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

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...

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Autores principales: Wang, Jia, Chen, Guangyuan, Gong, Hanlin, Huang, Wei, Long, Dan, Tang, Wenfu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388070/
https://www.ncbi.nlm.nih.gov/pubmed/22768339
http://dx.doi.org/10.1371/journal.pone.0040160
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author Wang, Jia
Chen, Guangyuan
Gong, Hanlin
Huang, Wei
Long, Dan
Tang, Wenfu
author_facet Wang, Jia
Chen, Guangyuan
Gong, Hanlin
Huang, Wei
Long, Dan
Tang, Wenfu
author_sort Wang, Jia
collection PubMed
description 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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spelling pubmed-33880702012-07-05 Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell Wang, Jia Chen, Guangyuan Gong, Hanlin Huang, Wei Long, Dan Tang, Wenfu PLoS One Research Article 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. Public Library of Science 2012-07-02 /pmc/articles/PMC3388070/ /pubmed/22768339 http://dx.doi.org/10.1371/journal.pone.0040160 Text en Wang et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Wang, Jia
Chen, Guangyuan
Gong, Hanlin
Huang, Wei
Long, Dan
Tang, Wenfu
Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell
title Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell
title_full Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell
title_fullStr Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell
title_full_unstemmed Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell
title_short Amelioration of Experimental Acute Pancreatitis with Dachengqi Decoction via Regulation of Necrosis-Apoptosis Switch in the Pancreatic Acinar Cell
title_sort amelioration of experimental acute pancreatitis with dachengqi decoction via regulation of necrosis-apoptosis switch in the pancreatic acinar cell
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388070/
https://www.ncbi.nlm.nih.gov/pubmed/22768339
http://dx.doi.org/10.1371/journal.pone.0040160
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