Search Results (112)

Traumatic brain injury (TBI) is a major global health problem and a leading cause of long-term neurological disability. TBI produces a spectrum of persistent symptoms, including cognitive impairment, mood and behavioral disturbances, sleep disruption, fatigue, and autonomic dysregulation. Chronic pain is among the most debilitating sequelae, affecting physical, emotional, and social functioning. The etiology of post-TBI pain is multifactorial, arising from initial structural and biochemical injury to the nervous system, maladaptive neuroplastic changes, neuroinflammation, and psychological comorbidities that amplify pain perception and chronicity. This review explores the complex pathophysiology of post-TBI pain and outlines a multidisciplinary framework for management. Pain syndromes are classified according to the International Association for the Study of Pain’s mechanistic framework as nociceptive pain (resulting from tissue injury and inflammation), neuropathic pain (due to lesion or disease of the somatosensory nervous system), and nociplastic pain (arising from altered nociceptive processing without clear evidence of tissue or nerve damage). Many patients exhibit mixed pain phenotypes driven by neuroinflammation and central sensitization. Pharmacologic approaches, including anti-inflammatory agents, anticonvulsants, and antidepressants, require cautious titration due to TBI-related comorbidities. Equally essential are non-pharmacologic strategies such as physical and occupational therapy, cognitive behavioral therapy, and neuromodulation techniques, which target both biomechanical and psychosocial contributors. Emerging innovations, machine learning for prognostication, blood biomarkers for structural injury, and neuro-reparative agents, represent the next frontier in personalized management. Effective care for post-TBI pain requires an integrated strategy that combines mechanistic classification, multidisciplinary treatments, and advancing diagnostic technologies. Full article

Background: Severe traumatic brain injury (TBI) often leads to elevated intracranial pressure (ICP) that requires aggressive management. Inducing burst suppression with deep sedation is an established therapy for refractory intracranial hypertension. Traditionally, barbiturate coma has been used to achieve burst-suppression EEG in TBI patients, but alternative sedative agents (propofol, midazolam, ketamine, dexmedetomidine) are increasingly utilized in modern neurocritical care. This review compares barbiturates with these alternatives for inducing burst suppression in adult TBI, focusing on protocols, mechanisms, efficacy in controlling ICP, safety profiles, and impacts on neurological outcomes. Methods: A search of the literature was performed, including clinical trials, observational studies, and guidelines on deep sedation for ICP control in adult TBI. Studies comparing high-dose barbiturates to other sedatives (propofol, midazolam, ketamine, dexmedetomidine) in the context of burst suppression or severe TBI management were included. Data on sedative protocols (dosing and EEG targets), mechanisms of action, ICP-lowering efficacy, complications, and patient outcomes were extracted and analyzed qualitatively. Results: High-dose barbiturates (e.g., pentobarbital or thiopental) and propofol are both effective at inducing burst-suppression EEG and reducing ICP via cerebral metabolic suppression. Barbiturate coma remains a third-tier intervention reserved for ICP refractory to other treatments. Propofol infusion has become first-line for routine ICP control due to rapid titratability and shorter half-life, though it can also achieve burst suppression at high doses. Midazolam infusions provide sedation and seizure prophylaxis but yield less metabolic suppression and ICP reduction compared to barbiturates or propofol, and are associated with longer ventilation duration and delirium. Ketamine, once avoided for fear of raising ICP, has shown neutral or lowering effects on ICP when used in ventilated TBI patients, thanks to its analgesic properties and maintenance of blood pressure; however, ketamine alone does not reliably produce burst-suppression patterns. Dexmedetomidine offers sedative and anti-delirium benefits with minimal respiratory depression, but it is generally insufficient for deep burst-suppressive sedation and has only a modest effect on ICP. In comparative clinical evidence, propofol and barbiturates both effectively lower ICP, but neither has demonstrated clear improvement in long-term neurological outcome when used prophylactically. Early routine use of barbiturate coma may increase complications (hypotension, immunosuppression), and thus, current practice restricts it to refractory cases. Modern sedation protocols emphasize using the minimal necessary sedation to maintain ICP < 22 mmHg, with continuous EEG monitoring to titrate therapy to a burst-suppression target (commonly 2–5 bursts per minute) when deep coma is employed. Conclusions: In adult TBI patients with intracranial hypertension, propofol-based sedation is favored for first-line ICP control and can achieve burst suppression if needed, whereas high-dose barbiturates are reserved for ICP crises unresponsive to standard measures. Compared to barbiturates, alternative agents (propofol, midazolam, ketamine, dexmedetomidine) offer differing advantages: propofol provides potent, fast-acting metabolic suppression; midazolam adds anticonvulsant sedation for prolonged use at the cost of slower wake-up; ketamine supports hemodynamics and analgesia; dexmedetomidine aids lighter sedation and delirium control. The choice of agent is guided by the clinical scenario, balancing ICP reduction needs against side effect profiles. While all sedatives can transiently reduce ICP, careful monitoring and a tiered therapy approach are essential, as no sedative has conclusively improved long-term neurological outcomes in TBI. EEG monitoring for burst suppression and meticulous titration is required when employing barbiturate or propofol coma. Ongoing research into optimal combinations and protocols may further refine sedation strategies to improve safety and outcomes in severe TBI. Full article

Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent and debilitating urological condition affecting approximately 2–10% of men globally, with a substantial impact on quality of life, productivity, and healthcare utilization. Despite the availability of multiple pharmacological options, their comparative efficacy remains uncertain. This meta-analysis evaluated the efficacy of pharmacological interventions for CP/CPPS based on the NIH-Chronic Prostatitis Symptom Index (NIH-CPSI). Methods: A systematic search of PubMed, Scopus, ScienceDirect, and Google Scholar was conducted from database inception to January 2025 for randomized controlled trials (RCTs) comparing pharmacological therapies with placebo. The primary outcome was a mean reduction in NIH-CPSI total score, with a clinically meaningful improvement defined as a ≥6-point reduction. Pooled mean differences (MDs) with 95% confidence intervals (CIs) were calculated using random-effects models, and risk of bias was assessed using the Cochrane Risk of Bias tool. The certainty of evidence was evaluated using the GRADE approach. Results: Alpha-blockers demonstrated the most consistent benefit (MD: −5.13; 95% CI: −6.87 to −3.39; Low certainty), followed by Traditional Chinese Medicine (TCM) (MD: −3.14; 95% CI: −5.38 to −0.90; Low certainty) and analgesics (MD: −2.47; 95% CI: −4.24 to −0.70; Low certainty). In contrast, antibiotics (MD: −2.45; 95% CI: −5.53 to 0.64; Very Low certainty), pollen extracts (MD: −2.56; 95% CI: −10.83 to 5.71; Very Low certainty), and other agents such as botulinum toxin A and anticonvulsants (MD: −6.94; 95% CI: −19.79 to 5.91; Very Low certainty) did not achieve statistical significance. The certainty for all interventions was downgraded from High due to risk of bias and substantial heterogeneity (I² > 75%). Funnel plot asymmetry suggested potential publication bias; however, Egger’s test did not confirm statistical significance (p = 0.626). Conclusions: Among available pharmacological options, alpha-blockers and TCM provide the most reliable symptom improvement in men with CP/CPPS, while analgesics offer modest benefit. Antibiotics, pollen extracts, and other agents show inconsistent or non-significant effects. The high heterogeneity and generally low certainty of evidence reflect variability in study quality and populations, underscoring the need for rigorously designed, standardized future trials to guide patient-centered therapy selection. Full article

