Parvizi Mohammad Reza, Parviz Mohsen, Tavangar Seyed Mohammad, Soltani Nepton, Kadkhodaee Mehri, Seifi Behjat, Azizi Yaser, Keshavarz Mansoor
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
J Diabetes Metab Disord. 2014 Aug 16;13(1):84. doi: 10.1186/s40200-014-0084-3. eCollection 2014.
Diabetic nephropathy is a serious complication of T1D (type one diabetes mellitus). Persistent hyperglycemia and subsequent hypomagnesemia is believed to develop kidney damage by activation of oxidative stress. We conducted this study to investigate the renoprotective effect of magnesium sulfate (MgSO4) on renal histopathology and oxidative stress in diabetic rats.
The study included 70 male rats. The animals were divided into seven groups: control (CRL), control receiving MgSO4 (CRL + Mg1 & CRL + Mg8), diabetic (DM1 & DM8) and diabetic receiving MgSO4 (DM + Mg1 & DM + Mg8). Rats were given 20 mg/kg (i.p) Streptozocin (STZ) for 5 consecutive days in (MLD) multiple low doses to induce T1D. At day 10 treatment groups were received MgSO4 (10 g/l) in drinking water, for 1 or 8 weeks. The blood glucose, BUN and creatinine levels were measured. Renal tissue levels of malondialdehyde (MDA) were measured by thiobarbituric acid (TBA) method to evaluate the oxidative stress. Renal histopathology was done using H & E staining method.
Treatment with MgSO4 significantly decreased the blood glucose in DM + Mg1 and DM + Mg8 groups as compared with DM1 and DM8. Magnesium treatment also decreased serum BUN and tissue level of MDA significantly in both short and long term treatment. The body weight loss and kidney weight to body weight ratio was improved by MgSO4. Histological results showed there were no differences between DM and DM + Mg groups.
Our findings showed that diabetic nephropathy is associated with high blood glucose level and oxidative stress (significant increase in MDA level). The renal dysfunction and oxidative stress can be improved by magnesium sulfate administration. It is suggested that protection against development of diabetic nephropathy by MgSO4 treatment involves changes in the blood glucose and oxidative stress.
糖尿病肾病是1型糖尿病（T1D）的一种严重并发症。持续性高血糖及随后出现的低镁血症被认为可通过激活氧化应激导致肾损伤。我们开展本研究以探讨硫酸镁（MgSO4）对糖尿病大鼠肾脏组织病理学及氧化应激的肾脏保护作用。
本研究纳入70只雄性大鼠。动物被分为7组：对照组（CRL）、接受MgSO4的对照组（CRL + Mg1和CRL + Mg8）、糖尿病组（DM1和DM8）以及接受MgSO4的糖尿病组（DM + Mg1和DM + Mg8）。大鼠连续5天接受20 mg/kg（腹腔注射）链脲佐菌素（STZ），采用多次低剂量（MLD）诱导T1D。在第10天，治疗组饮用含MgSO4（10 g/l）的水，持续1或8周。测量血糖、血尿素氮（BUN）和肌酐水平。采用硫代巴比妥酸（TBA）法测量肾组织丙二醛（MDA）水平以评估氧化应激。使用苏木精和伊红（H&E）染色法进行肾脏组织病理学检查。
与DM1和DM8组相比，MgSO4治疗显著降低了DM + Mg1和DM + Mg8组的血糖。镁治疗在短期和长期治疗中均显著降低了血清BUN和MDA组织水平。MgSO4改善了体重减轻及肾重与体重比。组织学结果显示DM组和DM + Mg组之间无差异。
我们的研究结果表明，糖尿病肾病与高血糖水平及氧化应激（MDA水平显著升高）相关。硫酸镁给药可改善肾功能障碍和氧化应激。提示MgSO4治疗预防糖尿病肾病的发生涉及血糖和氧化应激的改变。
