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Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell

机译:大承气汤通过调节胰腺腺泡细胞坏死-凋亡开关的作用改善实验性急性胰腺炎

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摘要

Severity of acute pancreatitis contributes to the modality of cell death. Pervious studies have demonstrated that the herb medicine formula “Dachengqi Decoction” (DCQD) could ameliorate the severity of acute pancreatitis. However, the biological mechanisms governing its action of most remain unclear. The role of apoptosis/necrosis switch within acute pancreatitis has attracted much interest, because the induction of apoptosis within injured cells might suppress inflammation and ameliorate the disease. In this study, we used cerulein (10−8 M)-stimulated AR42J cells as an in vitro model of acute pancreatitis and retrograde perfusion into the biliopancreatic duct of 3.5% sodium taurocholate as an in vivo rat model. After the treatment of DCQD, cell viability, levels of apoptosis and necrosis, reactive oxygen species positive cells, serum amylase, concentration of nitric oxide and inducible nitric oxide syntheses, pancreatic tissue pathological score and inflammatory cell infiltration were tested. Pretreatment with DCQD increased cell viability, induced apoptosis, decreased necrosis and reduced the severity of pancreatitis tissue. Moreover, treatment with DCQD reduced the generation of reactive oxygen species in AR42J cells but increased the concentration of nitric oxide of pancreatitis tissues. Therefore, the regulation of apoptosis/necrosis switch by DCQD might contribute to ameliorating the pancreatic inflammation and pathological damage. Further, the different effect on reactive oxygen species and nitric oxide may play an important role in DCQD-regulated apoptosis/necrosis switch in acute pancreatitis.
机译:急性胰腺炎的严重程度有助于细胞死亡。以往的研究表明,草药配方“大成奇汤”(DCQD)可以减轻急性胰腺炎的严重程度。但是,控制其大多数作用的生物学机制仍不清楚。凋亡/坏死转换在急性胰腺炎中的作用引起了人们的极大兴趣,因为在受损细胞中诱导凋亡可能会抑制炎症并改善疾病。在这项研究中,我们使用铜蓝蛋白(10 −8 M)刺激的AR42J细胞作为急性胰腺炎的体外模型,并将3.5%牛磺胆酸钠钠逆行灌注到胆胰管中作为体内大鼠模型。 DCQD处理后,检测细胞活力,凋亡和坏死水平,活性氧阳性细胞,血清淀粉酶,一氧化氮浓度和诱导型一氧化氮合成,胰腺组织病理学评分和炎性细胞浸润。 DCQD预处理可提高细胞活力,诱导细胞凋亡,减少坏死并降低胰腺炎组织的严重程度。此外,用DCQD的治疗减少了AR42J细胞中活性氧的产生,但增加了胰腺炎组织中一氧化氮的浓度。因此,DCQD对细胞凋亡/坏死开关的调节可能有助于减轻胰腺炎症和病理损害。此外,对活性氧和一氧化氮的不同作用可能在DCQD调节的急性胰腺炎细胞凋亡/坏死转换中起重要作用。

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