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Gallic acid (GA) is a phenolic molecule found naturally in a wide range of fruits as well as in medicinal plants. It has many health benefits due to its antioxidant properties. This study focused on finding out the neurobiological effects and mechanisms of GA using published data from reputed databases. For this, data were collected from various sources, such as PubMed/Medline, Science Direct, Scopus, Google Scholar, SpringerLink, and Web of Science. The findings suggest that GA can be used to manage several neurological diseases and disorders, such as Alzheimer’s disease, Parkinson’s disease, strokes, sedation, depression, psychosis, neuropathic pain, anxiety, and memory loss, as well as neuroinflammation. According to database reports and this current literature-based study, GA may be considered one of the potential lead compounds to treat neurological diseases and disorders. More preclinical and clinical studies are required to establish GA as a neuroprotective drug.

Fruits and vegetables are used not only for nutritional purposes but also as therapeutics to treat various diseases and ailments. These food items are prominent sources of phytochemicals that exhibit chemopreventive and therapeutic effects against several diseases. Hirsutine (HSN) is a naturally occurring indole alkaloid found in various Uncaria species and has a multitude of therapeutic benefits. It is found in foodstuffs such as fish, seafood, meat, poultry, dairy, and some grain products among other things. In addition, it is present in fruits and vegetables including corn, cauliflower, mushrooms, potatoes, bamboo shoots, bananas, cantaloupe, and citrus fruits. The primary emphasis of this study is to summarize the pharmacological activities and the underlying mechanisms of HSN against different diseases, as well as the biopharmaceutical features. For this, data were collected (up to date as of 1 July 2023) from various reliable and authentic literature by searching different academic search engines, including PubMed, Springer Link, Scopus, Wiley Online, Web of Science, ScienceDirect, and Google Scholar. Findings indicated that HSN exerts several effects in various preclinical and pharmacological experimental systems. It exhibits anti-inflammatory, antiviral, anti-diabetic, and antioxidant activities with beneficial effects in neurological and cardiovascular diseases. Our findings also indicate that HSN exerts promising anticancer potentials via several molecular mechanisms, including apoptotic cell death, induction of oxidative stress, cytotoxic effect, anti-proliferative effect, genotoxic effect, and inhibition of cancer cell migration and invasion against various cancers such as lung, breast, and antitumor effects in human T-cell leukemia. Taken all together, findings from this study show that HSN can be a promising therapeutic agent to treat various diseases including cancer.

Sedatives promote calmness or sleepiness during surgery or severely stressful events. In addition, depression is a mental health issue that negatively affects emotional well-being. A group of drugs called anti-depressants is used to treat major depressive illnesses. The aim of the present work was to evaluate the effects of quercetin (QUR) and linalool (LIN) on thiopental sodium (TS)-induced sleeping mice and to investigate the combined effects of these compounds using a conventional co-treatment strategy and in silico studies. For this, the TS-induced sleeping mice were monitored to compare the occurrence, latency, and duration of the sleep-in response to QUR (10, 25, 50 mg/kg), LIN (10, 25, 50 mg/kg), and diazepam (DZP, 3 mg/kg, i.p.). Moreover, an in silico investigation was undertaken to assess this study’s putative modulatory sedation mechanism. For this, we observed the ability of test and standard medications to interact with various gamma-aminobutyric acid A receptor (GABAA) subunits. Results revealed that QUR and LIN cause dose-dependent antidepressant-like and sedative-like effects in animals, respectively. In addition, QUR-50 mg/kg and LIN-50 mg/kg and/or DZP-3 mg/kg combined were associated with an increased latency period and reduced sleeping times in animals. Results of the in silico studies demonstrated that QUR has better binding interaction with GABAA α3, β1, and γ2 subunits when compared with DZP, whereas LIN showed moderate affinity with the GABAA receptor. Taken together, the sleep duration of LIN and DZP is opposed by QUR in TS-induced sleeping mice, suggesting that QUR may be responsible for providing sedation-antagonizing effects through the GABAergic interaction pathway.

Scientific evidence suggests that quercetin (QUR) has anxiolytic-like effects in experimental animals. However, the mechanism of action responsible for its anxiolytic-like effects is yet to be discovered. The goal of this research is to assess QUR’s anxiolytic effects in mouse models to explicate the possible mechanism of action. After acute intraperitoneal (i.p.) treatment with QUR at a dose of 50 mg/kg (i.p.), behavioral models of open-field, hole board, swing box, and light–dark tests were performed. QUR was combined with a GABAergic agonist (diazepam) and/or antagonist (flumazenil) group. Furthermore, in silico analysis was also conducted to observe the interaction of QUR and GABA (α5), GABA (β1), and GABA (β2) receptors. In the experimental animal model, QUR had an anxiolytic-like effect. QUR, when combined with diazepam (2 mg/kg, i.p.), drastically potentiated an anxiolytic effect of diazepam. QUR is a more highly competitive ligand for the benzodiazepine recognition site that can displace flumazenil (2.5 mg/kg, i.p.). In all the test models, QUR acted similar to diazepam, with enhanced effects of the standard anxiolytic drug, which were reversed by pre-treatment with flumazenil. QUR showed the best interaction with the GABA (α5) receptor compared to the GABA (β1) and GABA (β2) receptors. In conclusion, QUR may exert an anxiolytic-like effect on mice, probably through the GABA-receptor-interacting pathway.

