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The effects of carnosine in an experimental rat model of septic shock

机译:肌肽在实验性脓毒性休克大鼠模型中的作用

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Background To examine the effect of carnosine on liver function and histological findings in experimental septic shock model, 24 Sprague-Dawley rats were used. Material and Methods Rats were divided into control, septic shock, and carnosine-treated septic shock groups. Femoral vein and artery catheterization were performed on all rats. Rats in the control group underwent laparotomy and catheterization; in the test groups, cecal ligation-perforation and bladder cannulation were added. Rats in the treatment group received a single intraperitoneal (IP) injection of 250 mg/kg carnosine 60 minutes after cecal ligationperforation. Rats were monitored for blood pressure, heart rate, and body temperature to assess the postoperative septic response, and body fluids were replaced as necessary. At the end of 24 hours, rats were sacrificed and liver samples were collected. Results Statistically significant improvements were observed in liver function, tissue and serum MDA levels, and histological findings in rats treated with carnosine, compared to rats with untreated sepsis. HB and HCT values did not change significantly during the course of the experiment. Rats exposed to septic shock and treated with carnosine exhibited decreased sinusoidal dilatation and cellular inflammation into the portal region, compared to the sepsis group; the livers of rats in this group had near-normal histological structure. Conclusions We conclude that carnosine may be an effective treatment for oxidative damage due to liver tissue perfusion defects in cases of septic shock.
机译:背景为了研究肌肽对实验性败血性休克模型的肝功能和组织学结果的影响,使用了24只Sprague-Dawley大鼠。材料和方法将大鼠分为对照组,败血性休克和肌肽治疗的败血性休克组。对所有大鼠进行股静脉和动脉导管插入术。对照组的大鼠行剖腹术和导尿。在测试组中,增加盲肠结扎穿孔和膀胱插管。在盲肠结扎穿孔后60分钟,治疗组的大鼠腹膜内(IP)注射250 mg / kg肌肽。监测大鼠的血压,心率和体温以评估术后脓毒症反应,并根据需要更换体液。在24小时结束时,处死大鼠并收集肝脏样品。结果与未治疗的脓毒症大鼠相比,肌肽治疗的大鼠的肝功能,组织和血清MDA水平以及组织学发现在统计学上有显着改善。在实验过程中,HB和HCT值没有明显变化。与败血症组相比,暴露于败血性休克并用肌肽治疗的大鼠表现出减少的正弦曲线扩张和进入门区的细胞炎症。该组大鼠肝脏组织学结构接近正常。结论我们得出结论,肌苷可能是败血性休克引起的肝组织灌注缺陷引起的氧化损伤的有效治疗方法。

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