An important class of heterocyclic chemicals are pyrimidine derivatives, providing a wide spectrum of biological activities in the form of antibacterial, antifungal, anti-HIV, anti-hypertensive, anti-inflammatory, anti-cancer, anti-convulsant, anti-depressant, and anti-tuberculosis acts. The chalcone group also has a significant impact on the pharmacological activity of compounds used for therapeutic purposes, acting as antibiotics, antioxidants, and anti-cancer agents. In this research, the derivative 1-(4-(4-(dimethylamino)-2-hydroxyphenyl)-6-methyl-2-thioxo-1,2,3,4-tetrahydropyrimidin-5-yl) ethan-1-one was prepared. From the reaction of thiourea with acetyl acetone and 4-dimethylamino-2-hydroxybenzaldehyde, the product was then reacted with some aldehydes in the presence of ethanol and a little hydrochloric acid as a catalyst, after which the product was reacted with some aldehydes to prepare chalcone. The prepared derivatives were characterized by FT-IR, ¹H-NMR, and ¹³C-NMR spectra, the melting point was measured, and the biological activity of the prepared compounds as antibacterials was studied. Molecular docking also determined the anti-breast cancer potential of these derivatives by docking the prepared derivatives with PDB:3eqm protein using the MOE 2015.10 program. The prepared compounds showed good efficacy as antibacterial agents against Gram-negative bacteria at diluted concentrations. Additionally, molecular docking studies demonstrated good efficacy of some derivatives as breast cancer inhibitors, along with a study of the toxic effects of the prepared compounds using the ProTox 3.0 program prediction of toxicity of chemicals. Full article

This review focuses on hydrogel-based systems specifically designed for non-opioid analgesics, aiming to improve efficacy, safety, and translational applicability. The opioid crisis has intensified the need for safer and more effective alternatives in pain management. Non-opioid analgesics including NSAIDs, acetaminophen, gabapentinoids, antidepressants, anticonvulsants, NMDA receptor antagonists, topical agents, and cannabinoids offer promising options but are limited by rapid clearance, short half-lives, and off-target effects. Hydrogel-based drug delivery systems present a novel solution by enabling controlled, localized, and sustained release of analgesics, thus improving therapeutic efficacy and minimizing systemic toxicity. Advances in stimulus-responsive, self-healing, mechanically robust, and hybrid or nanocomposite hydrogels have broadened their biomedical applications and clinical relevance. This narrative review summarizes key hydrogel technologies and their integration with non-opioid analgesic agents. We explore encapsulation strategies, drug release mechanisms, and emerging clinical data, while also addressing critical challenges such as biocompatibility, mechanical durability, and translational scalability. Interdisciplinary collaboration between material scientists, clinicians, and regulatory experts is essential to advance hydrogel-based therapies from bench to bedside. Overall, hydrogel platforms hold transformative potential in optimizing non-opioid analgesic delivery and redefining the future of pain management. Full article

Background: Epilepsy is a high-burden neurological disorder worldwide, and several sedative drugs are used as therapy. Topiramate is among the more recent drugs shown to be effective in some patients, although its benefits are limited. Two carbohydrate derivatives, FB1 (from D-fructose) and AB1 (from D-arabinose), as well as phenylboronic acid, were recently reported as sedative and safe agents in mice. Their sedative properties and structural similarity to topiramate suggest potential antiseizure activity. Objective: The objective of this study was to evaluate the antiseizure potential of FB1 and AB1. Methods: Boron-containing compounds were administered to mice with seizures induced by pentylenetetrazol (a GABA-A receptor antagonist), 4-aminopyridine (a non-selective K⁺ channel blocker), or pilocarpine (a muscarinic agonist) to assess efficacy across models and explore potential mechanisms of action. Neuronal and glial toxicity was evaluated both in vitro and in vivo. Results: AB1 reduced seizure activity after intraperitoneal administration, whereas FB1 did not exhibit anticonvulsant effects, although it modified motor performance and limited neuronal loss. The effect of AB1 was comparable to that of topiramate across all three seizure models. Docking studies suggested that these compounds can interact with GABA-A (chloride), NMDA (glutamate), calcium, and potassium channels. Toxicity assays indicated that the concentrations required to affect neurons or glial cells were ≥300 µM, supporting the safety of these compounds. Conclusions: This preliminary evaluation demonstrates the antiseizure potential of AB1. Further experimental studies are needed to clearly establish its mechanism(s) of action. Full article

