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Honokiol attenuates the severity of acute pancreatitis and associated lung injury via acceleration of acinar cell apoptosis

机译:和厚朴酚减弱急性的严重程度胰腺炎和相关肺损伤通过加速度的腺泡细胞的凋亡

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摘要

Severe acute pancreatitis remains a life-threatening disease with a high mortality rate among a defined proportion of those affected. Apoptosis has been hypothesized to be a beneficial form of cell death in acute pancreatitis. Honokiol, a low-molecular-weight natural product, possesses the ability of anti-inflammation and apoptosis induction. Here, we investigate whether honokiol can ameliorate severe acute pancreatitis and the associated acute lung injury in a mouse model. Mice received six injections of cerulein at 1-h intervals, then given one intraperitoneal injection of bacterial lipopolysaccharide for the induction of severe acute pancreatitis. Moreover, mice were intraperitoneally given vehicle or honokiol 10 min after the first cerulein injection. Honokiol protected against the severity of acute pancreatitis in terms of increased serum amylase and lipase levels, pancreas pathological injury, and associated acute lung injury. Honokiol significantly reduced the increases in serum tumor necrosis factor-α, interleukin 1, and nitric oxide levels 3 h and serum high-mobility group box 1 24 h after acute pancreatitis induction. Honokiol also significantly decreased myeloperoxidase activities in the pancreas and the lungs. Endoplasmic reticulum stress-related molecules eIF2α (phosphorylated) and CHOP protein expressions, apoptosis, and caspase-3 activity were increased in the pancreas of mice with severe acute pancreatitis, which was unexpectedly enhanced by honokiol treatment. These results suggest that honokiol protects against acute pancreatitis and limits the spread of inflammatory damage to the lung in a severe acute pancreatitis mouse model. The acceleration of pancreatic cell apoptosis by honokiol may play a pivotal role.
机译:严重的急性胰腺炎仍然是一个威胁生命的疾病,死亡率很高率定义的比例受到影响。有益的形式在急性细胞死亡胰腺炎。自然产品,拥有的能力抗炎和诱导细胞凋亡。我们调查和厚朴酚是否可以改善严重的急性胰腺炎和相关联的急性肺损伤小鼠模型。六个注射cerulein每隔1小时给定一个腹腔内注射的细菌脂多糖诱导的严重急性胰腺炎。腹腔内车辆或10和厚朴酚分钟后第一个cerulein注入。防止急性的严重程度胰腺炎血清淀粉酶的增加和脂肪酶水平,胰腺病理损伤,和相关的急性肺损伤。显著降低血清的增加肿瘤坏死因子-α,白介素1,3 h和血清一氧化氮水平的高机动1急性胰腺炎后24 h组框归纳。髓过氧物酶在胰腺和活动肺部。蛋白质分子eIF2α(磷酸化)和排骨表达式、细胞凋亡和caspase-3活动增加小鼠的胰腺中严重的急性胰腺炎,这是出乎意料的增强和厚朴酚治疗。建议和厚朴酚预防急性胰腺炎和限制的传播炎症严重急性肺损伤胰腺炎小鼠模型。和厚朴酚可能扮演一个胰腺细胞凋亡关键作用。

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