Quercetin (3,3',4',5,7-pentahydroxyflavone) is found in vegetables and fruits. It is one of the major flavonoids that is part of human diets. Quercetin has several pharmacological effects in the nervous system as a neuroprotective agent. In this review, we summarize the research on quercetin and its role in memory in both animals and humans. Articles were chosen from the Scopus, PubMed, and Web of Science databases. In this review, we describe and summarize the importance of quercetin's presence in the body, particularly in the brain; its kinetics, including its absorption, metabolism, distribution, and excretion; its behavioral effects; and some of the possible mechanisms of action of quercetin on memory in different animal models. Several important pathways that may be involved in the processes of learning and memory, long-term potentiation, and cognition may be impaired during neurological diseases or other medical conditions. As dietary quercetin is important, provision of its best formulation for delivery to the brain as a nutraceutical and in clinical translational research for the prevention or treatment of Alzheimer's disease and other types of dementia is necessary.

Vitexin is an apigenin flavone glycoside found in food and medicinal plants. It has a variety of pharmacological effects, including antioxidant, anti‐inflammatory, anticancer, antinociceptive, and neuroprotective effects. This review study summarizes all the protective effects of vitexin as an antioxidant against reactive oxygen species, lipid peroxidation, and other oxidative damages in a variety of oxidative stress‐related diseases, including seizure, memory impairment, cerebral ischemia, neurotoxicity, myocardial and respiratory injury, and metabolic dysfunction, with possible molecular and cellular mechanisms. This review describes any activation or inhibition of the signaling pathways that depend on the antioxidant activity of vitexin. More basic research is needed on the antioxidative effects of vitexin in vivo, and carrying out clinical trials for the treatment of oxidative stress‐related diseases is also recommended.

Coronavirus disease 2019 (COVID‐19) is a viral disease caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). The disease was first reported in December 2019 in Wuhan, China, but now more than 200 countries have been affected and the coronavirus pandemic is still ongoing. The severity of COVID‐19 symptoms can range from mild to severe. FDA approved remdesivir as a treatment of COVID‐19 so far. Various clinical trials are underway to find an effective method to treat patients with COVID‐19. This review aimed at summarizing 219 registered clinical trials in the ClinicalTrials.gov database with possible mechanisms, and novel findings of them, and other recent publications related to COVID‐19. According to our analyses, various treatment approaches and drugs are being investigated to find an effective drug to cure COVID‐19 and among all strategies, three important mechanisms are suggested to be important against COVID‐19 including antiviral, anti‐inflammatory, and immunomodulatory properties. Our review can help future studies get on the way to finding an effective drug for COVID‐19 treatment by providing ideas for similar researches.

No abstract

No abstract

Potassium ion (K+) channels are pore-forming transmembrane proteins that control the transport of K+ ions. Medicinal plants are widely used as complementary therapies for several disorders. Studies have shown that the modulation of K+ channels is most likely involved in various pharmacological effects of medicinal plants. This review aimed to evaluate the modulatory effects of medicinal plants and their active constituents on K+ channels under pathological conditions. This systematic review was prepared according to the Preferred Reporting Items for the Systematic Reviews and Meta-analyses (PRISMA) 2020 guideline. Four databases, including PubMed, Web of Science, embase, and Scopus, were searched. We identified 687 studies from these databases, from which we selected 13 in vivo studies for the review by using the Population, Intervention, Comparison, Outcomes, Study (PICOS) tool. The results of the 13 selected studies showed a modulatory effect of medicinal plants or their active constituents on ATP-sensitive potassium channels (KATP), and small (SKCa) and large (BKCa) conductance calcium-activated K+ channels in several pathological conditions such as nociception, brain ischemia, seizure, diabetes, gastric ulcer, myocardial ischemia-reperfusion, and hypertension via possible involvement of the nitric oxide/cyclic GMP pathway and protein kinase. K+ channels should be considered as significant therapeutic milestones in the treatment of several diseases. We believe that understanding the mechanism behind the interaction of medicinal plants with K+ channels can facilitate drug development for the treatment of various K+ channel-related disorders.

Recent studies have indicated that dysfunction of gut microbiota, living microorganisms of the digestive tract, plays a role in the pathogenesis of neurodegenerative disorders, indicating the valuable impact of probiotics as a potential preventive or therapeutic strategy. Saccharomyces boulardii is a yeast probiotic with beneficial effects on various disorders, ranging from inflammatory gastrointestinal diseases to brain and behavioral disorders. Herein, we examined the effect of S. boulardii on memory impairment induced by lipopolysaccharide (LPS) in Wistar rats. Four groups of rats were used in this study (N = 10): (1) control [Cnt], (2) LPS, (3) LPS + S. boulardii [LPS + S], and (4) S. boulardii [S]. Animals were orally administered S. boulardii (250 mg/ rat) or saline by gavage for 4 weeks. From the 14th day of the study, animals were administered intraperitoneal LPS (0.25 mg/kg/ day) or saline for 9 days. We assessed memory impairment, neuroinflammation, and amyloid-β deposition. S. boulardii ameliorated LPS-induced memory dysfunction. We observed that S. boulardii significantly reduced the elevated levels of serum interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, as well as hippocampal levels of NLRP3 and caspase-1 in the LPS model. Moreover, S. boulardii alleviated amyloid-β deposition in the rat hippocampus. Collectively, our findings indicated that S. boulardii could inhibit memory impairment, neuroinflammation, and amyloid-β accumulation induced by LPS, possibly by modifying the gut microbiota.

No abstract