The ameliorating effects of Vitamin E on hepatotoxicity of ecstasy.

BACKGROUND: The production of stress oxidative condition in body which is caused by consumption of ecstasy (3,4-methylenedioxymethamphetamine [MDMA]) leads to a liver damage. As an antioxidant, Vitamin E can protect cells and tissues against the deleterious effects of free radicals. This study evaluates the protective effects of Vitamin E on MDMA induced liver toxicity. MATERIALS AND METHODS: Twenty-eight male albino mice were randomly assigned to four equal groups. Group 1 received saline (control), Group 2 received MDMA and saline, Group 3 received MDMA, and Vitamin E and Group 4 received Vitamin E. MDMA was injected with single daily dose, three sequential days/week for 5 weeks. At the end of the period, blood samples were collected for a biochemical analysis and then the mice were sacrificed by cervical dislocation for histopathological and biochemical examinations of liver. RESULTS: The administration of Vitamin E attenuated the increased levels of alanine transaminase, aspartate transaminase, and alkaline phosphatase enzymes in serum. Vitamin E treatments significantly restored endogenous antioxidant enzymes (reduced glutathione and superoxide dismutase enzyme) activities as compared with MDMA-treated animals. Histological examination of liver revealed significant morphological tissue injuries in hepatocytes after MDMA being used, but in coadministration of vitamin E and MDMA, these morphological alterations reduced. CONCLUSION: The study showed that MDMA administration has adverse effects on the liver. Vitamin E lessened the deleterious impact considerably.

Neutrophil-to-lymphocyte ratio as a predictive biomarker for early diagnosis of depression: A narrative review.

Depression is a mood disorder that causes persistent feelings of sadness, hopelessness, loss of interest, and decreased energy. Early diagnosis of depression can improve its negative impacts and be effective in its treatment. Previous studies have indicated that inflammation plays an important role in the initiation and development of depression, hence, various inflammatory biomarkers have been investigated for early diagnosis of depression, the most popular of which are blood biomarkers. The Neutrophil to lymphocyte ratio (NLR) may be more informative in the early diagnosis of depression than other widely used markers, such as other leukocyte characteristics or interleukins. Considering the importance of early diagnosis of depression and the role of NLR in early diagnosis of depression, our paper reviews the literature on NLR as a diagnostic biomarker of depression, which may be effective in its treatment. Various studies have shown that elevated NLR is associated with depression, suggesting that NLR may be a valuable, reproducible, easily accessible, and cost-effective method for the evaluation of depression and it may be used in outpatient clinic settings. Closer follow-up can be performed for these patients who have higher NLR levels. However, it seems that further studies on larger samples, taking into account important confounding factors, and assessing them together with other inflammatory markers are necessary to draw some conclusive statements.

Sleep deprivation and NLRP3 inflammasome: Is there a causal relationship?

In the modern era, sleep deprivation (SD) is one of the most common health problems that has a profound influence on an individual's quality of life and overall health. Studies have identified the possibility that lack of sleep can stimulate inflammatory responses. NLRP3 inflammasome, a key component of the innate immune responses, initiates inflammatory responses by enhancing proinflammatory cytokine release and caspase-1-mediated pyroptosis. In this study, NLRP3 modification, its proinflammatory role, and potential targeted therapies were reviewed with regard to SD-induced outcomes. A growing body of evidence has showed the importance of the mechanistic connections between NLRP3 and the detrimental consequences of SD, but there is a need for more clinically relevant data. In animal research, (i) some animals show differential vulnerability to the effects of SD compared to humans. (ii) Additionally, the effects of sleep differ depending on the SD technique employed and the length of SD. Moreover, paying attention to the crosstalk of all the driving factors of NLRP3 inflammasome activation such as inflammatory responses, autonomic control, oxidative stress, and endothelial function is highly recommended. In conclusion, targeting NLRP3 inflammasome or its downstream pathways for therapy could be complicated due to the reciprocal and complex relationship of SD with NLRP3 inflammasome activation. However, additional research is required to support such a causal claim.