PDF(Pubmed)
Abstract：
UNASSIGNED: Intestinal ischemia-reperfusion injury (i-IRI) involves a blood flow interruption in an intestinal segment followed by blood flow restoration. When blood flow is restored, oxidative and inflammatory molecules are distributed throughout the bloodstream, triggering both local and systemic damage. Our goal was to evaluate the potential of three antioxidant and/or anti-inflammatory compounds (curcumin, dexmedetomidine and α-tocopherol) to prevent or reverse local and systemic damage induced by i-IRI.
UNASSIGNED: i-IRI was induced by placing a microvascular clip in the superior mesenteric artery of female WAG/RijHsd rats; the clip was removed after 1h and reperfusion was allowed for 4h. Curcumin (200 mg/kg, orally), α-tocopherol (20 mg/kg, i.p.), and dexmedetomidine (5 or 20 µg/kg, s.c.; DEX5 and DEX20, respectively) were administered. Blood and terminal ileum specimens were collected for biochemical and histological determination. Furthermore, D-xylose absorption test was performed to evaluate intestinal absorption; after completing the 1-hour ischemia and 4-hour reperfusion period, 1 mL of aqueous D-xylose solution (0.615 mg/mL) was administered orally, and one hour later, plasma D-xylose levels were quantified.
UNASSIGNED: The histological injury degree (HID) measured by the Chiu scale was significantly reduced when the treatments were applied (non-treated rats, 2.6 ± 0.75; curcumin, 1.54 ± 0.8; DEX5, 1.47 ± 0.7; DEX20 1.14 ± 0.5; and α-tocopherol, 1.01 ± 0.6); intestinal absorptive capacity also improved in all cases healthy rats (2.06 ± 0.07 µg/mL; non-treated, 1.18 ± 0.07 µg/mL; curcumin 1.76 ± 0.3 µg/mL; DEX5, 2.29 ± 0.2 µg/mL; DEX20, 2.25 ± 0.26 µg/mL; and α-tocopherol 1.66 ± 0.21 µg/mL). However, it failed to reduce liver enzyme levels. Finally, only dexmedetomidine significantly reduced urea and creatinine levels compared to non-treated animals.
UNASSIGNED: All drugs were effective in reducing HID, although α-tocopherol was effective to a greater extent. Only dexmedetomidine reverted intestinal absorption to normal values of healthy animals.
UNASSIGNED: i-IRI was induced by placing a microvascular clip in the superior mesenteric artery of female WAG/RijHsd rats; the clip was removed after 1h and reperfusion was allowed for 4h. Curcumin (200 mg/kg, orally), α-tocopherol (20 mg/kg, i.p.), and dexmedetomidine (5 or 20 µg/kg, s.c.; DEX5 and DEX20, respectively) were administered. Blood and terminal ileum specimens were collected for biochemical and histological determination. Furthermore, D-xylose absorption test was performed to evaluate intestinal absorption; after completing the 1-hour ischemia and 4-hour reperfusion period, 1 mL of aqueous D-xylose solution (0.615 mg/mL) was administered orally, and one hour later, plasma D-xylose levels were quantified.
UNASSIGNED: The histological injury degree (HID) measured by the Chiu scale was significantly reduced when the treatments were applied (non-treated rats, 2.6 ± 0.75; curcumin, 1.54 ± 0.8; DEX5, 1.47 ± 0.7; DEX20 1.14 ± 0.5; and α-tocopherol, 1.01 ± 0.6); intestinal absorptive capacity also improved in all cases healthy rats (2.06 ± 0.07 µg/mL; non-treated, 1.18 ± 0.07 µg/mL; curcumin 1.76 ± 0.3 µg/mL; DEX5, 2.29 ± 0.2 µg/mL; DEX20, 2.25 ± 0.26 µg/mL; and α-tocopherol 1.66 ± 0.21 µg/mL). However, it failed to reduce liver enzyme levels. Finally, only dexmedetomidine significantly reduced urea and creatinine levels compared to non-treated animals.
UNASSIGNED: All drugs were effective in reducing HID, although α-tocopherol was effective to a greater extent. Only dexmedetomidine reverted intestinal absorption to normal values of healthy animals.
摘要：
■肠缺血再灌注损伤（i-IRI）涉及肠段中的血流中断，然后恢复血流。当血流恢复时，氧化和炎症分子分布在整个血液中，引发局部和系统性损害。我们的目标是评估三种抗氧化剂和/或抗炎化合物（姜黄素，右美托咪定和α-生育酚）以预防或逆转i-IRI引起的局部和全身损伤。
■i-IRI是通过在雌性WAG/RijHsd大鼠的肠系膜上动脉中放置微血管夹来诱导的；1h后将夹子取出，再灌注4h。姜黄素（200mg/kg，口头)，α-生育酚（20mg/kg，i.p.),和右美托咪定(5或20µg/kg，分别给予s.c.;DEX5和DEX20)。收集血液和回肠末端标本进行生化和组织学测定。此外，进行D-木糖吸收试验以评估肠吸收；在完成1小时缺血和4小时再灌注期后，口服1毫升D-木糖水溶液（0.615毫克/毫升），一小时后，定量血浆D-木糖水平。
■通过Chiu量表测量的组织学损伤程度（HID）在应用治疗时（未治疗的大鼠，2.6±0.75；姜黄素，1.54±0.8；DEX5，1.47±0.7；DEX201.14±0.5；和α-生育酚，1.01±0.6）；所有健康大鼠的肠道吸收能力也得到改善（2.06±0.07µg/mL；未治疗，1.18±0.07µg/mL；姜黄素1.76±0.3µg/mL；DEX5，2.29±0.2µg/mL；DEX20，2.25±0.26µg/mL；和α-生育酚1.66±0.21µg/mL）。然而,它不能降低肝酶水平。最后,与未治疗的动物相比,只有右美托咪定显著降低尿素和肌酐水平.
■所有药物都能有效降低HID，虽然α-生育酚在更大程度上有效。只有右美托咪定使健康动物的肠吸收恢复到正常值。
■i-IRI是通过在雌性WAG/RijHsd大鼠的肠系膜上动脉中放置微血管夹来诱导的；1h后将夹子取出，再灌注4h。姜黄素（200mg/kg，口头)，α-生育酚（20mg/kg，i.p.),和右美托咪定(5或20µg/kg，分别给予s.c.;DEX5和DEX20)。收集血液和回肠末端标本进行生化和组织学测定。此外，进行D-木糖吸收试验以评估肠吸收；在完成1小时缺血和4小时再灌注期后，口服1毫升D-木糖水溶液（0.615毫克/毫升），一小时后，定量血浆D-木糖水平。
■通过Chiu量表测量的组织学损伤程度（HID）在应用治疗时（未治疗的大鼠，2.6±0.75；姜黄素，1.54±0.8；DEX5，1.47±0.7；DEX201.14±0.5；和α-生育酚，1.01±0.6）；所有健康大鼠的肠道吸收能力也得到改善（2.06±0.07µg/mL；未治疗，1.18±0.07µg/mL；姜黄素1.76±0.3µg/mL；DEX5，2.29±0.2µg/mL；DEX20，2.25±0.26µg/mL；和α-生育酚1.66±0.21µg/mL）。然而,它不能降低肝酶水平。最后,与未治疗的动物相比,只有右美托咪定显著降低尿素和肌酐水平.
■所有药物都能有效降低HID，虽然α-生育酚在更大程度上有效。只有右美托咪定使健康动物的肠吸收恢复到正常值。
