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玛赫西AK - 4对过氧化氢诱导的离体大鼠心脏氧化应激的影响。

Effect of Maharishi AK-4 on H2O2-induced oxidative stress in isolated rat hearts.

作者信息

Cullen W J, Dulchavsky S A, Devasagayam T P, Venkataraman B V, Dutta S

机构信息

Department of Surgery, Wayne State University School of Medicine, Detroit, MI 48201, USA.

出版信息

J Ethnopharmacol. 1997 May;56(3):215-22. doi: 10.1016/s0378-8741(97)01526-2.

Abstract

Oxidative damage to crucial biomolecules due to excess generation of reactive oxygen species has been implicated as a major cause of organ damage and hence compounds capable of negating such damage have potential benefits. Using hydrogen peroxide (H2O2) as a model pro-oxidant to induce oxidative stress, we have examined the ability of natural food supplement Maharishi Amrit Kalash (MAK-4) to decrease oxidative damage in potassium-arrested isolated rat hearts. The protocol was that hearts isolated from male Sprague-Dawley rats were retrograde-perfused with Krebs-Henseleit (K-H) solution for 30 min for equilibration. After this period, the hearts were subjected to cardioplegia with high potassium (26-30 mM), followed by reperfusion with K-H solution in the presence or absence of 200 microM H2O2. As expected, H2O2 treatment following cardioplegia induced a high degree of oxidative stress as assessed by release of lactate dehydrogenase (LDH, a marker of plasma membrane damage) and total glutathione (GSH + GSSG). H2O2 also impaired the ability of heart to regain developed tension during the testing period. However, addition of MAK-4 in the perfusate containing H2O2 decreased oxidative stress in terms of release of LDH and glutathione. In parallel with these biochemical studies, in a few experiments the cardiac function was assessed by measuring developed contractile tension. These preliminary studies also showed that in the presence of MAK-4 the H2O2-treated hearts were able to regain better developed tension. Further in vitro studies to examine the possible mechanisms of MAK-4 action reveal that this formulation contains H2O2 binding activity which resulted in the decreased availability of H2O2 itself. Our studies hence reveal that the ayurvedic food supplement MAK-4 may have potential benefits in reducing oxidative stress.

摘要

由于活性氧的过量产生而对关键生物分子造成的氧化损伤,已被认为是器官损伤的主要原因,因此能够消除此类损伤的化合物具有潜在益处。我们以过氧化氢(H₂O₂)作为诱导氧化应激的模型促氧化剂,研究了天然食品补充剂玛赫西阿姆里特卡拉什(MAK - 4)减轻钾停搏离体大鼠心脏氧化损伤的能力。实验方案如下:从雄性斯普拉格 - 道利大鼠分离出的心脏,用克雷布斯 - 亨泽莱特(K - H)溶液逆行灌注30分钟以达到平衡。在此之后,心脏用高钾(26 - 30 mM)进行心脏停搏,随后在有或没有200微摩尔H₂O₂的情况下用K - H溶液再灌注。正如预期的那样,心脏停搏后进行H₂O₂处理会诱导高度的氧化应激,这通过乳酸脱氢酶(LDH,质膜损伤的标志物)和总谷胱甘肽(GSH + GSSG)的释放来评估。H₂O₂还损害了心脏在测试期间恢复舒张期张力的能力。然而,在含有H₂O₂的灌注液中添加MAK - 4,就LDH和谷胱甘肽的释放而言,可降低氧化应激。与这些生化研究并行,在一些实验中通过测量舒张期收缩张力来评估心脏功能。这些初步研究还表明,在MAK - 4存在的情况下,经H₂O₂处理的心脏能够更好地恢复舒张期张力。进一步的体外研究以探究MAK - 4作用的可能机制,结果显示该制剂具有H₂O₂结合活性,这导致H₂O₂本身的可用性降低。因此,我们的研究表明,阿育吠陀食品补充剂MAK - 4在减轻氧化应激方面可能具有潜在益处。

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