Shirahige Akinori, Mizushima Takaaki, Matsushita Koki, Sawa Kiminari, Ochi Koji, Ichimura Mitsuko, Tanioka Hiroaki, Shinji Toshiyuki, Koide Norio, Tanimoto Mitsune
Laboratory of Medicine, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
J Gastroenterol Hepatol. 2008 Feb;23(2):321-7. doi: 10.1111/j.1440-1746.2007.05127.x. Epub 2007 Aug 30.
The mechanism of pancreatic fibrosis is unclear. Taurine is used in the clinical treatment of a wide variety of diseases, but its effect on improving pancreatic fibrosis is unknown. We examined whether a diet with added taurine improves pancreatic fibrosis induced by dibutyltin dichloride (DBTC) in an experimental chronic pancreatitis rat model. In addition, we examined the influence of taurine on pancreatic stellate cells.
Pancreatic fibrosis was induced by DBTC. Rats were fed a taurine-containing diet or a normal diet and were killed at 4 weeks. Pancreatic stellate cells were isolated from male Wistar rats. Cultured pancreatic stellate cells were incubated with or without taurine chloramine. Type I collagen and transforming growth factor-beta1 secretion was evaluated by ELISA, and matrix metalloproteinase activity was assessed by gelatin zymography. Interleukin-6, interleukin-2, and transforming growth factor-beta1 levels in the supernatants of pancreatic tissue homogenates were measured.
Pancreatic fibrosis induced by DBTC was improved remarkably by the oral administration of the taurine-containing diet. Taurine chloramine decreased type I collagen, transforming growth factor-beta1, and matrix metalloproteinases 2 of the pancreatic stellate cell culture supernatant. Increased interleukin-6 and decreased interleukin-2 were found in the supernatants of the pancreatic tissue homogenates of DBTC-induced pancreatitis rats compared with other groups.
The oral administration of taurine improves pancreatic fibrosis. Taurine chloramine inhibits transforming growth factor-beta1 produced from activated pancreatic stellate cells and improves pancreatic fibrosis.
胰腺纤维化的机制尚不清楚。牛磺酸被用于多种疾病的临床治疗，但其对改善胰腺纤维化的作用尚不清楚。我们研究了在实验性慢性胰腺炎大鼠模型中，添加牛磺酸的饮食是否能改善二氯化二丁基锡（DBTC）诱导的胰腺纤维化。此外，我们还研究了牛磺酸对胰腺星状细胞的影响。
用DBTC诱导胰腺纤维化。给大鼠喂食含牛磺酸的饮食或正常饮食，并在4周后处死。从雄性Wistar大鼠中分离胰腺星状细胞。将培养的胰腺星状细胞与牛磺氯胺一起孵育或不孵育。通过ELISA评估I型胶原蛋白和转化生长因子-β1的分泌，并通过明胶酶谱法评估基质金属蛋白酶活性。测量胰腺组织匀浆上清液中的白细胞介素-6、白细胞介素-2和转化生长因子-β1水平。
口服含牛磺酸的饮食可显著改善DBTC诱导的胰腺纤维化。牛磺氯胺降低了胰腺星状细胞培养上清液中的I型胶原蛋白、转化生长因子-β1和基质金属蛋白酶2。与其他组相比，DBTC诱导的胰腺炎大鼠胰腺组织匀浆上清液中白细胞介素-增加，白细胞介素-2降低。
口服牛磺酸可改善胰腺纤维化。牛磺氯胺抑制活化的胰腺星状细胞产生的转化生长因子-β1，改善胰腺纤维化。
