extract at 500 mg/kg bwt activated SOD and Nrf2 expression more than glibenclamide in rats with alloxan-induced diabetes.
本研究旨在比较[具体物质未提及]与格列本脲对四氧嘧啶诱导的糖尿病的作用，并确定食用蘑菇的水提取物如何调节糖尿病雄性Wistar大鼠模型中核因子红细胞2相关因子2（Nrf2）的表达、氧化应激生物标志物和肾毒性。25只成年雄性Wistar大鼠随机分为五组，每组五只。第1组和各治疗组给予正常饲料和水。第2组腹腔注射一水合四氧嘧啶（150mg/kg体重）。第3组给予一水合四氧嘧啶和格列本脲（5mg/kg体重），第4组给予一水合四氧嘧啶加提取物（250mg/kg体重），第5组给予一水合四氧嘧啶加提取物（500mg/kg体重）。格列本脲加提取物口服给药14天。格列本脲和提取物降低了四氧嘧啶诱导糖尿病大鼠的血糖水平、过氧化氢酶和谷胱甘肽过氧化物酶活性，增加了超氧化物歧化酶（SOD）活性。500mg/kg体重的提取物降低了治疗大鼠的血浆尿素和钠浓度。提取物和格列本脲可通过激活Nrf2表达来解毒四氧嘧啶，并恢复其诱导的肾变性、肾小球萎缩、肾内出血和炎症以及氧化生物标志物。药物格列本脲和[具体物质未提及]具有明显的降血糖活性，并具有恢复大鼠正常肾脏结构的潜力，因此它们具有相似的治疗效果。此外，在四氧嘧啶诱导糖尿病的大鼠中，500mg/kg体重的提取物比格列本脲更能激活SOD和Nrf2表达。