Background: Hyponatremia (serum sodium concentration < 135 mmol/L) represents the most common electrolyte disturbance in clinical practice, particularly among high-risk populations such as older adults. Its severity ranges from moderately severe to life-threatening symptoms, contributing to increased mortality. Its etiology is widely heterogeneous and leads to different classifications according to volume status such as hypovolemic, euvolemic and hypervolemic hyponatremia. Drug-induced hyponatremia presents itself as one of the most prevalent but frequently overlooked causes, since many confounding factors like associated comorbidities and polypharmacy complicate the identification of specific medicines as the main offenders. Objectives: This narrative review was performed to provide a comprehensive analysis on drug-induced hyponatremia, focusing not only on the underlying pharmacological mechanisms, but also on management strategies in clinical practice. Methods: A narrative literature review was conducted using PubMed, Science Direct and Google Scholar. Results: This narrative review focused not only on the most common drug classes to induce hyponatremia through different mechanisms, including diuretics, antidepressants, anticonvulsants, and antipsychotics, but also on other pharmacological classes, that, although to a lesser extent, might also be associated with decreasing serum sodium levels (antineoplastic and immunomodulating agents, drugs acting on digestive and locomotor systems, anti-infective drugs, endocrine diseases drugs, among others). It also explores recommendations on the management of drug-induced hyponatremia and it emphasizes the role of healthcare providers in addressing this electrolyte disorder. Conclusions: As drug-induced hyponatremia poses significant challenges in clinical practice, understanding its mechanisms, coupled with effective management strategies, can enhance patient safety. Full article

Quinazolin-4(3H)-ones are nitrogen heterocycles that have attracted considerable interest over many years due to their important biological and pharmacological properties. It has been shown that quinazolinone derivatives exhibit, e.g., analgesic, anti-inflammatory, antibacterial, anticonvulsant, antifungal, and antitumor activities. Some of these compounds have found applications in medicine; for instance, Zydelig (Idelalisib) has been approved for the treatment of several types of blood cancers. Furthermore, the quinazolinone skeleton is an important structural moiety present in many naturally occurring alkaloids, such as Febrifugine, a potent anti-malarial agent. To date, numerous synthetic methods have been developed for the synthesis of quinazolinone derivatives. Among them, multicomponent reactions (MCRs) have emerged as a powerful tool, allowing for the rapid and straightforward construction of the quinazolinone scaffold from readily available substrates. This review article presents a concise overview of selected strategies for synthesizing quinazolinone frameworks via one-pot MCRs. The reported methods are categorized into three main groups: metal-catalyzed reactions; isatoic-anhydride-based strategies, utilizing isatoic anhydride as a key starting material, and alternative approaches involving, among others, the utilization of N-(2-aminobenzoyl)benzotriazoles or aryldiazonium salts as efficient building materials. Full article

