促炎细胞因子
髓过氧化物酶
急性胰腺炎
虾青素
腹腔注射
细胞因子
H&E染色
医学
白细胞介素
药理学
内科学
脂多糖
细胞凋亡
自噬
胰弹性蛋白酶
坏死
弹性蛋白酶
胰腺炎
化学
炎症
免疫组织化学
酶
生物化学
类胡萝卜素
作者
Hui Zhang,Wenjuan Yang,Yueyue Li,Liang-Kai Hu,Ying Dai,Jianqing Chen,Shuqi Xu,Xuanfu Xu,Jiang Hai-qiong
标识
DOI:10.1016/j.intimp.2018.01.011
摘要
A various of pharmacological effects of astaxanthin has been confirmed. However, the mechanism underlying protective effect of astaxanthin on acute pancreatitis (AP) induced by cerulein still unclear. The present study is to investigate the mechanism underlying the effect of astaxanthin on autophagy and apoptosis via the JAK/STAT3 pathway. Intraperitoneal injection of cerulein at hourly intervals followed by lipopolysaccharide injection were used in Balb/C mice. Vehicle or astaxanthin, which intraperitoneal injected in two doses (20 mg/kg and 40 mg/kg), were injected in mice 1 h before the first cerulein injection. At 3 h after the last injection, when the pathological changes were most severe, pancreatic tissue was analyzed by pathologically scored and hematoxylin and eosin (H&E) staining. The severity of AP was assessed by histological grading, proinflammatory cytokine levels, biochemistry, myeloperoxidase (MPO) activity, and analysis of JAK/STAT3 activity. Astaxanthin administration markedly reduced serum digestive enzyme activities, pancreatic histological scores, proinflammatory cytokine levels (tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), and Interleukin-6 (IL-6)), MPO and JAK/STAT3 activity. Collectively, these results indicate that astaxanthin inhibits pancreatic injury in AP by targeting JAK/STAT3-mediated apoptosis and autophagy.
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