Current Pharmaceutical Design - Online First

Millions of people have died from zoonotic illnesses, like COVID-19 and Nipahvirus infection (NiV), throughout history. Fruit bats (Pteropus sp.) are the main reservoir host for NiV, an RNA virus belonging to the Henipavirus group, which causes extremely infectious illnesses, such as COVID-19. NiV outbreaks have posed significant public health concerns, especially in South and Southeast Asia. The Nipah virus (NiV) infection is caused by a virus that belongs to the Paramyxoviridae family's Henipavirus genus. It is the source of zoonosis, which causes respiratory and neurological symptoms.

This study has reviewed the epidemiology, pathophysiology, genetic diversity, and phylogenetics of NiV. It has explored NiV’s clinical features, cellular monitoring, infection factors, and the virus’ reservoir host.

Phylogenetic analysis has identified two circulating NiV lineages. Additionally, the study has examined the role of phytochemicals in combating viral infections. Despite the absence of a focused therapy for COVID-19, phytochemicals have been investigated for their potential antiviral properties. Evidence suggests that plants and their components may possess resistance against NiV by modulating the immune system and inhibiting viral replication.

The investigation into plant-derived compounds has offered a novel direction for NiV treatment, potentially enhancing viral resistance through immune modulation. Continued research on natural antivirals could bridge current gaps in therapeutic options for emerging zoonotic diseases.

The study has highlighted the transmission risk, detection challenges, and the potential of phytochemicals in managing NiV infections. The therapeutic potential of plants and their antiviral properties offer promising insights into future treatments for serious viral diseases, like NiV.

Wound healing is a complex and dynamic biological process involving hemostasis, inflammation, proliferation, and tissue remodeling. Conventional wound dressings provide only passive protection and fail to maintain an optimal healing microenvironment. Synthetic polymers, such as polyvinyl alcohol (PVA), polycaprolactone (PCL), poly(lactic-co-glycolic acid) (PLGA), and polyethylene glycol (PEG), have emerged as promising materials in advanced wound care due to their tunable physicochemical properties, biocompatibility, and enhanced therapeutic functionality.

This review aims to evaluate the potential of synthetic polymers in wound healing applications, focusing on their structural and functional advantages, challenges, and opportunities in the development of next-generation wound dressings.

A comprehensive literature review was conducted on recent developments in polymer-based wound dressings. In this review, we conducted a systematic literature search across Google Scholar, ScienceDirect, Scopus, Web of Science, and PubMed for publications between 2015 and 2025. The search strategy employed keywords, such as “wound healing”, “polyvinyl alcohol”, “polycaprolactone”, “poly(lactic-co-glycolic acid)”, “polyethylene alcohol”, “physicochemical characteristics”, “drug delivery capabilities”, and ” clinical trial” to capture the research landscape.

Synthetic polymers demonstrated significant potential in overcoming limitations of natural biomaterials, such as poor mechanical strength and rapid degradation. PEG-based hydrogels exhibited excellent hydrophilicity and sustained drug release. PCL scaffolds offered mechanical durability and supported tissue regeneration. PLGA allowed controlled therapeutic release through tunable degradation, while PVA ensured prolonged wound protection due to its structural stability. Polymer modifications, including crosslinking and blending, further enhanced wound healing efficacy.

Synthetic polymers provide versatile platforms for designing multifunctional wound dressings with improved healing outcomes. Future research should emphasize biodegradable, patient-specific, and smart wound dressings integrating controlled drug delivery, infection prevention, and angiogenic stimulation, thereby revolutionizing wound management practices.

Nitrergic transmission and oxidative stress are complicated factors in the seizure’s pathophysiology. Syringic acid has been revealed to exert numerous pharmacological properties, including neuroprotective effects. Hence, this research was designed to explore the anticonvulsant effects of syringic acid, focusing on its possible impact on nitrergic transmission and oxidative stress in the prefrontal cortex (PFC) in mice that underwent induction of seizure using pentylenetetrazole (PTZ).

Forty male NMRI mice were randomly divided into five groups, including mice that received saline containing Tween 80 at a concentration of 1% (10 ml/kg), syringic acid at doses of 10, 20, and 30 mg/kg, and diazepam (10 mg/kg). Syringic acid was dissolved in saline containing Tween 80 at a concentration of 1%. All drugs were injected intraperitoneally one hour before seizure induction by PTZ. Seizure threshold, total antioxidant capacity (TAC), nitrite, and malondialdehyde (MDA) levels, as well as inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) gene expressions, were assessed in the PFC.

