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首页> 外文期刊>Life sciences >Aqueous extract of black tea (Camellia sinensis) prevents ethanol+cholecystokinin-induced pancreatitis in a rat model.
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Aqueous extract of black tea (Camellia sinensis) prevents ethanol+cholecystokinin-induced pancreatitis in a rat model.

机译：红茶（茶花）的水提取物可预防乙醇+胆囊收缩素诱发的大鼠胰腺炎。

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摘要

Black Tea Extract (BTE), a phytocompound has been attributed with a plethora of health-promoting actions. We have previously demonstrated that BTE inhibits chronic hepatitis in a rat model induced with high-fat and ethanol (EtOH). This study reports that BTE prevents altered pancreatic acinar cell functions, oxidative stress, inflammatory changes and DNA damage in the EtOH+cholecystokinin (CCK)-induced model of pancreatitis. The EtOH+CCK model rats were administered with BTE, and were examined the activity of pancreatic digestive enzymes (amylase and lipase), proinflammatory cytokines (IL-6 and TNF-alpha), oxidative and antioxidative enzymes (nitric oxide, NO; malondialdehyde, MDA; superoxide dismutase, SOD; catalase, CAT), antioxidant level (glutathione, GSH), histopathological changes and the integrity of genomic DNA. Results show that because of chronic EtOH treatment, serum level of amylase and lipase (two biomarkers for pancreatitis) and pancreatic levels of MDA and NO (two biomarkers of oxidativestress) increased significantly, which could be effectively blunted by BTE. BTE could normalize EtOH+CCK-induced suppressed activities of SOD and CAT, and GSH content of pancreatic tissue. Also, histopathological and inflammatory changes during EtOH+CCK-induced pancreatitis could be blunted by BTE. Furthermore, BTE could effectively reduce EtOH+CCK-induced increase in DNA fragmentation and damage. These findings suggest that BTE prevents pancreatitis caused by chronic EtOH+CCK toxicity presumably by enhancing antioxidant, anti-inflammatory and antiapoptotic activity in rats.
机译：红茶提取物（BTE）是一种植物化合物，被认为具有多种促进健康的作用。先前我们已经证明BTE在高脂和乙醇（EtOH）诱导的大鼠模型中抑制慢性肝炎。这项研究报告说，在EtOH +胆囊收缩素（CCK）诱发的胰腺炎模型中，BTE可以防止胰腺腺泡细胞功能改变，氧化应激，炎症变化和DNA损伤。给予EtOH + CCK模型大鼠BTE，并检查其胰消化酶（淀粉酶和脂肪酶），促炎细胞因子（IL-6和TNF-α），氧化酶和抗氧化酶（一氧化氮，NO;丙二醛， MDA;超氧化物歧化酶，SOD;过氧化氢酶，CAT），抗氧化剂水平（谷胱甘肽，GSH），组织病理学变化和基因组DNA的完整性。结果表明，由于长期接受EtOH治疗，血清淀粉酶和脂肪酶（胰腺炎的两个生物标志物）的血清水平以及胰腺中MDA和NO（氧化应激的两个生物标志物）的水平显着增加，这可能被BTE有效地抑制了。 BTE可以使EtOH + CCK抑制的SOD和CAT活性以及胰腺组织GSH含量正常化。此外，BTE可能会抑制EtOH + CCK诱发的胰腺炎期间的组织病理学和炎症变化。此外，BTE可以有效减少EtOH + CCK诱导的DNA片段化和损伤增加。这些发现表明，BTE可能通过增强大鼠的抗氧化，抗炎和抗凋亡活性来预防由EtOH + CCK慢性毒性引起的胰腺炎。

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