Background: Epilepsy is a chronic, non-communicable brain disorder characterized by recurrent seizures. Some derivatives of 1,2,3,4-tetrahydroisoquinolines have demonstrated anticonvulsant effects. This study aims to investigate the effects of 33 derivatives of 1-aryl-1,2,3,4-tetrahydroisoquinoline on seizures induced by nicotine and strychnine. Methods: The anticonvulsant effects of 1-aryl-1,2,3,4-tetrahydroisoquinoline derivatives were evaluated in white male mice. Convulsant agents were administered subcutaneously at doses of 10.0 mg/kg for nicotine and 1.5 mg/kg for strychnine, 60 min after the oral administration of the test compounds at doses ranging from 0.1 to 10 mg/kg. The onset time, duration of tremors and seizures, and survival rate of the animals were recorded. The docking studies were conducted for 32 tested compounds targeting the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (PDB ID: 1FTL). Furthermore, a predictive ADMET study was conducted to evaluate the pharmacokinetic and toxicity profiles of the compounds. Results: Compounds 20 and 25 exhibited the highest activity against strychnine-induced seizures. When evaluating the effects of 1-aryl-1,2,3,4-tetrahydroisoquinolines and reference drugs on the tremorogenic and convulsive actions of nicotine at doses of 0.1–5 mg/kg, compounds 3, 6, 8, 14, 16, 25, 27, 29, 30, 31, and 34 demonstrated comparable activity to the reference drugs. The docking results targeting AMPA (PDB ID: 1FTL) revealed comparable binding interactions for most of the compounds, with a (−)C-Docker interaction energy range of 33.82–45.41 Kcal/mol, compared to that of the ligand (41.60 Kcal/mol). The structural requirements of the studied scaffold were analyzed to identify the essential pharmacophoric features for anticonvulsant activity. Furthermore, a predictive ADMET study was conducted to evaluate the pharmacokinetic and toxicity profiles of the compounds. Conclusions: Certain derivatives of 1,2,3,4-tetrahydroisoquinolines may serve as potential anticonvulsant agents for epilepsy. Full article

Background: Epilepsy is a cluster of central nervous system (CNS) disorders identified by recurrent seizures, which affects about 60 million people around the world. In this research, a total of 40 types of 3,4,5-trimethoxycinnamic acid (TMCA) piperazine amide derivatives were designed and synthesized, inspired by the traditional Chinese medicine (TCM) herb pair drugs Polygala tenuifolia and Acori tatarinowii, followed by determination of their anticonvulsant potency. Methods: All the TMCA analogues were tested for their anticonvulsant potential through two acute models of seizures induced in mice: the maximal electroshock (MES) and sc-pentylenetetrazole (PTZ) models. In addition, the lactate dehydrogenase (LDH) inhibitory activity was determined in vitro. Results: The results showed that compounds A3, A9, A12, A14, B9, and B12 exhibited preferable anticonvulsant activity in the primary evaluation. In addition, the molecular docking results predicted good interactions of screened analogues with the LDH. Molecular dynamic simulation was used to reveal the consensual binding affinity between the most promising compound (B9) and active site interactions with LDH. Electroencephalogram (EEG) analysis and silver and immunofluorescence staining were performed to illustrate the anti-epilepsy potential of compound B9. Conclusions: Novel derivatives in this study provide new cores for the further design and optimization inspired by TCM herb pair drugs P. tenuifolia and A. tatarinowii, with the aim to explore new anticonvulsant agents. Full article

Diabetic neuropathy (DN) remains a major clinical burden, characterized by progressive sensory dysfunction, pain, and impaired quality of life. Despite the available symptomatic treatments, there is a pressing need for disease-modifying therapies. In recent years, preclinical research has highlighted the potential of repurposed pharmacological agents, originally developed for other indications, to target key mechanisms of DN. This narrative review examines the main pathophysiological pathways involved in DN, including metabolic imbalance, oxidative stress, neuroinflammation, ion channel dysfunction, and mitochondrial impairment. A wide array of repurposed drugs—including antidiabetics (metformin, empagliflozin, gliclazide, semaglutide, and pioglitazone), antihypertensives (amlodipine, telmisartan, aliskiren, and rilmenidine), lipid-lowering agents (atorvastatin and alirocumab), anticonvulsants (topiramate and retigabine), antioxidant and neuroprotective agents (melatonin), and muscarinic receptor antagonists (pirenzepine, oxybutynin, and atropine)—have shown promising results in rodent models, reducing neuropathic pain behaviors and modulating underlying disease mechanisms. By bridging basic mechanistic insights with pharmacological interventions, this review aims to support translational progress toward mechanism-based therapies for DN. Full article

