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

被引:27
作者
Wang, Jia [1 ]
Chen, Guangyuan [1 ]
Gong, Hanlin [1 ]
Huang, Wei [2 ]
Long, Dan [3 ]
Tang, Wenfu [1 ]
机构
[1] Sichuan Univ, Dept Integrated Tradit Chinese & Western Med, W China Hosp, Chengdu 610064, Peoples R China
[2] Univ Liverpool, Physiol Lab, Liverpool L69 3BX, Merseyside, England
[3] Sichuan Univ, Dept Lab Transplant Engn & Immunol, W China Hosp, Chengdu 610064, Peoples R China
关键词
CHENG-QI DECOCTION; NITRIC-OXIDE; NECROTIZING PANCREATITIS; INFLAMMATORY RESPONSE; OXIDATIVE STRESS; DEATH; RATS; CYTOKINES; SEVERITY; RADICALS;
D O I
10.1371/journal.pone.0040160
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
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.
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页数:7
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