Su Shi-Bing, Motoo Yoshiharu, Xie Min-Jue, Mouri Hisatsugu, Asayama Kohtaro, Sawabu Norio
Department of Internal Medicine and Medical Oncology, Cancer Research Institute, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-0934, Japan.
Pancreas. 2002 Mar;24(2):146-52. doi: 10.1097/00006676-200203000-00005.
Free radicals and their scavengers are supposed to be involved in pancreatitis.
To investigate the expression of superoxide dismutase (SOD) in rat pancreatic acinar cell injury.
As an in vivo model, male WBN/Kob rats were used. Chronic pancreatitis developed spontaneously at 12 weeks in this model and progressed thereafter, but acinar regeneration was recognized at 20 weeks. By semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR), manganese SOD (MnSOD) mRNA expression peaked at 8 and 20 weeks, whereas copper/zinc SOD (CuZnSOD) mRNA expression peaked at 12 and 20 weeks. Immunohistochemistry confirmed the localization of SOD in acinar cells. Acinar cell apoptosis peaked at 12 and 20 weeks. In an in vitro study, MnSOD mRNA expression peaked at 2 hours after the addition of arginine to culture medium, whereas apoptosis was increased at 24 hours.
Thus, the induction of SOD around the onset and at the late stage of chronic pancreatitis in the WBN/Kob rats implies pancreatic ischemia and acinar remodeling, respectively. From the in vitro results, MnSOD expression might reflect a defensive mechanism of acinar cells against oxidative stress or pro-apoptotic stimuli.
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