Dept. of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking Univ., 38 Xueyuan Road, Beijing 100191, People's Republic of China.
Am J Physiol Gastrointest Liver Physiol. 2014 Jan;306(2):G111-22. doi: 10.1152/ajpgi.00123.2013. Epub 2013 Nov 14.
Intestinal ischemia and reperfusion (I/R) is a clinical problem occurred for diverse causes with high mortality. Prophylaxis and treatment of intestinal I/R remains a challenge for clinicians. The purpose of the present study was to explore the role of Notoginsenoside R1 (R1), a major component form of Panax notoginseng, in management of intestinal I/R injury. Intestinal I/R was induced in male Sprague-Dawley rats by clamping the superior mesenteric artery for 90 min followed by reperfusion for 60 min or 3 days. R1 (10 mg·kg(-1)·h(-1)) was administered either 20 min before ischemia or 20 min after reperfusion. Intestinal microcirculation was evaluated by intravital microscopy over 60 min reperfusion. Sixty minutes or 3 days after reperfusion, rats were killed for histological examination of the jejunum tissue and immunohistochemical localization of myeloperoxidase and CD68. ATP, ADP, and AMP content in jejunum tissue was assessed by ELISA. Activation of nuclear factor-κB (NF-κB) and expression of ATP5D and tight junction proteins were determined by Western blotting. The results demonstrated that R1 is capable of attenuating intestinal I/R-induced microvascular hyperpermeability, inflammatory cytokine production, NF-κB activation, and loss of tight junction proteins, as well as improving energy metabolism during I/R. The results of the present study suggest R1 as an option in protecting against intestinal I/R injury.
肠缺血再灌注(I/R)是由多种原因引起的临床问题,死亡率较高。预防和治疗肠 I/R 仍然是临床医生面临的挑战。本研究的目的是探讨三七总皂苷 R1(R1)在肠 I/R 损伤治疗中的作用。通过夹闭肠系膜上动脉 90 min 后再灌注 60 min 或 3 天,在雄性 Sprague-Dawley 大鼠中诱导肠 I/R。R1(10 mg·kg(-1)·h(-1))在缺血前 20 min 或再灌注后 20 min 给药。在再灌注 60 min 期间通过活体显微镜评估肠微循环。再灌注 60 min 或 3 天后,处死大鼠以评估空肠组织的组织学检查和髓过氧化物酶和 CD68 的免疫组织化学定位。通过 ELISA 评估空肠组织中 ATP、ADP 和 AMP 的含量。通过 Western 印迹测定核因子-κB(NF-κB)的激活和 ATP5D 及紧密连接蛋白的表达。结果表明,R1 能够减轻肠 I/R 引起的微血管通透性增加、炎症细胞因子产生、NF-κB 激活和紧密连接蛋白丢失,以及改善 I/R 期间的能量代谢。本研究的结果表明 R1 是一种预防肠 I/R 损伤的选择。