PDF(Pubmed)
Abstract：
BACKGROUND: This study aims to explore whether Xuebijing (XBJ) can improve intestinal microcirculation dysfunction in sepsis and its mechanism.
METHODS: A rat model of sepsis was established by cecal ligation and puncture (CLP). A total of 30 male SD rats were divided into four groups: sham group, CLP group, XBJ + axitinib group, and XBJ group. XBJ was intraperitoneally injected 2 h before CLP. Hemodynamic data (blood pressure and heart rate) were recorded. The intestinal microcirculation data of the rats were analyzed via microcirculation imaging. Enzyme-linked immunosorbent assay (ELISA) kits were used to detect the serum levels of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α) in the rats. Histological analysis and transmission electron microscopy were used to analyze the injury of small intestinal microvascular endothelial cells and small intestinal mucosa in rats. The expression of vascular endothelial growth factor A (VEGF-A), phosphoinositide 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (Akt), and phosphorylated Akt (p-Akt) in the small intestine was analyzed via Western blotting.
RESULTS: XBJ improved intestinal microcirculation dysfunction in septic rats, alleviated the injury of small intestinal microvascular endothelial cells and small intestinal mucosa, and reduced the systemic inflammatory response. Moreover, XBJ upregulated the expression of VEGF-A, p-PI3K/total PI3K, and p-Akt/total Akt in the rat small intestine.
CONCLUSIONS: XBJ may improve intestinal microcirculation dysfunction in septic rats possibly through the VEGF-A/PI3K/Akt signaling pathway.
METHODS: A rat model of sepsis was established by cecal ligation and puncture (CLP). A total of 30 male SD rats were divided into four groups: sham group, CLP group, XBJ + axitinib group, and XBJ group. XBJ was intraperitoneally injected 2 h before CLP. Hemodynamic data (blood pressure and heart rate) were recorded. The intestinal microcirculation data of the rats were analyzed via microcirculation imaging. Enzyme-linked immunosorbent assay (ELISA) kits were used to detect the serum levels of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α) in the rats. Histological analysis and transmission electron microscopy were used to analyze the injury of small intestinal microvascular endothelial cells and small intestinal mucosa in rats. The expression of vascular endothelial growth factor A (VEGF-A), phosphoinositide 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (Akt), and phosphorylated Akt (p-Akt) in the small intestine was analyzed via Western blotting.
RESULTS: XBJ improved intestinal microcirculation dysfunction in septic rats, alleviated the injury of small intestinal microvascular endothelial cells and small intestinal mucosa, and reduced the systemic inflammatory response. Moreover, XBJ upregulated the expression of VEGF-A, p-PI3K/total PI3K, and p-Akt/total Akt in the rat small intestine.
CONCLUSIONS: XBJ may improve intestinal microcirculation dysfunction in septic rats possibly through the VEGF-A/PI3K/Akt signaling pathway.
摘要：
背景：本研究旨在探讨血必净（XBJ）是否能改善脓毒症肠微循环功能障碍及其机制。
方法：采用盲肠结扎穿孔法(CLP)建立脓毒症大鼠模型。将30只雄性SD大鼠分为4组:假手术组,CLP集团,XBJ+阿西替尼组，和XBJ组。CLP前2小时腹腔注射XBJ。记录血液动力学数据（血压和心率）。通过微循环成像分析大鼠的肠道微循环数据。酶联免疫吸附试验(ELISA)试剂盒检测血清白细胞介素-6(IL-6)水平,C反应蛋白(CRP),和大鼠肿瘤坏死因子-α（TNF-α）。采用组织学分析和透射电镜分析大鼠小肠微血管内皮细胞和小肠黏膜的损伤情况。血管内皮生长因子A(VEGF-A)的表达,磷酸肌醇3-激酶（PI3K），磷酸化PI3K（p-PI3K），蛋白激酶B（Akt），通过Western印迹分析小肠中磷酸化的Akt(p-Akt)。
结果：XBJ改善脓毒症大鼠肠道微循环功能障碍，减轻了小肠微血管内皮细胞和小肠粘膜的损伤，减少全身炎症反应。此外，XBJ上调VEGF-A的表达,p-PI3K/总PI3K,和大鼠小肠中的p-Akt/总Akt。
结论：XBJ可能通过VEGF-A/PI3K/Akt信号通路改善脓毒症大鼠肠道微循环功能障碍。
方法：采用盲肠结扎穿孔法(CLP)建立脓毒症大鼠模型。将30只雄性SD大鼠分为4组:假手术组,CLP集团,XBJ+阿西替尼组，和XBJ组。CLP前2小时腹腔注射XBJ。记录血液动力学数据（血压和心率）。通过微循环成像分析大鼠的肠道微循环数据。酶联免疫吸附试验(ELISA)试剂盒检测血清白细胞介素-6(IL-6)水平,C反应蛋白(CRP),和大鼠肿瘤坏死因子-α（TNF-α）。采用组织学分析和透射电镜分析大鼠小肠微血管内皮细胞和小肠黏膜的损伤情况。血管内皮生长因子A(VEGF-A)的表达,磷酸肌醇3-激酶（PI3K），磷酸化PI3K（p-PI3K），蛋白激酶B（Akt），通过Western印迹分析小肠中磷酸化的Akt(p-Akt)。
结果：XBJ改善脓毒症大鼠肠道微循环功能障碍，减轻了小肠微血管内皮细胞和小肠粘膜的损伤，减少全身炎症反应。此外，XBJ上调VEGF-A的表达,p-PI3K/总PI3K,和大鼠小肠中的p-Akt/总Akt。
结论：XBJ可能通过VEGF-A/PI3K/Akt信号通路改善脓毒症大鼠肠道微循环功能障碍。
