Ascitic fluid and serum from rats with acute pancreatitis injure rat pancreatic tissues and alter the expression of heat shock protein 60 |
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Authors: | Yong-Yu Li Xue-Jin Li Shuai Lv Kun Li Yan-Na Li Zhi-Rong Gao Jia-Yan Feng Chang-Jie Chen Claus Schaefer |
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Institution: | (1) Institute of Digestive Disease, Department of Pathophysiology, School of Medicine, Tongji University, 1239 Si Ping Road, Shanghai, 200092, China;(2) Department of Internal Medicine II, Klinikum Grosshadern, Ludwig Maximilian University, Munich, Germany |
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Abstract: | Acute pancreatitis (AP) is an inflammatory process in which cytokines and chemokines are involved. After onset, extrapancreatic
stimuli can induce the expression of cytokines in pancreatic acinar cells, thereby amplifying this inflammatory loop. To further
determine the role and mechanism of irritating agents in the pathogenesis of AP, rat pancreatic tissues were stimulated with
ascitic fluid (APa) and serum (APs) from rats with AP or with lipopolysaccharide (LPS). In addition, the alteration of heat
shock protein 60 (HSP60) expression was evaluated. Rat pancreas was removed and meticulously snipped to fragments. The snips
were cultured for up to 48 h. During this period, the tissue viability as well as amylase and TNF-α levels in the supernatant
and the HSP60 expression in the pancreatic tissue before and after stimulation by APa, APs, and LPS were assayed time-dependently.
At different time-points during the culture, the viability and the amylase activity in the pancreatic tissue remained largely
stable. After stimulation with APa, APs, or LPS for 1 h, the pancreatic tissues showed some damage, and this was followed
by a sharp decrease in the viability accompanied by increased levels of amylase and TNF-α in the culture medium 2 or 4 h after
stimulation (p < 0.05). In contrast, both the HSP60 mRNA and protein levels had a relatively high expression in the freshly prepared tissue
fragments (0 h). As the culturing period was extended, the expression of HSP60 mRNA decreased only slightly; at the same time,
the HSP60 protein levels decreased over a prolonged culture time, significantly so from 12 through 48 h (p < 0.05). After stimulation with APs, APa, or LPS, both the expression of HSP60 mRNA and protein in the tissue fragments increased
slightly at 1 h and decreased significantly thereafter at 2 and 4 h (p < 0.05). APa, APs, or LPS induce injuries on isolated pancreatic tissues, accompanied by an altered HSP60 expression pattern
in a time-dependent manner. |
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Keywords: | Acute pancreatitis Pancreatic tissue fragments Heat shock protein 60 |
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