Miao Chengfeng, Chen Hanbin, Li Yulian, Guo Ying, Xu Feifei, Chen Qi, Zhang Yanyan, Hu Mengjun, Chen Guorong
Department of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR China.
Department of Radiation Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR China.
Diabetol Metab Syndr. 2021 Feb 18;13(1):21. doi: 10.1186/s13098-021-00638-3.
Diabetic encephalopathy is a severe diabetes complication with cognitive dysfunction and neuropsychiatric disability. The mechanisms underlying diabetic encephalopathy is believed to be relevant with oxidative stress, vascular amylin deposition, immune receptors, inflammation, etc. This study wanted to evaluate the ability of curcumin and its analog A13 to alleviate oxidative stress and inflammation in diabetes-induced damages in brain.
Sixty adult male Sprague-Dawley rats were divided into 5 groups: normal control (NC) group, diabetes mellitus (DM) group, curcumin-treated diabetes mellitus (CUR) group, high dose of A13-treated diabetes mellitus (HA) group, low dose of A13-treated diabetes mellitus (LA) group. Activation of the nuclear factor kappa-B (NF-κB p65) pathway was detected by RT-qPCR, immunohistochemical (IHC) staining and Western blot; oxidative stress was detected by biochemical detection kit; brain tissue sections were stained with hematoxylin-eosin (HE) staining and Myelin staining.
RT-qPCR, IHC staining and Western blot showed that curcumin and A13 treatment could inhibit the NF-κB p65 pathway. Curcumin and A13 increased the activity of superoxide dismutase and decreased the malondialdehyde level in the brain of diabetic rats. Furthermore, HE staining and Myelin staining demonstrated that the histological lesions of the brain in diabetic rats could be significantly ameliorated by curcumin and A13.
Curcumin analog A13 could alleviate the damages in the brain of diabetes rats by regulating the pathways of inflammation and oxidative stress. A13 may be a new potential therapeutic agent for diabetic encephalopathy.
糖尿病性脑病是一种严重的糖尿病并发症，伴有认知功能障碍和神经精神残疾。糖尿病性脑病的潜在机制被认为与氧化应激、血管淀粉样蛋白沉积、免疫受体、炎症等有关。本研究旨在评估姜黄素及其类似物A13减轻糖尿病诱导的脑损伤中氧化应激和炎症的能力。
将60只成年雄性Sprague-Dawley大鼠分为5组：正常对照组（NC）、糖尿病组（DM）、姜黄素治疗糖尿病组（CUR）、高剂量A13治疗糖尿病组（HA）、低剂量A13治疗糖尿病组（LA）。通过RT-qPCR、免疫组织化学（IHC）染色和蛋白质印迹法检测核因子κB（NF-κB p65）通路的激活情况；使用生化检测试剂盒检测氧化应激；对脑组织切片进行苏木精-伊红（HE）染色和髓鞘染色。
RT-qPCR、IHC染色和蛋白质印迹法显示，姜黄素和A13治疗可抑制NF-κB p65通路。姜黄素和A13可提高糖尿病大鼠脑中超氧化物歧化酶的活性，降低丙二醛水平。此外，HE染色和髓鞘染色表明，姜黄素和A13可显著改善糖尿病大鼠脑的组织学损伤。
姜黄素类似物A13可通过调节炎症和氧化应激途径减轻糖尿病大鼠脑损伤。A13可能是糖尿病性脑病的一种新的潜在治疗药物。
