Eltahawy N A, Saada H N, Hammad A S
Radiation Biology Department, National Center for Radiation Research and Technology (NCRRT), Egyptian Atomic Energy Authority (EAEA), Cairo, Egypt.
Indian J Clin Biochem. 2017 Jun;32(2):207-213. doi: 10.1007/s12291-016-0597-2. Epub 2016 Jul 30.
The aim of the current study was to evaluate the role of γ-amino butyric acid (GABA) in insulin disturbance and hyperglycemia associated with brain oxidative damage in streptozotocin-treated rats. Streptozotocin (STZ) was administered to male albino rats as a single intraperitoneal dose (60 mg/kg body weight). GABA (200 mg/Kg body weight/day) was administered daily via gavages during 3 weeks to STZ-treated-rats. Male albino rats (10 ± 2 weeks old; 120 ± 10 g body weight) were divided into 4 groups of 6 rats and treated in parallel. (1) Control group: received distilled water, (2) GABA group: received GABA, (3) STZ group: STZ-treated rats received distilled water, (4) STZ + GABA group: STZ-treated rats received GABA. Rats were sacrificed after a fasting period of 12 h next last dose of GABA. The results obtained showed that STZ-treatment produced hyperglycemia and insulin deficiency (similar to type1 Diabetes). These changes were associated with oxidative damage in brain tissue and notified by significant decreases of superoxide dismutase and catalase activities in parallel to significant increases of malondialdehyde and advanced oxidation protein products levels. The histopathology reports also revealed that STZ-treatment produced degeneration of pancreatic cells. The administration of GABA to STZ-treated rats preserved pancreatic tissue with improved insulin secretion, improved glucose level and minimized oxidative stress in brain tissues. It could be concluded that GABA might protect the brain from oxidative stress and preserve pancreas tissues with adjusting glucose and insulin levels in Diabetic rats and might decrease the risk of neurodegenerative disease in diabetes.
本研究的目的是评估γ-氨基丁酸（GABA）在链脲佐菌素处理的大鼠中与脑氧化损伤相关的胰岛素紊乱和高血糖中的作用。将链脲佐菌素（STZ）以单次腹腔注射剂量（60mg/kg体重）给予雄性白化大鼠。在3周内，每天通过灌胃向经STZ处理的大鼠给予GABA（200mg/Kg体重/天）。将雄性白化大鼠（10±2周龄；体重120±10g）分为4组，每组6只大鼠，并进行平行处理。（1）对照组：接受蒸馏水；（2）GABA组：接受GABA；（3）STZ组：经STZ处理的大鼠接受蒸馏水；（4）STZ + GABA组：经STZ处理的大鼠接受GABA。在末次给予GABA后禁食12小时后处死大鼠。获得的结果表明，STZ处理导致高血糖和胰岛素缺乏（类似于1型糖尿病）。这些变化与脑组织中的氧化损伤相关，并通过超氧化物歧化酶和过氧化氢酶活性的显著降低以及丙二醛和晚期氧化蛋白产物水平的显著升高而得以体现。组织病理学报告还显示，STZ处理导致胰腺细胞变性。向经STZ处理的大鼠给予GABA可保护胰腺组织，改善胰岛素分泌，改善血糖水平，并使脑组织中的氧化应激最小化。可以得出结论，GABA可能保护大脑免受氧化应激，在糖尿病大鼠中保护胰腺组织，调节血糖和胰岛素水平，并可能降低糖尿病中神经退行性疾病的风险。
