Yang Tie-Cheng, Zhang Shu-Wen, Sun Li-Na, Wang Hong, Ren Ai-Min
Intensive Care Unit and Medical Department of Infection, Beijing Friendship Hospital, Capital Medical University, No. 95, Yong An Road, Beijing 100050, China.
World J Gastroenterol. 2008 Dec 28;14(48):7353-60. doi: 10.3748/wjg.14.7353.
To investigate the protective effects of magnolol on sepsis-induced inflammation and intestinal dysmotility.
Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide (LPS). Male Wistar rats were randomly assigned to one of three treatment groups: magnolol prior to LPS injection (LPS/Mag group); vehicle prior to LPS injection (LPS/Veh group); vehicle prior to injection of saline (Control/Veh). Intestinal transit and circular muscle mechanical activity were assessed 12 h after LPS injection. Tumor necrosis factor-alpha (TNF-alpha), interleukin-10 (IL-10), monocyte chemoattractant protein-1 (MCP-1) and inducible nitric oxide synthase (iNOS) mRNA in rat ileum were studied by RT-PCR 2 h after LPS injection. Nuclear factor-kappaB (NF-kappaB) activity in the intestine was also investigated at this time using electrophoretic mobility shift assay. In addition, antioxidant activity was determined by measuring malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity in the intestine 2 h after LPS injection.
Magnolol significantly increased intestinal transit and circular muscle mechanical activity in LPS-treated animals. TNF-alpha, MCP-1 and iNOS mRNA expression in the small intestine were significantly reduced after magnolol treatment in LPS-induced septic animals, compared with untreated septic animals. Additionally, magnolol significantly increased IL-10 mRNA expression in septic rat ileum. Magnolol also significantly suppressed NF-kappaB activity in septic rat intestine. In addition, magnolol significantly decreased MDA concentration and increased SOD activity in rat ileum.
Magnolol prevents sepsis-induced suppression of intestinal motility in rats. The potential mechanism of this benefit of magnolol appears to be modulation of self-amplified inflammatory events and block of oxidative stress in the intestine.
研究厚朴酚对脓毒症诱导的炎症反应及肠道运动障碍的保护作用。
通过单次腹腔注射脂多糖（LPS）诱导脓毒症。雄性Wistar大鼠随机分为三个治疗组之一：LPS注射前给予厚朴酚（LPS/厚朴酚组）；LPS注射前给予赋形剂（LPS/赋形剂组）；注射生理盐水前给予赋形剂（对照/赋形剂组）。在LPS注射后12小时评估肠道转运和环行肌机械活性。在LPS注射后2小时，通过逆转录聚合酶链反应（RT-PCR）研究大鼠回肠中肿瘤坏死因子-α（TNF-α）、白细胞介素-10（IL-10）、单核细胞趋化蛋白-1（MCP-1）和诱导型一氧化氮合酶（iNOS）mRNA的表达。此时还使用电泳迁移率变动分析研究肠道中核因子-κB（NF-κB）的活性。此外，在LPS注射后2小时，通过测量肠道中丙二醛（MDA）浓度和超氧化物歧化酶（SOD）活性来测定抗氧化活性。
厚朴酚显著增加了LPS处理动物的肠道转运和环行肌机械活性。与未处理的脓毒症动物相比，厚朴酚处理后，LPS诱导的脓毒症动物小肠中TNF-α、MCP-1和iNOS mRNA表达显著降低。此外，厚朴酚显著增加了脓毒症大鼠回肠中IL-10 mRNA的表达。厚朴酚还显著抑制了脓毒症大鼠肠道中NF-κB的活性。此外，厚朴酚显著降低了大鼠回肠中MDA浓度并增加了SOD活性。
厚朴酚可预防脓毒症诱导的大鼠肠道运动抑制。厚朴酚这种有益作用的潜在机制似乎是调节肠道中自我放大的炎症事件并阻断氧化应激。
