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马齿苋乙醇提取物对小鼠的抗缺氧活性。

Anti-hypoxic activity of the ethanol extract from Portulaca oleracea in mice.

作者信息

Chen Cheng-Jie, Wang Wan-Yin, Wang Xiao-Li, Dong Li-Wei, Yue Yi-Tian, Xin Hai-Liang, Ling Chang-Quan, Li Min

机构信息

Department of Naval Medicine, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, PR China.

出版信息

J Ethnopharmacol. 2009 Jul 15;124(2):246-50. doi: 10.1016/j.jep.2009.04.028. Epub 2009 May 3.

Abstract

AIM OF THE STUDY

To investigate the effects of the ethanol extract from Portulaca oleracea (EEPO) on hypoxia models mice and to find the possible mechanism of its anti-hypoxic actions so as to elucidate the anti-hypoxia activity and provide scientific basis for the clinical use of Portulaca oleracea.

MATERIALS AND METHODS

EEPO was evaluated on anti-hypoxic activity in several hypoxia mice models, including closed normobaric hypoxia and sodium nitrite or potassium cyanide toxicosis. To verify the possible mechanism(s), we detected the activities of pyruvate kinase (PK), phosphofructokinase (PFK), lactate dehydrogenase (LDH) and the level of adenosine triphosphate (ATP) in mice cortices.

RESULTS

Given orally, the EEPO at doses of 100, 200, 400 mg/kg could dose-dependently enhance the survival time of mice in both of the normobaric and chemical hypoxia models. The activity of the glycolysis enzymes and the level of ATP were higher than those of the control. In the pentobarbital sodium-induced sleeping time test and the open-field test, EEPO neither significantly enhanced the pentobarbital sodium-induced sleeping time nor impaired the motor performance, indicating that the observed anti-hypoxic activity was unlikely due to sedation or motor abnormality.

CONCLUSIONS

These results demonstrated that the EEPO possessed notable anti-hypoxic activity, which might be related to promoting the activity of the key enzymes in glycolysis and improving the level of ATP in hypoxic mice.

摘要

研究目的

研究马齿苋乙醇提取物(EEPO)对缺氧模型小鼠的影响,探讨其抗缺氧作用的可能机制,以阐明马齿苋的抗缺氧活性,为马齿苋的临床应用提供科学依据。

材料与方法

在多种缺氧小鼠模型中评估EEPO的抗缺氧活性,包括常压缺氧和亚硝酸钠或氰化钾中毒。为验证可能的机制,检测小鼠皮质中丙酮酸激酶(PK)、磷酸果糖激酶(PFK)、乳酸脱氢酶(LDH)的活性以及三磷酸腺苷(ATP)水平。

结果

口服给药时,100、200、400 mg/kg剂量的EEPO可剂量依赖性地延长常压和化学性缺氧模型小鼠的存活时间。糖酵解酶活性和ATP水平高于对照组。在戊巴比妥钠诱导的睡眠时间试验和旷场试验中,EEPO既未显著延长戊巴比妥钠诱导的睡眠时间,也未损害运动性能,表明观察到的抗缺氧活性不太可能是由于镇静或运动异常所致。

结论

这些结果表明,EEPO具有显著的抗缺氧活性,这可能与促进缺氧小鼠糖酵解关键酶的活性和提高ATP水平有关。

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