A Review on Herbal Plants used in Brain Ischemic and Reperfusion Injury

A stroke causes serious and long term brain disability due to disruption in the blood flow to the brain. Clinically major changes occur in brain functions are seen after brain ischemia and reperfusion. Patients show emotional, behavioural, and cognitive alterations during retrieval time. Cerebral injury by transient ischemia distresses the number of patients globally with death or long term disability. In recent years a great deal of research has been carried out to find the effectiveness of the herbal drug for the treatment of stroke. Both thrombolytic and neuro-protective activities of herbal drugs may be a new strategy for effective stroke treatment. This article reviews the list of universally used plants effective for brain stroke therapies. The purpose of this article was to collect the herbal drugs useful in brain stroke therapies. Keywords: ischemia-reperfusion, brain injury, stroke, herbal drugs, tissue

The Role of Cardiac N-Methyl-D-Aspartate Receptors in Heart Conditioning—Effects on Heart Function and Oxidative Stress

As well as the most known role of N-methyl-D-aspartate receptors (NMDARs) in the nervous system, there is a plethora of evidence that NMDARs are also present in the cardiovascular system where they participate in various physiological processes, as well as pathological conditions. The aim of this study was to assess the effects of preconditioning and postconditioning of isolated rat heart with NMDAR agonists and antagonists on heart function and release of oxidative stress biomarkers. The hearts of male Wistar albino rats were subjected to global ischemia for 20 min, followed by 30 min of reperfusion, using the Langendorff technique, and cardiodynamic parameters were determined during the subsequent preconditioning with the NMDAR agonists glutamate (100 µmol/L) and (RS)-(Tetrazol-5-yl)glycine (5 μmol/L) and the NMDAR antagonists memantine (100 μmol/L) and MK-801 (30 μmol/L). In the postconditioning group, the hearts were perfused with the same dose of drugs during the first 3 min of reperfusion. The oxidative stress biomarkers were determined spectrophotometrically in samples of coronary venous effluent. The NMDAR antagonists, especially MK-801, applied in postconditioning had a marked antioxidative effect with a most pronounced protective effect. The results from this study suggest that NMDARs could be a potential therapeutic target in the prevention and treatment of ischemic and reperfusion injury of the heart.

PREVENTION AND TREATMENT OF ISCHEMIA-REPERFUSION SYNDROME

The main negative consequences of ischemia-reperfusion of the kidneys are the early developing severe chronic dysfunction of the graft, and in the most severe cases the function of the transplanted kidney is not restored (primary non-functioning graft). As a result of loss of transplant function, the patient usually returns to dialysis. These complications are more common in kidney transplants from “donors with extended criteria,” since these organs are most sensitive to damage resulting from ischemia-reperfusion syndrome (IR syndrome). At the same time, the share of such (suboptimal) donors is gradually increasing in Russia. Cold preservation of the organ in special solutions remains the gold standard for kidney transplantation, however, it is not able to fully protect the organ. The article presents the main promising methods that reduce the severity of ischemic and reperfusion injury: donor conditioning, ischemic preconditioning, various variants of kidney preservation, effects on inflammatory mediators, application of biological target drugs. Nevertheless, the pathogenesis of ischemia-reperfusion syndrome has been studied much better than the methods of its correction. Currently, there are only indirect or experimental evidence that the severity of the syndrome of IR can be reduced due to the pharmacoprotection of the ogran before donation, during preservation, as well as in the early postoperative period. Further research is needed to find ways to reduce the severity of ischemic and reperfusion injury of the graft.

Novel Aspects of Cardiac Ischemia and Reperfusion Injury Mechanisms

Introduction.The present article, in which a contemporary analysis of the literature on the pathophysiology of ischemic and reperfusion injury (IRI) of the myocardium is presented, focuses on the possible role played by of the calpain system and oxidative stress. Several process development options were proposed, including cytosolic and mitochondrial Ca2+ overload, reactive oxygen stress release, acute inflammatory response and metabolic degradation. The combined effect of all of the above factors produces irreversible ischemic and reperfused damage of cardiomyocytes.Materials and methods.The role of the calpain system in the creation of myocardial IRI was experimentally investigated. It was found that active calpain substrates play a significant role in the processes of cell cycle, apoptosis and differentiation, adversely affecting cardiomyocyte functionality. The calpain system is part of an integrated proteolytic system that is critical to the relationship between the structure and function of the cardiac sarcomere. Uncontrolled activation of calpain is indicated in the pathophysiology of many cardiovascular disorders. As shown by research, inhibitor calpain reduces the size of the zone of infarction following ischemia reperfusion and thus lessens the risk of “stunning” the myocardium. As is known, a consequence of IRI is acute myocardial infarction (AMI), which is a central factor in cardiovascular disease (CVD) and is one of the primary causes of mortality. Understanding the exact pathophysiological mechanisms remains an urgent problem for clinical physicians. To date, the mechanisms of IRI are not fully known, which creates certain difficulties in further treatment and prevention tactics. In addition, myocardial IRI is also an important issue for pathoanatomical service, since sudden coronary death can occur despite timely reperfusion therapy following AMI.Conclusion.The development of strategies for creating conditions that limit the degree of damage to myocardial tissues significantly increases the ability of the heart to withstand ischemic damage.

