慢性胰腺炎 (CP) 是一种与组织学改变相关的胰腺炎性疾病，包括纤维化、腺泡细胞丧失和免疫细胞浸润，并导致胰腺损伤，进而导致疼痛、体重减轻和胰腺功能丧失。儿茶素或儿茶素水合物 (CH) 具有抗氧化、抗癌和免疫调节作用。然而，与其他儿茶素不同，儿茶素水合物 (+)‑CH 在许多疾病中，包括 CP，其抗纤维化作用尚未得到广泛研究。因此，本研究评估了 (+)‑CH 对 CP 的抗纤维化效果。为了评估 CH 的预防效果，先给予 (+)‑CH (1、5 或 10 mg/kg) 或乙醇于首次注射 cerulein (50 µg/kg) 前 1 小时。为了评估治疗效果，(+)-CH (5 mg/kg) 或乙醇在 cerulein 注射后的一至两周内给予。在这两种方法中，每隔一个小时将 cerulein 腹腔注射给予小鼠，每天六次，每周四次，共三周，以诱导 CP。数据显示，(+)‑CH 显著抑制了 CP 过程中的腺体破坏和炎症。此外，(+)‑CH 阻止了胰腺星状细胞 (PSC) 的活化以及基质成分的产生，如纤维连接蛋白 1 和胶原蛋白，这表明它可能作为一种新的治疗药物。此外，还在离体 PSCs 中研究了 (+)‑CH 对胰腺纤维化的机制和有效性。(+)-CH 抑制了通过转化生长因子‑β(TGF‑β)或血小板源生长因子作用的 Smad2 激活和纤维化因子。这些发现表明，(+)‑CH 通过失活 TGF‑β/Smad2 信号传导，在 cerulein 诱导的 CP 中表现出抗纤维化作用。

Chronic pancreatitis (CP) is a pancreatic inflammatory disease associated with histological changes, including fibrosis, acinar cell loss and immune cell infiltration, and leads to damage of the pancreas, which results in pain, weight loss and loss of pancreas function. Catechin or catechin hydrate (CH) has antioxidant, anticancer and immune‑regulatory effects. However, unlike other catechins, the antifibrotic effects of (+)‑CH have not been widely studied in many diseases, including CP. Therefore, the anti‑fibrotic effects of (+)‑CH against CP were evaluated in the present study. To assess the prophylactic effects of CH, (+)‑CH (1, 5 or 10 mg/kg) or ethanol was administered 1 h before first cerulein (50 µg/kg) injection. To assess the therapeutic effects, (+)‑CH (5 mg/kg) or ethanol was administered after cerulein injection for one or two weeks. In both methods, cerulein was injected intraperitoneally into mice once every hour, six times a day, four times a week, for a total of three weeks, to induce CP. The data showed that (+)‑CH markedly inhibited glandular destruction and inflammation during CP. Moreover, (+)‑CH prevented pancreatic stellate cell (PSC) activation and the production of extracellular matrix components, such as fibronectin 1 and collagens, which suggested that it may act as a novel therapeutic agent. Furthermore, the mechanism and effectiveness of (+)‑CH on pancreatic fibrosis were investigated in isolated PSCs. (+)‑CH suppressed the activation of Smad2 and fibrosis factors that act through transforming growth factor‑β (TGF‑β) or platelet‑derived growth factor. These findings suggest that (+)‑CH exhibits antifibrotic effects in cerulein‑induced CP by inactivating TGF‑β/Smad2 signaling.