姜黄素抑制幽门螺杆菌感染大鼠胃 NF-κB 激活和大分子渗漏。
Curcumin suppresses gastric NF-kappaB activation and macromolecular leakage in Helicobacter pylori-infected rats.
机构信息
Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
出版信息
World J Gastroenterol. 2010 Aug 28;16(32):4039-46. doi: 10.3748/wjg.v16.i32.4039.
AIM
To investigate whether curcumin could attenuate nuclear factor (NF)-kappaB p65 expression and macromolecular leakage in the gastric mucosa of Helicobacter pylori (H. pylori)-infected rats.
METHODS
Twenty-five male Sprague-Dawley rats were equally divided into five groups: control rats (Control), control rats supplemented with 600 mg/kg curcumin, H. pylori-infected rats (Hp), H. pylori-infected rats supplemented with 200 mg/kg curcumin (Hp + curI), and H. pylori-infected rats supplemented with 600 mg/kg curcumin (Hp + curII). In H. pylori-infected groups, rats were inoculated with H. pylori suspension twice a day at an interval of 4 h for 3 d. Two weeks later, 200 or 600 mg/kg curcumin was given once daily to curcumin-supplemented groups for 7 d. On the day of the experiment, macromolecular leakage in gastric mucosa was examined by intravital fluorescence microscopy. The stomach tissue was removed to examine NF-kappaB p65 expression in gastric epithelial cells by immunohistochemistry.
RESULTS
The expression of NF-kappaB p65 in gastric epithelial cells and the macromolecular leakage from gastric mucosal microcirculation significantly increased in the Hp group compared with the Control group. The percentages of NF-kappaB p65 immunoreactive cells in Control and Hp groups were 10.72% +/- 2.10% vs 16.02% +/- 2.98%, P = 0.004, respectively. The percentages of macromolecular leakage in Control and Hp groups were 10.69% +/- 1.43% vs 15.41% +/- 2.83%, P = 0.001, respectively. Curcumin supplementation in Hp + curI and Hp + curII groups significantly decreased NF-kappaB p65 immunoreactive cells and macromolecular leakage compared with results in the Hp group. The percentages of NF-kappaB p65 immunoreactive cells in Hp + curI and Hp + curII groups were 11.79% +/- 2.13% (P = 0.017) and 11.42% +/- 1.68% (P = 0.010), respectively. The percentages of macromolecular leakage in Hp + curI and Hp + curII groups were 12.32% +/- 2.13% (P = 0.025) and 12.14% +/- 1.86% (P = 0.018), respectively.
CONCLUSION
H. pylori-induced gastric inflammation in rats is associated with increased NF-kappaB activation and macromolecular leakage which can be reduced by curcumin supplementation.
目的
研究姜黄素是否可以减弱幽门螺杆菌（H. pylori）感染大鼠胃黏膜核因子（NF）-κB p65 的表达和大分子渗漏。
方法
25 只雄性 Sprague-Dawley 大鼠等分为 5 组：对照组（Control）、对照组给予 600mg/kg 姜黄素（Control+curI）、H. pylori 感染组（Hp）、H. pylori 感染组给予 200mg/kg 姜黄素（Hp+curI）、H. pylori 感染组给予 600mg/kg 姜黄素（Hp+curII）。在 H. pylori 感染组，大鼠每天间隔 4 小时分两次接种 H. pylori 混悬液，共 3 天。2 周后，姜黄素补充组每天给予 200 或 600mg/kg 姜黄素，共 7 天。实验当天，通过活体荧光显微镜检查胃黏膜大分子渗漏。通过免疫组织化学检查胃上皮细胞中 NF-κB p65 的表达。
结果
与对照组相比，H. pylori 感染组胃上皮细胞 NF-κB p65 的表达和胃黏膜微循环中的大分子渗漏明显增加。Control 组和 Hp 组 NF-κB p65 免疫反应细胞的百分比分别为 10.72%±2.10%和 16.02%±2.98%，P=0.004。Control 组和 Hp 组大分子渗漏的百分比分别为 10.69%±1.43%和 15.41%±2.83%，P=0.001。与 Hp 组相比，Hp+curI 和 Hp+curII 组的姜黄素补充显著降低了 NF-κB p65 免疫反应细胞和大分子渗漏。Hp+curI 和 Hp+curII 组 NF-κB p65 免疫反应细胞的百分比分别为 11.79%±2.13%（P=0.017）和 11.42%±1.68%（P=0.010）。Hp+curI 和 Hp+curII 组大分子渗漏的百分比分别为 12.32%±2.13%（P=0.025）和 12.14%±1.86%（P=0.018）。
结论
H. pylori 诱导的大鼠胃炎症与 NF-κB 激活和大分子渗漏增加有关，姜黄素补充可减少这种增加。
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