Cardioprotection by ginseng: experimental and clinical evidence and underlying mechanisms

Protection of the ischemic and reperfused myocardium represents a major therapeutic challenge. Translating results from animal studies to the clinical setting has been disappointing, yet the need for effective intervention, particularly to limit heart damage following infarction or surgical procedures such as coronary artery bypass grafting, is substantial. Among the many compounds touted as cardioprotective agents is ginseng, a medicinal herb belonging to the genus Panax, which has been used as a medicinal agent for thousands of years, particularly in Asian societies. The biological actions of ginseng are very complex and reflect composition of many bioactive components, although many of the biological and therapeutic effects of ginseng have been attributed to the presence of steroid-like saponins termed ginsenosides. Both ginseng and many ginsenosides have been shown to exert cardioprotective properties in experimental models. There is also clinical evidence that traditional Chinese medications containing ginseng exert cardioprotective properties, although such clinical evidence is less robust primarily owing to the paucity of large-scale clinical trials. Here, we discuss the experimental and clinical evidence for ginseng, ginsenosides, and ginseng-containing formulations as cardioprotective agents against ischemic and reperfusion injury. We further discuss potential mechanisms, particularly as these relate to antioxidant properties.

Morphological illustration of alterations in the arterial endothelium in ischemic and reperfusion injuries

Background. Reperfusion syndrome is an inevitable event in recovery of the blood flow after a longstanding ischemia. The article is dedicated to the study of the expressiveness of this condition. Aim – to compare the depth of morphological alterations of the arterial endothelium in ischemic and reperfusion injury in experiment. Materials and Мethods. The work was conducted on 90 laboratory animals – rats of Wistar line. Models of ischemia and reperfusion were obtained by compression of the abdominal part of the aorta (1st group) with further conditioning (2nd group). The animals were withdrawn from the experiment and the vessel wall was taken on the 1st, 3d, 5th, 7th day. Preparations were studied in a transmission electron microscope «Libra 120» with automatic scanning of images. Results. Comparison of pathomorphological data obtained in examination of the aortas and iliac arteries of the two groups of animals («ischemia» and «reperfusion») showed that the cascade of pathomorphological changes includes several main stages. Transient ischemia leads to injury (alteration) of the main components of the vessel wall. Under action of this factor endotheliocytes exhibit a nonspecific response changing their synthetic activity that was manifested by a complex of morphological signs in the nucleus, karyolemma, cytoplasm and plasmalemma. In some cells the changes took an irreversible character and were accompanied by rupture of mitochondrial membranes, of general purpose organelles and of plasmalemma. Such endotheliocytes died and were desquamated. Because of short duration of ischemia these changes were insignificant. Subendothelial structures underwent edema which is logical in view of derangement of the barrier function of the epithelium and presence of a mild inflammatory component (in response to death of a part of endotheliocytes and cells of the vascular wall stroma). Examination of the ultrastructure of the vessel wall in the ischemiareperfusion group revealed adaptive and pathological changes in the endothelial cells. Data were obtained that evidence a significant disorder in microhemodynamics in tissues in reperfusion. Conclusion. No significant structural and ultrastructural differences in injuries and reactive changes in «ischemia» and «reperfusion» groups were found. In view of this, for subtle differentiation of pathomorphogenesis of these two conditions it is reasonable to use examination methods with higher resolution.

Morphological illustration of alterations in the arterial endothelium in ischemic and reperfusion injuries

Background. Reperfusion syndrome is an inevitable event in recovery of the blood flow after a longstanding ischemia. The article is dedicated to the study of the expressiveness of this condition. Aim – to compare the depth of morphological alterations of the arterial endothelium in ischemic and reperfusion injury in experiment. Materials and Мethods. The work was conducted on 90 laboratory animals – rats of Wistar line. Models of ischemia and reperfusion were obtained by compression of the abdominal part of the aorta (1st group) with further conditioning (2nd group). The animals were withdrawn from the experiment and the vessel wall was taken on the 1st, 3d, 5th, 7th day. Preparations were studied in a transmission electron microscope «Libra 120» with automatic scanning of images. Results. Comparison of pathomorphological data obtained in examination of the aortas and iliac arteries of the two groups of animals («ischemia» and «reperfusion») showed that the cascade of pathomorphological changes includes several main stages. Transient ischemia leads to injury (alteration) of the main components of the vessel wall. Under action of this factor endotheliocytes exhibit a nonspecific response changing their synthetic activity that was manifested by a complex of morphological signs in the nucleus, karyolemma, cytoplasm and plasmalemma. In some cells the changes took an irreversible character and were accompanied by rupture of mitochondrial membranes, of general purpose organelles and of plasmalemma. Such endotheliocytes died and were desquamated. Because of short duration of ischemia these changes were insignificant. Subendothelial structures underwent edema which is logical in view of derangement of the barrier function of the epithelium and presence of a mild inflammatory component (in response to death of a part of endotheliocytes and cells of the vascular wall stroma). Examination of the ultrastructure of the vessel wall in the ischemiareperfusion group revealed adaptive and pathological changes in the endothelial cells. Data were obtained that evidence a significant disorder in microhemodynamics in tissues in reperfusion. Conclusion. No significant structural and ultrastructural differences in injuries and reactive changes in «ischemia» and «reperfusion» groups were found. In view of this, for subtle differentiation of pathomorphogenesis of these two conditions it is reasonable to use examination methods with higher resolution.