Background: The development of cerebral organoids created from human pluripotent stem cells in 3D culture may greatly improve the discovery of neuropsychiatric medicines. Methods: In the current study we differentiated neural organoids from a human pluripotent stem cell line in vitro, recorded the development of neurophysiological activity using multielectrode arrays (MEAs) and characterized the neuropharmacology of synaptic signaling over 8 months in vitro. In addition, we investigated the ability of these organoids to display epileptiform activity in response to a convulsant agent and the effects of antiseizure medicines to inhibit this abnormal activity. Results: Single and bursts of action potentials from individual neurons and network bursts were recorded on the MEA plates and significantly increased and became more complex from week 7 to week 30, consistent with neural network formation. Neural spiking was reduced by the Na channel blocker tetrodotoxin but increased by the inhibitor of K_V7 potassium channels XE991, confirming the involvement of voltage-gated sodium and potassium channels in action potential activity. The GABA antagonists bicuculline and picrotoxin each increased the spike rate, consistent with inhibitory synaptic signaling. In contrast, the glutamate receptor antagonist kynurenic acid inhibited the spike rate, consistent with excitatory synaptic transmission in the organoids. The convulsant 4-aminopyridine increased spiking, bursts and synchronized firing, consistent with epileptiform activity in vitro. The anticonvulsants carbamazepine, ethosuximide and diazepam each inhibited this epileptiform neural activity. Conclusions: Together, our data demonstrate that neural organoids form inhibitory and excitatory synaptic circuits, generate epileptiform activity in response to a convulsant agent and detect the antiseizure properties of diverse antiepileptic drugs, supporting their value in drug discovery. Full article

Background/Objectives: Approximately 1% of people worldwide suffer from epilepsy. The development of safer and more effective antiepileptic medications (AEDs) is still urgently needed because all AEDs have some unwanted side effects and roughly 30% of epileptic patients cannot stop having seizures when taking current AEDs. It should be noted that the derivatives of pyrazolo[3,4-b]pyridine are important core structures in many drug substances. The aim of this study is to synthesize new derivatives of piperazino-substituted pyrazolo[3,4-c]-2,7-naphthyridines and 9,11-dimethylpyrimido[1′,2′:1,5]pyrazolo[3,4-c]-2,7-naphthyridines for the evaluation of their neurotropic activity. Methods: The synthesis of the target compounds was performed starting from 1-amino-3-chloro-2,7-naphthyridines and using well-known methods. The structures of all the synthesized compounds were confirmed by spectroscopic data. Compounds were studied for their potential neurotropic activities (anticonvulsant, sedative, anti-anxiety, and antidepressive), as well as side effects, in 450 white mice of both sexes and 50 male Wistar rats. The anticonvulsant effect of the newly synthesized compounds was investigated by using the following tests: pentylenetetrazole, thiosemicarbazide-induced convulsions, and maximal electroshock. The psychotropic properties of the selected compounds were evaluated by using the following tests: the Open Field test, the Elevated Plus Maze (EPM), the Forced Swimming test, and Rotating Rod Test to study muscle relaxation. For the docking studies, AutoDock 4 (version 4.2.6) was used, as well as the structures of the GABA_A receptor (PDB ID: 4COF), the SERT transporter (PDB ID: 3F3A), and the 5-HT_1A receptor (PDB ID: 3NYA) obtained from the Protein Data Bank. Results: A series of piperazino-substituted pyrazolo[3,4-c]-2,7-naphthyridines (3a–j) and 9,11-dimethylpyrimido[1′,2′:1,5]pyrazolo[3,4-c]-2,7-naphthyridines (4a–j), as well as new heterocyclic systems, i.e., isoxazolo[5,4-c]-2,7-naphthyridines 6a–d, were synthesized and evaluated for their neurotropic activity. The investigation showed that some of these compounds (3a,b,d,f–i and 4a,d,f,i) display high anticonvulsant activity, especially in the test of antagonism with pentylenetetrazol, surpassing the well-known antiepileptic drug ethosuximide. Thus, the most active compounds in the pentylenpotetrazole test are 3h, 3i, and 4i; the ED50 of compound 4i is 23.8, and the therapeutic index is more than 33.6, which is the highest among these three active compounds. On the other hand, they simultaneously exhibit psychotropic (anxiolytic, antidepressant, or sedative) or behavioral depressant) effects. The effective compounds do not cause myorelaxation at the tested doses and have high therapeutic indices. Docking on the most active compounds, i.e., 3h, 3i, and 4i, is in agreement with the experimental results. Conclusions: The studies reveled that some of these compounds (3i, 4a, and 4i) display high anticonvulsant and psychotropic activities. The most active compounds contained methyl and diphenylmethyl groups in the piperazine ring. The docking studies identified compounds 3i, 4i, and 4a as the most potent anticonvulsants, showing strong affinity for GABA_A, 5-HT_1A receptors, and the SERT transporter. Notably, compound 4i formed two hydrogen bonds with Thr176 and Arg180 on GABA_A and exhibited a binding energy (−8.81 kcal/mol) comparable to that of diazepam (−8.90 kcal/mol). It also showed the strongest binding to SERT (−7.28 kcal/mol), stabilized by interactions with Gly439, Ile441, and Arg11. Furthermore, 4i displayed the best docking score with 5-HT_1A (−9.10 kcal/mol) due to multiple hydrogen bonds and hydrophobic interactions, supporting its potential as a dual-acting agent targeting both SERT and 5-HT_1A. Full article

