ABSTRACT
The kidneys have a close functional relationship with other organs especially the lungs. This connection makes the kidney and the lungs as the most organs involved in the multi-organ failure syndrome. The combination of acute lung injury (ALI) and renal failure results a great clinical significance of 80% mortality rate. Acute kidney injury (AKI) leads to an increase in circulating cytokines, chemokines, activated innate immune cells and diffuse of these agents to other organs such as the lungs. These factors initiate pathological cascade that ultimately leads to ALI and acute respiratory distress syndrome (ARDS). We comprehensively searched the English medical literature focusing on AKI, ALI, organs cross talk, renal failure, multi organ failure and ARDS using the databases of PubMed, Embase, Scopus and directory of open access journals. In this narrative review, we summarized the pathophysiology and treatment of respiratory distress syndrome following AKI. This review promotes knowledge of the link between kidney and lung with mechanisms, diagnostic biomarkers, and treatment involved ARDS induced by AKI.
ABSTRACT
Background and Objectives: irradiation is common treatment in most cancers but the effect of radiation on healthy cells, could be prevented its use in high doses. Ascorbic acid is known as a potent antioxidant. In this study the role of vitamin c to reduce cell death and complications after radiotherapy was tested
Materials and Methods: in this study, 3 groups of race bulb-c mice [control, irradiation, treatment with ascorbic acid] were chosen. Two groups received 6 Gray of radiation. Medications was given intraperitoneally to them one week prior to radiotherapy and then after a week of radiotherapy, again they were given the drug again for a week and at the end of treatment, y-maze memory test and shuttle box test were done and then the brain of rats was fixed by paraformaldehyde perfusion and removed and was prepared for histological studies
Results: nissl staining applied to counting necrotic cells of hippocampus. Tunnel kit was used to quantify apoptotic cell death while to short term memory scale; we applied maze and shuttle box tests. Memory tests were indicated to reduction of irradiation effects on short-term memory in treatment group. Nissl staining showed significant decrease in necrotic cells, Evaluation of cell apoptosis, also showed significant decrease in apoptotic cells in treatment group
Conclusion: treatment the mice with ascorbic acid caused reduction of cell death and complications after Radiotherapy
ABSTRACT
Preliminary studies confirmed reduction of cell death following treatment with antioxidants. According to this finding we investigated the relationship between consumption of CoQ10 and expression of bax and bcl2 in hippocampus ischemia that this expression related to cell programmed death. We studied the protective role of CoQ10 against ischemia-reperfusion. Experimental design includes four groups: intact [N=7], ischemic control [N=7], sham control [N=7] and treatment groups with CoQ10 [N=7]. The mice [treatment group] treated with CoQ10 as Pre-Treatment for a week. Then, ischemia induced by common carotid artery ligation and following the reduction in inflammation [a week] the treatment group post-treated with CoQ10 for a week. Nissl staining applied to counting necrotic cells of hippocampus and the western blotting performed to measurement the bax and bcl2 expression. Tunnel kit was used to quantify apoptotic cell death while to short term memory scale, we apply Y-maze. Cell death was significantly lower when mice treated with CoQ10. Bax expression was significantly high in ischemic group but in treatment group was less and reversely the bcl2 expression in ischemic group was lower than treatment and vehicle groups. The memory test results were consistent with cell death results. Ischemia for 15 minutes induced cell death in hippocampus with more potent effect on CA1. CoQ10 intake significantly reduced cell death and decreased memory loss. with prevent of expression of bax and increase in expression of bcl2