Flavonoids are metabolites of plants and fungus. Flavonoid research has been paid special attention to in recent times after the observation of their beneficial effects on the cardiovascular system. These favorable effects are exerted by flavonoids mainly due to their antioxidant properties, which result from the ability to decrease the oxidation of low-density lipoproteins, thus improving the lipid profiles. The other positive effect exerted on the cardiovascular system is the ability of flavonoids to produce vasodilation and regulate the apoptotic processes in the endothelium. Researchers suggested that these effects, including their anti-inflammatory function, are consequences of flavonoids’ potent antioxidant properties, but recent studies have shown multiple signaling pathways linked to them, thus suggesting that there are more mechanisms involved in the beneficial effect of the flavonoids on the human body. This review aims to present the latest data on the classification of these substances, their main mechanisms of action in the human body, and the beneficial effects on the physiological and pathological status of the cardiovascular system.

Nitric oxide, a ubiquitous molecule found throughout the natural world, is a key molecule implicated in many central and benefic molecular pathways and has a well-established role in the function of the central nervous system, as numerous studies have previously shown. Dysregulation of its metabolism, mainly the upregulation of nitric oxide production, has been proposed as a trigger and/or aggravator for many neurological affections. Increasing evidence supports the implication of this molecule in prevalent neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease, or amyotrophic lateral sclerosis. The mechanisms proposed for its neurotoxicity mainly center around the increased quantities of nitric oxide that are produced in the brain, their cause, and, most importantly, the pathological metabolic cascades created. These cascades lead to the formation of neuronal toxic substances that impair the neurons’ function and structure on multiple levels. The purpose of this review is to present the main causes of increased pathological production, as well as the most important pathophysiological mechanisms triggered by nitric oxide, mechanisms that could help explain a part of the complex picture of neurodegenerative diseases and help develop targeted therapies.

Curcumin (CC) is known to have anti-inflammatory and anti-oxidative properties and has already been tested for its efficiency in different diseases including diabetes mellitus (DM). New formulations and route administration were designed to obtain products with higher bioavailability. Our study aimed to test the effect of intraperitoneal (i.p.) administration of liposomal curcumin (lCC) as pre-treatment in streptozotocin(STZ)-induced DM in rats on oxidative stress, liver, and pancreatic functional parameters. Forty-two Wistar-Bratislava rats were randomly divided into six groups (seven animals/group): control (no diabetes), control-STZ (STZ-induced DM —60 mg/100g body weight a single dose intraperitoneal administration, and no CC pre-treatment), two groups with DM and CC pre-treatment (1mg/100g bw—STZ + CC1, 2 mg/100g bw—STZ + CC2), and two groups with DM and lCC pre-treatment (1 mg/100g bw—STZ + lCC1, 2 mg/100g bw—STZ + lCC1). Intraperitoneal administration of Curcumin in diabetic rats showed a significant reduction of nitric oxide, malondialdehyde, total oxidative stress, and catalase for both evaluated formulations (CC and lCC) compared to control group (p < 0.005), with higher efficacy of lCC formulation compared to CC solution (p < 0.002, excepting catalase for STZ + CC2vs. STZ + lCC1when p = 0.0845). The CC and lCC showed hepatoprotective and hypoglycemic effects, a decrease in oxidative stress and improvement in anti-oxidative capacity status against STZ-induced DM in rats (p < 0.002). The lCC also proved better efficacy on MMP-2, and -9 plasma levels as compared to CC (p < 0.003, excepting STZ + CC2 vs. STZ + lCC1 comparison with p = 0.0553). The lCC demonstrated significantly better efficacy as compared to curcumin solution on all serum levels of the investigated markers, sustaining its possible use as adjuvant therapy in DM.

This systematic review investigates the potential health and wellness benefits of natural calcium-rich mineral waters. It emphasizes the importance of dietary calcium sourced from natural mineral waters in promoting bone health, maintaining cardiovascular function, aiding in weight management, and enhancing overall well-being. The review process involved the comprehensive analysis of peer-reviewed articles, clinical trials, and experimental studies published within the last decade. Findings reveal that consuming calcium-rich mineral water can contribute significantly to daily calcium intake, particularly for those with lactose intolerance or individuals adhering to plant-based diets. The unique bioavailability of calcium from such waters also appears to enhance absorption, thus potentially offering an advantage over other calcium sources. The potential benefits extend to the cardiovascular system, with some studies indicating a reduction in blood pressure and the prevalence of cardiovascular diseases. Emerging evidence suggests that calcium-rich mineral water might have a role in body weight management, though further research is needed. The review identifies several areas requiring additional research, such as the potential interaction between calcium-rich mineral water and other dietary components, the effects on populations with specific health conditions, and the long-term effects of consumption. In conclusion, natural calcium-rich mineral waters show promise as a readily accessible and bioavailable sources of dietary calcium, potentially beneficial for a broad range of individuals. However, further investigation is required to fully understand its range of health impacts and define optimal intake levels.

This review explores the emerging role of hydrogen sulfide (H₂S) in modulating epigenetic mechanisms involved in neurodegenerative diseases. Accumulating evidence has begun to elucidate the multifaceted ways in which H₂S influences the epigenetic landscape and, subsequently, the progression of various neurodegenerative disorders, including Alzheimer’s, Parkinson’s, and Huntington’s disease. H₂S can modulate key components of the epigenetic machinery, such as DNA methylation, histone modifications, and non-coding RNAs, impacting gene expression and cellular functions relevant to neuronal survival, inflammation, and synaptic plasticity. We synthesize recent research that positions H₂S as an essential player within this intricate network, with the potential to open new therapeutic avenues for these currently incurable conditions. Despite significant progress, there remains a considerable gap in our understanding of the precise molecular mechanisms and the potential therapeutic implications of modulating H₂S levels or its downstream targets. We conclude by identifying future directions for research aimed at exploiting the therapeutic potential of H₂S in neurodegenerative diseases.