Epilepsy is a chronic neurological disorder with significant treatment challenges, necessitating the search for alternative therapies. This study evaluates the anticonvulsant activity and toxicological profile of Verbesina persicifolia leaf extracts. Methanolic and sequential fractions (hexane, dichloromethane, ethyl acetate, and methanol) were tested using a pentylenetetrazole (PTZ)-induced seizure model in zebrafish (Danio rerio), measuring seizure latency, severity, and survival rates. Phytochemical screening confirmed the presence of flavonoids, alkaloids, and steroids, suggesting potential neuroactive properties. The hexane extracts significantly increased seizure latency and survival rates, with co-administration of hexane extract (5 µg/mL) and diazepam (35.5 µM) further enhancing these effects. Toxicity assessment in Artemia salina indicated low to moderate toxicity in methanolic extracts, while sequential fractions exhibited higher toxicity, particularly in hexane and ethyl acetate extracts. These findings suggest that V. persicifolia extracts exert anticonvulsant effects, likely through GABAergic modulation, and exhibit a favorable safety profile at therapeutic doses. The results support further investigations to isolate active constituents, confirm their mechanisms of action, and explore their potential as plant-derived anticonvulsant agents. Full article

Medicinal plants are well-known for synthesizing a wide range of bioactive compounds used mainly in the pharmaceutical, food and cosmetic industries. The therapeutic use of Passiflora species in Europe began in the 17th century, but few studies have been carried out on Passiflora caerulea L. This is a versatile plant, an herbaceous climber, belonging to the Passifloraceae family. In the past, P. caerulea L. has been mainly used as a sedative agent, but in recent years, scientific studies have focused on exploring its functionality and pharmacological use. Phytochemical analysis has revealed several classes of phytochemical components, some of which have promising biological potential. Recent studies have confirmed the therapeutic potential of P. caerulea by demonstrating its in vivo anxiolytic and antistress effects as well as antimicrobial, antioxidant, anticonvulsant, analgesic and gastroprotective activities. While these findings have been encouraging, there has been limited research conducted on the on the phytochemical profiling, biosafety and molecular mechanisms of the biological activity of extracts from Passiflora caerulea L. This review aims to summarize and analyze the recent scientific data on biological activities of Passiflora caerulea, including phytochemical profiling, mechanisms of action of individual compounds and potential therapeutic applications. Full article