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Glutamine induces heat-shock protein and protects against Escherichia coli lipopolysaccharide-induced vascular hyporeactivity in rats

机译:谷氨酰胺诱导热休克蛋白并预防大肠杆菌脂多糖诱导的大鼠血管低反应性

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IntroductionVascular hyporeactivity is an important problem associated with sepsis. Although the mechanism involves inflammatory pathway activation, specific therapeutic approaches have not been defined. Glutamine (Gln) has been shown to provide some anti-inflammatory effects and improve outcomes in sepsis. Here, we tested the hypothesis that Gln could reduce Escherichia coli lipopolysaccharide (LPS)-induced vascular hyporeactivity and evaluated the role of heat-shock protein 70 (HSP70) induction in this process.MethodsTwenty-four male Sprague-Dawley rats were divided into control, LPS shock, and alanyl-Gln dipeptide+LPS shock (Ala-Gln+LPS) groups. Six hours after administration of LPS, phenylephrine (PE) (0.5 to approximately 2.5 μg/kg) was applied intravenously to all groups, and the percentage increase in mean arterial pressure (MAP) was detected in the respective groups. The concentration-response curve of PE was obtained in tension experiments, and the average values of PE maximum efficacy (Emax) and median effective dose (EC50) were calculated. The plasma concentrations of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) were detected in all groups. The expressions of HSP70 from heart, liver, lung, and aorta were also assayed in all groups.ResultsThe maximal percentage increase in MAP induced by PE was significantly reduced to 12.7% in the LPS shock group (P < 0.05) and was restored to 15.6% in the Ala-Gln+LPS group (P < 0.05), whereas the control group was 24.7%. The average values of PE Emax and EC50 were significantly impaired in the LPS shock group (P < 0.05) but partially restored in the Ala-Gln+LPS group (P < 0.05). The expressions of HSP70 from the heart, aorta, lung, and liver were much higher in the Ala-Gln+LPS group than those in the LPS shock group (P < 0.05). The plasma concentrations of TNF-α, IL-6, and MDA were much lower in the Ala-Gln+LPS group than those in the LPS shock group.ConclusionGln effectively improves vascular reactivity by inducing the expression of HSP70, reducing inflammatory cytokine release and peroxide biosynthesis in LPS shock rats. These results suggest that Gln has a potentially beneficial therapeutic effect for septic shock patients.
机译:简介血管反应性低下是与败血症相关的重要问题。尽管该机制涉及炎性途径激活,但尚未定义具体的治疗方法。谷氨酰胺(Gln)已被证明可提供某些抗炎作用并改善败血症的预后。在本文中,我们检验了Gln可以降低大肠杆菌脂多糖(LPS)诱导的血管反应性降低的假设,并评估了热休克蛋白70(HSP70)诱导在此过程中的作用。方法将24只雄性Sprague-Dawley大鼠分为对照组,LPS休克和丙氨酰-Gln二肽+ LPS休克(Ala-Gln + LPS)组。在给予LPS六小时后,将苯肾上腺素(PE)(0.5至约2.5μg/ kg)静脉内应用于所有组,并在各组中检测到平均动脉压(MAP)的百分比增加。在拉伸实验中获得了PE的浓度-反应曲线,并计算了PE最大功效(Emax)和中值有效剂量(EC50)的平均值。在所有组中检测到血浆丙二醛(MDA),肿瘤坏死因子-α(TNF-α)和白介素6(IL-6)的浓度。同时检测各组心,肝,肺和主动脉中HSP70的表达。结果LPS休克组PE诱导的MAP最大增加百分比显着降低至12.7%(P <0.05),并恢复至15.6。在Ala-Gln + LPS组中,%(P <0.05),而对照组为24.7%。 LPS休克组的PE Emax和EC50平均值显着降低(P <0.05),但Ala-Gln + LPS组的PE Emax和EC50平均值有所恢复(P <0.05)。 Ala-Gln + LPS组心脏,主动脉,肺和肝脏中HSP70的表达均高于LPS休克组(P <0.05)。 Ala-Gln + LPS组的血浆TNF-α,IL-6和MDA的浓度远低于LPS休克组。结论Gln通过诱导HSP70的表达,减少炎性细胞因子的释放和LPS休克大鼠体内过氧化物的生物合成。这些结果表明,Gln对败血性休克患者具有潜在的有益治疗作用。

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