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目的研究姜黄素对糖尿病血管并发症的治疗作用及其可能的保护机制。方法 60只健康雄性SD大鼠分为空白对照组、模型组、阳性药物组、姜黄素低、中、高(100、200、400mg·g-1)剂量组。建立糖尿病血管并发症大鼠模型,观察灌胃给药姜黄素8周后大鼠空腹血糖浓度、TG、TC、LDL-C、ox-LDL、SOD及MDA等生化指标。体外培养正常大鼠胸主动脉血管外膜成纤维细胞,并用高糖诱导细胞损伤模型,观察姜黄素对血管外膜成纤维细胞损伤的保护作用及机制。结果经姜黄素治疗后,糖尿病血管并发症大鼠体质量均有所增加、空腹血糖及血脂水平降低,大鼠血清SOD活性明显升高,MDA含量有所降低(P<0.05),中剂量组作用最为明显。MTT结果表明与高糖组相比,浓度为25μmol·L-1姜黄素细胞存活率上升30.3%,提高最为明显(P<0.05)。Western blot结果表明姜黄素可显著上调血管外膜成纤维细胞中SIRT1和Beclin1蛋白的表达(P<0.01)。结论姜黄素不仅可降低糖尿病血管并发症大鼠血糖值、提高抗氧化水平,还可改善其脂代谢异常;其保护机制可能与氧化应激和自噬有关。
Objective To study the therapeutic effect of curcumin on diabetic vascular complications and its possible mechanism of protection. Methods Sixty healthy male SD rats were divided into blank control group, model group, positive drug group and curcumin low, medium and high doses (100, 200 and 400 mg · g -1). To establish a rat model of diabetic vascular complications and observe the fasting blood glucose levels, TG, TC, LDL-C, ox-LDL, SOD and MDA in rats after 8 weeks of intragastric administration of curcumin. The normal rat thoracic aorta fibroblasts were cultured in vitro, and the injury model was induced by high glucose. The protective effect and mechanism of curcumin on the injury of vascular adventitial fibroblasts were observed. Results After curcumin treatment, the body weight of diabetic rats with vascular complications increased, while the fasting blood glucose and blood lipid levels decreased. The activity of SOD in serum increased significantly and the content of MDA decreased (P <0.05) The most obvious role. MTT results showed that compared with high glucose group, the survival rate of 25μmol·L-1 curcumin cells increased by 30.3%, the most obvious increase (P <0.05). Western blot results showed that curcumin significantly up-regulated the expression of SIRT1 and Beclin1 in vascular adventitial fibroblasts (P <0.01). Conclusion Curcumin can not only reduce the blood sugar level and improve the level of anti-oxidation in diabetic rats with vascular complications, but also improve the abnormal lipid metabolism. Its protective mechanism may be related to oxidative stress and autophagy.