Department of Nephrology, Instituto Nacional de Cardiología Ignacio Chavez México City, 14080, Mexico.
Diabetes Res Clin Pract. 2012 Aug;97(2):276-82. doi: 10.1016/j.diabres.2012.02.022. Epub 2012 Mar 18.
Oxidative stress has been associated with diabetic complications like nephropathies. Recent studies indicate that ursodeoxycholic acid (UDCA) may be beneficial preventing diabetes-induced oxidative stress and secondary complications. Thus, we study if the UDCA-treatment decreases the expression of sodium-glucose cotransporter (SGLT2) and the oxidative stress in the kidney of diabetic rats.
The diabetes model was established by intraperitoneal injection of streptozotocin (50mg/kg). SGLT2 expression was evaluated by western blot and RT-PCR. Oxidative stress was assessed by catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase activities (SOD) and immunohistochemical analysis of 3-nitrotyrosine (3-NT).
Streptozotocin-induced diabetes caused hyperglycemia and lower body weight. The SGLT2 expression and mRNA levels increased in cortex of kidney from diabetic rats. The CAT activity decreased in cortex and medulla from diabetic rats, otherwise the GPx activity increased. Furthermore the 3-NT staining of kidney from diabetic rats increased compared to control rats. The UDCA treatment was able to decrease hyperglycemia and prevents the SGLT2 over-expression, restores the CAT and GPX activities and decreases 3-NT staining.
The UDCA treatment prevents the over-expression of SGLT2 and oxidative stress in kidney of diabetic rats.
氧化应激与糖尿病并发症有关，如肾病。最近的研究表明，熊去氧胆酸（UDCA）可能有益于预防糖尿病引起的氧化应激和继发并发症。因此，我们研究 UDCA 治疗是否会降低糖尿病大鼠肾脏中钠-葡萄糖共转运蛋白（SGLT2）的表达和氧化应激。
通过腹腔注射链脲佐菌素（50mg/kg）建立糖尿病模型。通过 Western blot 和 RT-PCR 评估 SGLT2 表达。通过过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）和超氧化物歧化酶（SOD）活性以及 3-硝基酪氨酸（3-NT）的免疫组织化学分析来评估氧化应激。
链脲佐菌素诱导的糖尿病导致高血糖和体重下降。糖尿病大鼠肾脏皮质 SGLT2 表达和 mRNA 水平增加。糖尿病大鼠皮质和髓质的 CAT 活性降低，而 GPx 活性增加。此外，与对照组大鼠相比，糖尿病大鼠肾脏的 3-NT 染色增加。UDCA 治疗能够降低高血糖，并防止 SGLT2 过度表达，恢复 CAT 和 GPX 活性并减少 3-NT 染色。
UDCA 治疗可预防糖尿病大鼠肾脏中 SGLT2 的过度表达和氧化应激。
