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The identification of anthocyanins from Padus racemosa and its protective effects on H2O2-induced INS-1 cells damage and STZ-induced diabetes mice
Chemistry & Biodiversity ( IF 2.9 ) Pub Date : 2020-10-06 , DOI: 10.1002/cbdv.202000382
Jianli Liu 1 , Siqi Tian 1 , Chong Xin 1 , Jia Liu 2 , Qiuyu Wang 1 , Yin He 1 , Meijia Liu 1 , Mingyang Fu 1 , Yang Yang 1 , Xiangyu Cao 1
Affiliation  

Oxidative damage in cells induced by reactive oxygen species (ROS) is a main factor in diabetes mellitus diseases progression. The composition of anthocyanins from Padus racemosa (APR) and the protective effects of APR on H2O2‐induced rat insulinoma (INS‐1) cells damage and streptozocin (STZ)‐induced diabetes mice were investigated in this study. The main components of APR were cyanidin‐cyanidin glucosyl‐rutinoside, cyanidin‐cyanidin xylosyl‐rutinoside, cyanidin‐xylosyl‐glucoside and cyanidin‐rutinoside, which were determined by liquid chromatography‐mass spectrometry (LC/MS). APR could scavenge the 2,2‐diphenyl‐1‐picrylhydrazyl (DPPH), hydroxyl radical and superoxide radical in vitro. ROS level was decreased and the cell viability was increased in INS‐1 cells after treated with APR. Cell apoptosis induced by H2O2 in INS‐1 cells was decreased after incubation with APR. APR could decrease the phosphorylation of p38 and the nuclear translocation of p65, which indicated that APR could inhibit the activation of p38 Mitogen‐activated protein kinase (MAPK) and Nuclear factor kappa B (NF‐κB) cell signaling pathways. Meanwhile, APR could effectively reduce the blood glucose and blood lipid in STZ‐induced diabetic mice. These results suggested that APR might be a potential agent for diabetes mellitus diseases treatment.

中文翻译:

总状花青素的鉴定及其对H2O2诱导的INS-1细胞损伤和STZ诱导的糖尿病小鼠的保护作用

由活性氧 (ROS) 诱导的细胞氧化损伤是糖尿病疾病进展的主要因素。本研究调查了总状花青素 (APR) 的花青素成分以及 APR 对 H2O2 诱导的大鼠胰岛素瘤 (INS-1) 细胞损伤和链脲佐菌素 (STZ) 诱导的糖尿病小鼠的保护作用。液相色谱-质谱法(LC/MS)测定APR的主要成分为花青素-花青素葡糖苷-芸香苷、花青素-木糖苷-芸香苷、花青素-木糖苷和花青素-芸香苷。APR可以在体外清除2,2-二苯基-1-苦基肼(DPPH)、羟基自由基和超氧自由基。用APR处理后,INS-1细胞中ROS水平降低,细胞活力增加。与 APR 孵育后,INS-1 细胞中 H2O2 诱导的细胞凋亡减少。APR可以降低p38的磷酸化和p65的核转位,表明APR可以抑制p38丝裂原活化蛋白激酶(MAPK)和核因子κB(NF-κB)细胞信号通路的激活。同时,APR可以有效降低STZ诱导的糖尿病小鼠的血糖和血脂。这些结果表明 APR 可能是治疗糖尿病疾病的潜在药物。APR可有效降低STZ诱导的糖尿病小鼠的血糖和血脂。这些结果表明 APR 可能是治疗糖尿病疾病的潜在药物。APR可有效降低STZ诱导的糖尿病小鼠的血糖和血脂。这些结果表明 APR 可能是治疗糖尿病疾病的潜在药物。
更新日期:2020-10-06
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