Saffron (Crocus sativus L.) is a medicinal plant, originally cultivated in the East and Middle East, and later in some Mediterranean countries. Saffron is obtained from the stigmas of the plant. Currently, the use of saffron is undergoing a revival. The medicinal virtues of saffron, its culinary use and its high added value have led to the clarification of its phytochemical profile and its biological and therapeutic characteristics. Saffron is rich in carotenoids and terpenes. The major products of saffron are crocins and crocetin (carotenoids) deriving from zeaxanthin, pirocrocin and safranal, which give it its taste and aroma, respectively. Saffron and its major compounds have powerful antioxidant and anti-inflammatory properties in vitro and in vivo. Anti-tumor properties have also been described. The goal of this review is to present the beneficial effects of saffron and its main constituent molecules on neuropsychiatric diseases (depression, anxiety and schizophrenia) as well as on the most frequent age-related diseases (cardiovascular, ocular and neurodegenerative diseases, as well as sarcopenia). Overall, the phytochemical profile of saffron confers many beneficial virtues on human health and, in particular, on the prevention of age-related diseases, which is a major asset reinforcing the interest for this medicinal plant.

Mitochondria are multifunctional organelles that participate in a wide range of metabolic processes, including energy production and biomolecule synthesis. The morphology and distribution of intracellular mitochondria change dynamically, reflecting a cell’s metabolic activity. Oxidative stress is defined as a mismatch between the body’s ability to neutralise and eliminate reactive oxygen and nitrogen species (ROS and RNS). A determination of mitochondria failure in increasing oxidative stress, as well as its implications in neurodegenerative illnesses and apoptosis, is a significant developmental process of focus in this review. The neuroprotective effects of bioactive compounds linked to neuronal regulation, as well as related neuronal development abnormalities, will be investigated. In conclusion, the study of secondary components and the use of mitochondrial features in the analysis of various neurodevelopmental diseases has enabled the development of a new class of mitochondrial-targeted pharmaceuticals capable of alleviating neurodegenerative disease states and enabling longevity and healthy ageing for the vast majority of people.

Coronavirus illness (COVID-19) is an infectious pathology generated by intense severe respiratory syndrome coronavirus 2 (SARS-CoV-2). This infectious disease has emerged in 2019. The COVID-19-associated pandemic has considerably affected the way of life and the economy in the world. It is consequently crucial to find solutions allowing remedying or alleviating the effects of this infectious disease. Natural products have been in perpetual application from immemorial time given that they are attested to be efficient towards several illnesses without major side effects. Various studies have shown that plant extracts or purified molecules have a promising inhibiting impact towards coronavirus. In addition, it is substantial to understand the characteristics, susceptibility and impact of diet on patients infected with COVID-19. In this review, we recapitulate the influence of extracts or pure molecules from medicinal plants on COVID-19. We approach the possibilities of plant treatment/co-treatment and feeding applied to COVID-19. We also show coronavirus susceptibility and complications associated with nutrient deficiencies and then discuss the major food groups efficient on COVID-19 pathogenesis. Then, we covered emerging technologies using plant-based SARS-CoV-2 vaccine. We conclude by giving nutrient and plants curative therapy recommendations which are of potential interest in the COVID-19 infection and could pave the way for pharmacological treatments or co-treatments of COVID-19.

Background: This study aims to examine the potential neuroprotective effects of flaxseed oil (FSO) on the brain activity of rat pups sired by females intoxicated with aluminum (Al). The brain is known to be particularly vulnerable to the deleterious effects of aluminum, which promotes oxidative stress and neuroinflammation. FSO is a rich source of omega-3 (ω-3) fatty acids (FA), essential components of neuronal membranes and neurotransmission. Methods: After collecting 36 offspring aged three weeks from a control group and an intoxicated female group that received an intraperitoneal injection of aluminum chloride (AlCl3) (75 mg/kg body weight, twice a week) in the morning for 30 days. Six subgroups of pup rats for each group (n = 6) were used, with control groups having free access to food and water and two experimental groups receiving low and high doses of FSO administered by gavage (0.5 and 2 mL/kg b.wt.). An intoxicated group was also tested with rats receiving low and high FSO concentrations and free access to water. The study appears to focus on the effect of omega-3 in the FSO on the brain's development of young rats a neurobehavioral study was carried out, followed by estimation of prooxidant parameters and neurotransmitter activity of the brain, and a lipid composition was carried out on the brain membrane by gas chromatography-mass spectrometry (GC-MS) analysis. Results: The FA profile of FSO revealed domination by ω-3 type (86.9%). The 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging capability was found at half maximal inhibitory concentration (IC₅₀) values of 18.12 g/mL. Neurobehavioral experiments showed significant hyperactivity and memory loss in intoxicated young rats, with decreased levels of lipid peroxidation (LPO) and nitric oxide (NO) and a significant increase in acetylcholinesterase (AChE) activity in the brain. However, ameliorative results were found in both concentrations of FSO administration when compared with intoxicated groups. GC-MS analysis of the brain membrane FA profile revealed the presence of elaidic acid in both the AL and AL+FSO. Neurobehavioral experiments showed significant hyperactivity and memory loss in intoxicated young rats, with decreased levels of lipid peroxidation (LPO) and nitric oxide (NO) and a significant increase in acetylcholinesterase (AChE) activity in the brain. However, ameliorative results were found in both concentrations of FSO administration when compared with intoxicated groups. GC-MS analysis of the brain membrane FA profile revealed the presence of elaidic acid in both the AL and AL+FSO” groups. In contrast, only the AL+FSO' group had eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) areas. Conclusions: Our results suggest that FSO supplementation at low concentrations has neuroprotective effects on developing rat brains, correcting and ameliorating the abnormalities brought on by embryo/fetal aluminum chloride toxicity.

Jujube (Ziziphus jujuba) has a long history of use in traditional medicine. It has many pharmacological properties, including neuroprotective, antioxidative, hepatoprotective, anti-cancer, anti-inflammatory, and immunomodulatory. Thus, this study aimed to evaluate the anti-inflammatory activity of the ethanolic extract of Ziziphus (EEZ) fruit and its wound-healing effect. The anti-inflammatory activity of EEZ was assessed in vivo by carrageenan-induced paw edema test. NIH-3T3 mouse embryonic fibroblast cells were used to evaluate the wound healing effect of EEZ. The effect of the extract on wound-healing was examined by in vitro scratch test. Also, the level of C-reactive protein (CRP) in the serum of rats was determined using the CRP latex test kit. The ethanol extract of jujube fruit induced wound closure in NIH-3T3 fibroblast cells for 18 h (88.5%) at 1 μ\umu g/mL concentration. Also, EEZ significantly inhibited carrageenan-induced edema in rat paws. However, a statistically significant decrease in CRP levels was observed in rats pre-treated with EEZ. As a result, Z. jujuba fruit extract had anti-inflammatory and wound healing effects, which might be strongly related to its phytochemical composition.