Piao Xuehua, Liu Baohai, Guo Lianyi, Meng Fanji, Gao Leming
Department of Traditional Chinese Medicine, The First Affiliated Hospital, Jinzhou Medical University, Jinzhou 121001, China.
Department of Gastroenterology, The First Affiliated Hospital, Jinzhou Medical University, Jinzhou 121001, China.
Oxid Med Cell Longev. 2017;2017:7085709. doi: 10.1155/2017/7085709. Epub 2017 Jun 21.
Picroside II, from the herb , has antioxidant and anti-inflammatory activities. However, its function on severe acute pancreatitis (SAP) and molecular mechanism remains unknown. The effects of picroside II on the SAP induced by cerulean were investigated. SAP rats were treated with picroside II (25 mg/kg). The severity of SAP was evaluated by using biochemical and histological analyses. Pancreatic cancer cell PANC-1 was transfected with ptfLC3 (an indicator of autophagic activity), pcDNA3.1-NF-B (nuclear factor kappa B), and pTZU6+1-NF-B-shRNA and then treated with picroside II. Relative molecules related with NF-B-dependent autophagy were detected by using Western blot. Autophagic activities were observed by phase-contrast and fluorescent microscopes. Acetylated LC3 was detected by immunoprecipitation. The results showed that picroside II treatment reduced the level of ALT, AST, NF-B, IL-1, IL-6, TNF-, and SIRT1 (NAD-dependent deacetylase) and increased the level of SOD and GSH. The autophagic activity was reduced when NF-B was silenced, and the levels of TNF- and SIRT1 were reduced. In contrast, the overexpression of NF-B increased autophagic activity and the level of TNF-, which activated SIRT1. SIRT1 deacetylated LC3 and increased autophagic activities. Picroside II ameliorates SAP by improving antioxidant and anti-inflammtory activities of SAP models via NF-B-dependent autophagy.
来源于该草药的胡黄连苷II具有抗氧化和抗炎活性。然而，其在重症急性胰腺炎（SAP）中的作用及分子机制尚不清楚。本研究探讨了胡黄连苷II对雨蛙肽诱导的SAP的影响。将SAP大鼠用胡黄连苷II（25mg/kg）进行治疗。通过生化和组织学分析评估SAP的严重程度。用ptfLC3（自噬活性指标）、pcDNA3.1-NF-κB（核因子κB）和pTZU6 + 1-NF-κB-shRNA转染胰腺癌细胞PANC-1，然后用胡黄连苷II进行处理。通过蛋白质免疫印迹法检测与NF-κB依赖性自噬相关的相对分子。通过相差显微镜和荧光显微镜观察自噬活性。通过免疫沉淀法检测乙酰化LC3。结果显示，胡黄连苷II处理降低了ALT、AST、NF-κB、IL-1、IL-6、TNF-α和SIRT1（烟酰胺腺嘌呤二核苷酸依赖性脱乙酰酶）的水平，并提高了SOD和GSH的水平。当NF-κB沉默时自噬活性降低，TNF-α和SIRT1的水平也降低。相反，NF-κB的过表达增加了自噬活性和TNF-α的水平，从而激活了SIRT1。SIRT1使LC3去乙酰化并增加自噬活性。胡黄连苷II通过NF-κB依赖性自噬改善SAP模型的抗氧化和抗炎活性，从而改善SAP。
