Ates Ozkan, Yucel Neslihan, Cayli Suleyman R, Altinoz Eyup, Yologlu Saim, Kocak Ayhan, Cakir Celal Ozbek, Turkoz Yusuf
Department of Neurosurgery, Turgut Ozal Medical Center, Inonu University, School of Medicine, 44069 Malatya, Turkey.
Neurochem Res. 2006 Jun;31(6):777-83. doi: 10.1007/s11064-006-9076-0. Epub 2006 Jun 21.
It is well known that hyperglycaemia due to diabetes mellitus leads to oxidative stress in the central nervous system. Oxidative stress plays important role in the pathogenesis of neurodegenerative changes. In the present study we investigated the possible neuroprotective effect of etomidate against streptozotocin-induced (STZ-induced) hyperglycaemia in the rat brain and spinal cord. A total of 40 rats were used in this study. Rats were divided into four groups: sham-control, diabetic, diabetic-etomidate treated and vehicle for etomidate treatment group. Diabetes mellitus was induced by a single injection of streptozotocin (60 mg/kg body weight). Three days after streptozotocin injection, etomidate (2 mg/kg) was injected intraperitoneally for etomidate group and lipid emulsion (10%) for vehicle group was injected with corresponding amount intraperitoneally every day for 6 weeks. Six weeks after streptozotocin injection, seven rats from each group were killed and brain, brain stem and cervical spinal cord were removed. The hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for the biochemical analysis (the level of malondialdehyde [MDA], total nitrite, reduced glutathione [GSH], and xanthine oxidase [XO] activity). STZ-induced diabetes resulted in significantly elevation of MDA, XO and nitrite levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the rats (P < 0.05) while etomidate treatment provided significantly lower values (P < 0.05). This study demonstrated that etomidate have neuroprotective effect on the neuronal tissue against the diabetic oxidative damage.
众所周知，糖尿病所致的高血糖会导致中枢神经系统氧化应激。氧化应激在神经退行性变的发病机制中起重要作用。在本研究中，我们调查了依托咪酯对链脲佐菌素诱导（STZ诱导）的大鼠脑和脊髓高血糖可能具有的神经保护作用。本研究共使用了40只大鼠。大鼠被分为四组：假手术对照组、糖尿病组、糖尿病依托咪酯治疗组和依托咪酯治疗的溶媒组。通过单次注射链脲佐菌素（60 mg/kg体重）诱导糖尿病。链脲佐菌素注射三天后，依托咪酯组腹腔注射依托咪酯（2 mg/kg），溶媒组每天腹腔注射相应剂量的脂质乳剂（10%），持续6周。链脲佐菌素注射6周后，每组处死7只大鼠，取出脑、脑干和颈脊髓。解剖海马、皮质、小脑、脑干和脊髓进行生化分析（丙二醛[MDA]水平、总亚硝酸盐、还原型谷胱甘肽[GSH]和黄嘌呤氧化酶[XO]活性）。STZ诱导的糖尿病导致大鼠海马、皮质、小脑、脑干和脊髓中MDA、XO和亚硝酸盐水平显著升高（P < 0.05），而依托咪酯治疗组的值显著降低（P < 0.05）。本研究表明，依托咪酯对神经元组织具有抗糖尿病氧化损伤的神经保护作用。
