Qingyi decoction attenuates severe acute pancreatitis in rats via inhibition of inflammation and protection of the intestinal barrier

被引:44
作者
Su, Song [1 ]
Liang, Tiancheng [2 ]
Zhou, Xiang [1 ]
He, Kai [1 ]
Li, Bo [1 ]
Xia, Xianming [1 ]
机构
[1] Southwest Med Univ, Affiliated Hosp, Dept Hepatobiliary Surg, 25 Taiping St, Luzhou 646000, Sichuan, Peoples R China
[2] Luzhou Tradit Chinese Med Hosp, Dept Surg 1, Luzhou, Sichuan, Peoples R China
关键词
Severe acute pancreatitis; Qingyi decoction; TLR4; NF-kappa B pathway; ZO-1; rat model; sodium taurocholate; PERMEABILITY; EXPRESSION; PROTEIN; GUT;
D O I
10.1177/0300060518809289
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Objective Qingyi decoction (QYD) has beneficial effects in severe acute pancreatitis (SAP). We assessed the therapeutic effect and mechanisms of QYD in SAP. Methods A rat model of SAP was induced by pancreatic ductal injection of sodium taurocholate. QYD was administered intragastrically immediately postoperatively and once every 12 hours. Serum amylase, endotoxin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and D-lactate levels were measured at 12, 24, and 48 hours. Histological changes in the pancreas and ileum were analyzed. Expression of nuclear factor kappa-light-chain-enhancer of activated B cells p65 (NF-kappa B p65), Toll-like receptor 4 (TLR4), and zonula occludens-1 (ZO-1) in the small intestinal mucosa was also assessed. Results Pancreatic tissue showed extracellular space expansion, inflammatory infiltration, vessels with necrotic walls, and hemorrhage. Ileal tissue showed hemorrhage, inflammatory infiltration, and ileal mucosa destruction. These histological features were dramatically improved by QYD. Increased serum levels of amylase, endotoxin, TNF-alpha, IL-6, and D-lactic acid were significantly decreased by QYD administration. Increased expression of NF-kappa B p65 and TLR4 and decreased expression of ZO-1 in the ileal mucosa were also restored to normal levels by QYD treatment. Conclusion QYD alleviates SAP by reducing intestinal barrier dysfunction, inhibiting intestinal bacteria and endotoxin translocation, and preventing NF-kappa B activation.
引用
收藏
页码:2215 / 2227
页数:13
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