Biol. Pharm. Bull. 30(6) 1091—1096 (2007)

ease, whose clinical features are intractable pain, loss of pancreatic exocrine and endocrine function. Fibrosis and loss of parenchymal cells in the pancreas are characteristic histopathologic features in chronic pancreatitis. Moreover, pancreatic fibrosis is suggested to contribute to the irreversibility of the disease. Therefore, to search for an available medicine against pancreatic fibrosis is urgently needed. The pathogenesis of chronic pancreatitis is not clear yet. Recent data demonstrate that pancreatic stellate cells (PSCs) play a major role in pancreatic fibrosis. PSCs, in their quiescent state, can be identified by the presence of vitamin A containing lipid droplets in their cytoplasm. After pancreas injury, they are activated and transform into myofibroblastlike cells which exhibit positive staining for the cytoskeletal protein a-smooth muscle actin (a-SMA), and synthesise and secrete increased amounts of extracellular matrix (ECM). TGF-b1 is a major mediator of fibrosis in pancreatic fibrosis. Increased evidences demonstrated that the expression of TGF-b1 was up-regulated in the fibrotic areas of the pancreas in human and animal with chronic pancreatitis, whereas with little expression in normal pancreas. Vogelmann R. et al. observed that overexpressed TGF-b1 developed pancreatic fibrosis in transgenic mice. Moreover, inhibition of TGFb1 by anti-TGF-b1 antibody suppressed ECM production in pancreas. Furthermore, TGF-b1 is important to regulate PSCs functions. For instance, TGF-b1 activates PSCs, inhibits PSC growth and enhances ECM production and secretion. As we know, tea is one of the most frequently consumed beverages in the world, next to water. Epigallocatechin gallate (EGCG) (Fig. 1) is the major constituent found in green tea polyphenols (GTP). EGCG is responsible for the majority of the potential health benefits attributed to green tea consumption. Over the past decade, a vast body of scientific research discovered that EGCG had a wide range of biologic activities, including hypolipidemic, anti-microbial, antitumour activities and anti-oxidative stress. Recent studies suggested that EGCG also had anti-inflammatory and anti-fibrosis effects and substantial evidence had shown the role of EGCG in hepatic fibrosis, including inhibiting activation and proliferation of hepatic stellate cells, interrupting TGF-b signaling and suppressing collagen production and collagenase activity. And as we known, the pathogenesis of pancreatic fibrosis is similar to that of hepatic fibrosis, so scholars have set about to investigate the effect of EGCG in pancreatitis. Recent investigations reported that GTP had a protective effect on the pathogenesis of acute pancreatitis. Furthermore, EGCG could inhibit activation and impede proliferation and migration of PSCs in vitro. But the correlative research literature in vivo has not been presented. Oxidative stress was reported to be involved in pancreatic fibrosis. Our previous report also confirmed this viewpoint. From this viewpoint, Matsumura N. et al. succeeded in inducing pancreatic fibrosis in rat using a superoxide dismutase inhibitor, diethyldithiocarbamate (DDC). This model is easy to handle, and it needn’t require long-term duration for the development of pancreatic fibrosis. The aim of the present study was to evaluate effects of EGCG on DDCinduced pancreatic fibrosis in rats.