The aim of this study is to assess the sedative impact of palmatine chloride (PME) in thiopental sodium-induced sleeping chicks and its underlying molecular mechanism by using in vivo and in silico approaches. Chicks received PME per orally (p.o.) at doses of 1.25, 2.5, and 5 mg/kg per body weight (b.w.), while diazepam (DZP) (2 mg/kg) served as a positive control and vehicle as a negative control. For the purpose of evaluating the experimental compounds synergistic or antagonistic effects, a combination of PME and DZP was administered to the chicks. After thirty minutes, thiopental sodium (40 mg/kg, intraperitoneal (i.p.)) was administered to induce sleep, and latency to sleep onset and sleep duration were measured. In vivo results showed that PME reduced sleep latency and prolonged sleep duration in a dose-dependent manner, with the combination therapy producing a significant enhancement of these effects. In silico docking revealed PME binding to gamma-aminobutyric acid A (GABA A ) receptor α1 and β2 subunits (–7.2 kcal/mol) with shared amino acids. Pharmacokinetic and toxicity analyses suggested favorable drug-like properties. These results indicate PME’s sedative potential, alone or with DZP, likely via GABAergic modulation, warranting further functional validation.

Frequent use of various food processing chemical agents sometimes causes damage to our bodies by inducing cytotoxicity, genotoxicity, and mutagenesis. In Bangladesh, among various chemical agents, formalin, saccharin, and urea are vastly used for processing foodstuffs by industry and local people. This study is focused to assess the toxic effects of formalin, saccharin, and urea on the popularly used eukaryotic test model, Allium cepa L. The assay was carried out by exposing different concentrations of test samples to A. cepa at 24, 48, and 72 h, where distilled water and CuSO4·5H2O (0.6 µg/mL) were utilized as the vehicle and positive control, respectively. The root length of the onions was measured in mm, and the results propose that all the chemical agents demonstrated toxicity in onions in a concentration- and exposure-time-dependent manner. The highest root length was examined at the lower concentrations, and with the increase in the concentration of the test sample and exposure time, the RG (root growth) was inhibited due to the deposition of chemicals and hampering of cell division in the root meristematic region of A. cepa. All the chemical agents also revealed a concentration- and time-dependent adaptive effect up to 72 h inspection of 24 h and a depletion of % root growth at 72 h inspection of 48 h. Our study suggests that sufficient precautions should be confirmed during its industrial and traditional usage as a toxicological response to the chemical agents observed in the A. cepa assay.

This research is designed to investigate the sedative effects of naringenin (NAR) and diazepam against thiopental sodium‐induced sleeping mice. NAR (5 and 10 mg kg), diazepam (DZP) (2 mg kg), flumazenil (FLN) (0.1 mg kg), and their combinations are administered intraperitoneally to mice. After 30 min, sleep is induced with intraperitoneal thiopental sodium (20 mg kg), and sleep latency and duration are measured. In silico analysis investigates the role of GABA receptors. NAR significantly reduces sleep latency and prolongs sleep duration in a dose‐dependent manner, with the combination of NAR‐10 and DZP‐2 showing a synergistic effect. The combination of the antagonist (FLN) (NAR‐10 and FLN‐0.1) indicates that latency increases and sleep duration decreases compared to NAR‐10 alone. Furthermore, in silico docking studies corroborates these results, demonstrating a significant binding affinity of NAR (−8.3 kcal mol), which is comparable to the standard ligand DZP (−8.7 kcal mol) and FLN (−7.0 kcal mol) for the GABAA (6X3X) receptor, indicating a GABAergic mechanism. Pharmacokinetics and toxicity evaluations confirm NAR's potential as a safe therapeutic agent, with a high LD50 (2000 mg kg) and minimal toxicity. These findings highlight NAR's potential as a GABAergic sedative agent, requiring further research before being used clinically to treat sleep disorders. The study investigates the sedative potential of naringenin (NAR) through in vivo and in silico approaches. NAR significantly enhances sleep duration and reduces latency in mice, especially when combined with diazepam. Molecular docking shows strong binding to GABAA receptors, suggesting a GABAergic mechanism. Pharmacokinetic and toxicity analyses support NAR's safety and drug‐likeness as a potential sedative agent.

