EVALUATION OF EZENUS IN AN EXPERIMENTAL MODEL OF DIET-INDUCED ALCOHOLIC AND NON-ALCOHOLIC FATTY LIVER CONDITION IN RATS

Objective: Alcoholic and non-alcoholic fatty liver disease are found to affect more than 10% of the general population. Fatty liver condition in humans is directly correlated with psychosocial stress. Herbal formulations for the management of stress may present an alternative for the treatment of fatty liver disease. Ezenus is a polyherbal candy containing herbs that can ameliorate stress and consequent liver abnormality. The present study aimed to evaluate the effect of Ezenus in experimentally induced alcoholic and non-acloholic fatty liver condition.Methods: Two models were studied simultaneously, prophylactic and therapeutic. Prophylactic groups received Ezenus along with fatty diet whereas the therapeutic groups received Ezenus only after induction of alcoholic or non-alcoholic fatty liver condition. Biochemical parameters were estimated in the serum on Days 0, 45 and 90. Lipid biochemistry of liver and histopathology were performed after terminal necropsy.Results: Fatty liver condition was induced in rats within 45 days of fatty diet administration with or without alcohol. Results of the present study suggested that prophylactic administration of Ezenus prevented the development of fatty liver condition in rats to a certain extent. Therapeutic intervention with Ezenus after fatty diet intake for 45 days was able to prevent the deranging effects of fatty liver disease. This beneficial effect of Ezenus was attributed to the adaptogenic and antioxidant effects of the ingredients present in Ezenus.Conclusion: Based on the results of the study, it was concluded that long term treatment of Ezenus exhibits a preventive effect in fatty liver disease. It not only protects the liver from toxic insults to a certain extent but also has the capability of maintaining the normal liver function.Â

Molecular hydrogen potentiates beneficial anti-infarct effect of hypoxic postconditioning in isolated rat hearts: Novel cardioprotective intervention

Generation of free radicals through incomplete reduction of oxygen during ischemia/ reperfusion is well-described. On the other hand, molecular hydrogen (H2) reduces oxidative stress due to its ability to react with strong oxidants and easily penetrate cells by diffusion, without disturbing metabolic redox reactions. This study was designed to explore cardioprotective potential of hypoxic postconditioning (HpostC) against ischemia/reperfusion (30-min global I/120-min R) in isolated rat hearts using oxygen-free Krebs-Henseleit buffer (KHB). Furthermore, the possibility to potentiate the effect of HpostC by H2 using oxygen-free KHB saturated with H2 (H2+HpostC) was tested. HPostC was induced by 4 cycles of 1-min perfusion with oxygen-free KHB intercepted by 1-min perfusion with normal KHB, at the onset of reperfusion. H2+HPostC was applied in a similar manner using H2 enriched oxygen-free KHB. Cardioprotective effects were evaluated on the basis of infarct size (IS, in % of area at risk, AR) reduction, post-I/R recovery of heart function and occurrence of reperfusion arrhythmias. HPostC significantly reduced IS/AR compared to non-conditioned controls. H2 present in KHB during HPostC further decreased IS/AR compared to the effect of HPostC, attenuated severe arrhythmias, and significantly restored heart function (vs. controls). Cardioprotection by hypoxic postconditioning can be augmented by molecular hydrogen infusion.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Potencial markers and metabolic processes involved in mechanism of radiation-induced heart injury

Irradiation of normal tissues leads to acute increase in reactive oxygen/nitrogen species that serve as intra and intercellular signaling to alter cell and tissue function. In the case of chest irradiation it can affect the heart, blood vessels and lungs, with consequent tissue remodelation and adverse side effects and symptoms. This complex process is orchestrated by a large number of interacting molecular signals, including cytokines, chemokines and growth factors. Inflammation, endothelial cell dysfunction, thrombogenesis, organ dysfunction and ultimate failing of the heart occur as a pathological entity - "radiation-induced heart disease" (RIHD) that is major source of morbidity and mortality. The purpose of the review is to bring insights into the basic mechanisms of RIHD that may lead to the identification of targets for intervention in the radiotherapy side effect. Studies of authors also provide knowledge how to select targeted drugs or biological molecules to modify the progression of radiation damage in the heart. New prospective studies are needed to validate that assessed factors and changes are useful as early markers of cardiac damage.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author