研究动态
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非洲红藻 (Erythrophleum africanum) 的临床前抗糖尿病和抗氧化作用对链脲佐菌素诱发的糖尿病肾病有害。

Preclinical antidiabetic and antioxidant effects of Erythrophleum africanum (benth.) harms in streptozotocin-induced diabetic nephropathy.

发表日期:2024 Jul 03
作者: Oluwafemi A Ojo, David Ajeigbe, Akingbolabo D Ogunlakin, Olalekan E Odesanmi, Mojisola Ayomipo, Godwin Berana, Peluola Ayeni, Omolola A Ajayi-Odoko, Damilare I Ayokunle, Adebola B Ojo, Basiru O Ajiboye, Omolara O Ojo, Samuel O Dahunsi
来源: ANTIOXIDANTS & REDOX SIGNALING

摘要:

本研究调查了非洲桉树皮甲醇提取物 (MEEA) 对链脲佐菌素 (STZ) 诱导的 Wistar 大鼠糖尿病肾病 (DN) 的抗糖尿病作用。测量了 MEEA 的体外酶(α-淀粉酶)抑制活性使用标准程序。空腹血糖高于 250mg/dL 的糖尿病大鼠被视为糖尿病,并分为以下组:对照组(蒸馏水处理)、糖尿病对照、糖尿病二甲双胍(100mg/kg)、糖尿病 MEEA(150mg/kg) )和糖尿病 MEEA(300 毫克/公斤),每天口服一次,持续 14 天。在实验期结束时,收集肾组织用于生化和组织学分析。通过实时定量PCR检测肾脏细胞凋亡和标记基因表达。MEEA具有α-淀粉酶抑制作用。 MEEA 显着 (p<0.05) 降低 STZ 诱导的血糖、血清尿素、血清肌酐、尿酸、丙氨酸氨基转移酶、碱性磷酸酶和丙二醛的升高,并增加 STZ 诱导的超氧化物歧化酶、过氧化氢酶和还原型谷胱甘肽的降低。此外,MEEA 通过显着下调环磷酸腺苷 (cAMP)、蛋白激酶 A (PKA)、cAMP 反应结合蛋白 (CREB) 和 cFOS 的 mRNA 表达以及上调 B 细胞淋巴瘤 2 (Bcl-2) 的 mRNA 表达来预防 DN ),表明MEEA的肾保护能力是由于cAMP/PKA/CREB/cFOS信号通路的调节。此外,MEEA 治疗可防止糖尿病大鼠中观察到的组织病理学改变。这项研究的数据表明,MEEA 调节 DN 大鼠的葡萄糖稳态并抑制氧化还原失衡。© 2024 Walter de Gruyter GmbH,柏林/波士顿。
This study investigated the antidiabetic effects of the methanolic extract of E. africanum (MEEA) stem bark on streptozotocin (STZ)-induced diabetic nephropathy (DN) in Wistar rats.The in vitro enzyme (α-amylase) inhibitory activity of MEEA was measured using a standard procedure. Diabetic rats with fasting blood glucose above 250 mg/dL were considered diabetic and were divided into the following groups: control (distilled water-treated), diabetic-control, diabetic metformin (100 mg/kg), diabetes + MEEA (150 mg/kg), and diabetes + MEEA (300 mg/kg) via oral gavage once daily for 14 days. At the end of the experimental period, kidney tissues were collected for biochemical and histological analyses. Kidney apoptosis and marker gene expression were measured by real-time quantitative PCR.MEEA exhibited α-amylase inhibitory effects. MEEA significantly (p<0.05) reduced the STZ-induced increases in blood glucose, serum urea, serum creatinine, uric acid, alanine aminotransferase, alkaline phosphatase, and malondialdehyde and increased the STZ-induced decreases in superoxide dismutase, catalase, and reduced glutathione. In addition, MEEA protects against DN by significantly downregulating the mRNA expression of cyclic adenosine monophosphate (cAMP), protein kinase A (PKA), cAMP-response binding protein (CREB), and cFOS and upregulating B-cell lymphoma 2 (Bcl-2), suggesting that the nephroprotective ability of MEEA is due to the modulation of the cAMP/PKA/CREB/cFOS signaling pathway. Furthermore, MEEA treatment protected against histopathological alterations observed in diabetic rats.The data from this study suggest that MEEA modulates glucose homeostasis and inhibits redox imbalance in DN rats.© 2024 Walter de Gruyter GmbH, Berlin/Boston.