Biotechnology and Structural Biology (BSB) Group, Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa 3886, South Africa.
Department of Biochemistry, College of Sciences, Afe Babalola University, PMB 5454, Ado-Ekiti 360001, Nigeria.
Molecules. 2017 Oct 2;22(10):1654. doi: 10.3390/molecules22101654.
This study sought to investigate the possible protective role of Parkia biglobosa seed protein isolate (PBPi) against streptozotocin-induced hepatic damage and oxidative stress in diabetic male rats. Prior to animal experiments, a HPLC fingerprint of PBPi was recorded. Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin (STZ; 60 mg/kg body weight). Diabetic rats were orally treated daily with PBPi (200 or 400 mg/kg body weight) or insulin (5 U/kg, i.p.) for 28 days. The degree of protection was evaluated using biochemical parameters such as malondialdehyde (MDA) levels, serum transaminases (ALT and AST), total protein, total glutathione (Total GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and interleukin-6 (IL-6) activities. Histology of liver sections was also performed. The HPLC fingerprint of PBPi revealed eleven distinct peaks; PBPi at tested doses significantly attenuates STZ-induced elevated levels of serum IL-6, ALT and AST; and hepatic TBARS levels. Hepatic antioxidants (Total GSH, GST, SOD, CAT) as well as total protein were markedly restored in a dose-dependent manner. Histopathological results strongly support the protective role of PBPi. These results suggest PBPi could confer protection by ameliorating hepatic damage and oxidative stress caused by STZ in animal model possibly via its anti-inflammatory and antioxidant properties.
本研究旨在探讨百香果酸豆分离蛋白(PBPi)对链脲佐菌素(STZ)诱导的糖尿病雄性大鼠肝损伤和氧化应激的可能保护作用。在动物实验之前,记录了 PBPi 的 HPLC 指纹图谱。通过单次腹腔注射链脲佐菌素(STZ;60mg/kg 体重)诱导大鼠糖尿病。糖尿病大鼠每日口服 PBPi(200 或 400mg/kg 体重)或胰岛素(5U/kg,ip)治疗 28 天。通过生化参数如丙二醛(MDA)水平、血清转氨酶(ALT 和 AST)、总蛋白、总谷胱甘肽(总 GSH)、谷胱甘肽-S-转移酶(GST)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和白细胞介素-6(IL-6)活性来评估保护程度。还对肝组织切片进行了组织学检查。PBPi 的 HPLC 指纹图谱显示有十一个独特的峰;PBPi 在测试剂量下可显著减轻 STZ 诱导的血清 IL-6、ALT 和 AST 升高以及肝 TBARS 水平。肝抗氧化剂(总 GSH、GST、SOD、CAT)和总蛋白呈剂量依赖性显著恢复。组织病理学结果强烈支持 PBPi 的保护作用。这些结果表明,PBPi 可能通过其抗炎和抗氧化特性改善 STZ 诱导的动物模型中的肝损伤和氧化应激来发挥保护作用。