The demand for medicinal plants and their derived substances is increasing day by day due to their relevance in the context of drug discovery and development. The goal of this investigation is to assess the pharmacological and phytochemical potentials of the grossly underexplored Antidesma montanum Blume (Family: Phyllanthaceae). The methanolic extract of the leave of this plant was fractionated and then followed by initial screening of phytochemical. The investigation of the pharmacological potential, which includes antioxidant, antidiarrheal, anti-inflammatory, analgesic, anti-pyretic, and anxiolytic evaluations, was accomplished using an in vitro free radical scavenging assay with 2,2-diphenyl-1-picrylhydrazyl (DPPH), castor oil-induced diarrheal test, egg albumin test, acetic acid-induced writhing model, brewer’s yeast induced fever test, swing test, open field, and light-dark test, respectively. The investigation o phytochemicals proposes that the methanol extract of A. montanum possesses flavonoids, tannins, terpenoids, saponins, amino acids, fixed oils, and sterols. Pharmacological evaluation suggests that A. montanum possesses significant antioxidant, anti-diarrheal, anti-inflammatory, and analgesic effects. The methanol and chloroform fractions exhibited better DPPH radical scavenging activities with an IC50: 103 ± 0.05 and 108.7 ± 0.05 µg/ml, respectively. The methanol and chloroform fractions also showed anti-inflammatory capacities in the egg albumin (IC50 values: 89.10 ± 0.07 and 92.85 ± 0.07 µg/ml, respectively) model. The plant also showed anti-pyretic and anxiolytic activities in a dose-dependent manner. One of the possible sources of phytotherapeutic lead compounds is A. montanum. To extract and analyze the key bioactive components of this essential therapeutic plant, more research is required.

The soy isoflavone daidzin (DZN) has been considered a hopeful bioactive compound having diverse biological activities, including anxiolytic, memory-enhancing, and antiepileptic effects, in experimental animals. However, its sedative and hypnotic effects are yet to be discovered. This study aimed to evaluate its sedative/hypnotic effect on Swiss mice. Additionally, in silico studies were also performed to see the possible molecular mechanisms behind the tested neurological effect. For this, male Swiss albino mice were treated with DZN (5, 10, or 20 mg/kg) intraperitoneally (i.p.) with or without the standard GABAergic medication diazepam (DZP) and/or flumazenil (FLU) and checked for the onset and duration of sleeping time using thiopental sodium-induced as well as DZP-induced sleeping tests. A molecular docking study was also performed to check its interaction capacity with the α1 and β2 subunits of the GABAA receptor. Findings suggest that DZN dose-dependently and significantly reduced the latency while increasing the duration of sleep in animals. In combination therapy, DZN shows synergistic effects with the DZP-2 and DZP-2 + FLU-0.01 groups, resulting in significantly (p < 0.05) reduced latency and increased sleep duration. Further, molecular docking studies demonstrate that DZN has a strong binding affinity of − 7.2 kcal/mol, which is closer to the standard ligand DZP (− 8.3 kcal/mol) against the GABAA (6X3X) receptor. Molecular dynamic simulations indicated stability and similar binding locations for DZP and DZN with 6X3X. In conclusion, DZN shows sedative effects on Swiss mice, possibly through the GABAA receptor interaction pathway.

Background Numerous studies suggest that morellic acid (MOR), highly available in Garcinia plants, has different physiological activities, including anti‐cancer, anti‐oxidant, and anti‐microbial activity. Aim In this investigation, we aimed to demonstrate the anxiolytic activity, along with the mechanism behind this activity of MOR, using in vivo and in silico studies. Methods For this, we used different doses of MOR (5 and 10 mg/kg) and administered this drug intraperitoneally to Swiss albino mice (male and female). Diazepam (DZP), a positive allosteric modulator of the GABAA receptor, was used as a positive control at a dose of 2 mg/kg (i.p), and vehicle was used as a control group. In this test, various test protocols are used to assess the behavioral patterns of mice, including swing, hole cross, light–dark testing, and open field testing. Results This investigation revealed that MOR remarkably reduced the locomotor activity of mice in a dose‐dependent manner and produced calming behaviors like DZP. However, the findings showed that the combination of MOR and DZP synergistically reduced the locomotion of mice compared to the single therapy. On the other hand, from the computational study, the result demonstrated that MOR exhibited the highest binding scores (−9.2 kcal/mol) towards the GABAA receptor α3 subunit and −7.6 kcal/mol towards the GABAA α2 receptor. Whereas, DZP showed −6.6 and −7.3 kcal/mol docking affinity and FLU exerted −6.2 and −6.3 kcal/mol docking scores towards the GABAA receptor α2 and α3 subunits, respectively. The ligand interacted with the receptor by forming different hydrogen and hydrophobic bonds. Conclusion However, it is recommended that more precise and comprehensive preclinical investigations be required to demonstrate the exact mechanism behind the anxiolytic effects and conduct clinical trials to determine efficacy and safety. Morellic acid (MOR) alone, dose‐dependently, and with the standard drug diazepam (DZP), significantly (p < 0.05) reduced the locomotive activities of Swiss mice. Additionally, the computational studies suggest that MOR exhibited the highest binding scores of −9.2 and −7.6 kcal/mol towards the GABAA receptor α3 and α2 subunits, respectively.