Syringic acid increased the seizure threshold and TAC, whereas it decreased MDA and nitrite levels in the PFC samples. Furthermore, syringic acid diminished the expression of iNOS and nNOS genes in the PFC.

Oxidative/nitrosative stress, which is involved in the pathophysiology of seizure, was alleviated by syringic acid.

It was concluded that, at least partially, the anticonvulsant property of syringic acid was mediated through the mitigation of oxidative stress and nitrergic transmission in the PFC in PTZ-induced seizures in male mice.

The purpose of this research is to review and evaluate both traditional and emerging biomarkers used in the diagnosis, monitoring, and treatment of liver diseases. The study aims to highlight how these biomarkers—such as liver enzymes, microRNAs, exosomes, and fibrosis-related proteins—can improve early detection, track disease progression, and support personalized treatment strategies for better patient outcomes.

This study uses a literature review to analyze both traditional (ALT, AST, ALP, bilirubin, etc.) and emerging biomarkers (microRNAs, exosomes, CRP, IL-6, MMPs, TIMPs) in liver disease. It focuses on their role in diagnosis, disease monitoring, and personalized treatment planning.

Traditional biomarkers (ALT, AST, ALP, bilirubin, albumin) are key for liver function assessment. Emerging markers like microRNAs, exosomes, MMPs, and TIMPs improve early detection and disease monitoring. Together, they enhance diagnostic accuracy and support personalized treatment.

The combination of traditional and novel biomarkers improves early detection, accurate diagnosis, and personalized treatment of liver diseases. New biomarkers, such as microRNAs and exosomes, offer higher sensitivity and specificity, enabling non-invasive diagnostics. The findings align with current research trends that promote the use of molecular and extracellular markers. These biomarkers provide deeper insights into liver disease mechanisms, particularly in fibrosis and hepatocellular carcinoma.

Traditional biomarkers are essential for liver assessment, while new ones like microRNAs, exosomes, MMPs, and TIMPs improve early diagnosis and monitoring. They support personalized care but need further validation for routine use.

Disorders of mood and post-traumatic stress disorder (PTSD) are common after major trauma, and one of the treatments used is Tricyclic Antidepressants (TCA). These medications work by inhibiting the re-uptake of neurotransmitters like serotonin and noradrenaline. Serotonin is known to have measurable effects on bone tissue due to the presence of specific receptors on bone cells. However, there are conflicting reports about how serotonin signaling affects bone tissue and the process of fracture healing. This study aimed to evaluate the effect of TCAs on fracture healing.

Twelve skeletally mature Wistar rats were used in the study. All rats underwent intra-medullary pinning of the right tibia, and a complete mid-diaphyseal fracture was created. The rats were then randomly split into two groups: a control group and a study group. For twenty-eight days, the study group received a daily dose of 10 mg/kg of amitriptyline via intraperitoneal infusion, while the control group received an equal volume of plain saline via the same route. On day twenty-eight, five hours after the final dose, all rats were euthanized to assess fracture healing using radiological, microscopic, and histological methods.

The study found a significant difference in the total volume of new bone formation between the two groups on day twenty-eight. The control group had a mean bone formation volume of 1.077 mm³, whereas the amitriptyline-treated group had a significantly higher mean volume of 1.824 mm³ (p<0.01).

The results suggest that TCAs positively influence the early phases of fracture healing. The increased new bone formation observed in the amitriptyline group indicates a potential therapeutic benefit beyond their known psychiatric effects. This finding adds to the existing literature on the complex relationship between serotonin signaling and bone metabolism, providing evidence that this class of antidepressants may enhance the process of bone repair.

Tricyclic Antidepressants, specifically amitriptyline, significantly increase new bone formation in the early stages of fracture healing in Wistar rats.

The Xianling Gubao capsule (XLGB), a traditional Chinese medicine formulation approved by the China Food and Drug Administration, has been effectively used to treat two common medical conditions: osteoarthritis (OA) and osteoporosis (OP). However, due to the complex ingredients, the molecular mechanisms underlying its therapeutic effects for OA and OP remain unknown.

This study identified XLGB-related therapeutic target genes and pathways for OA and OP by using bioinformatics and network pharmacology. Molecular docking assessed the interactions between core genes and compounds, while quantitative real-time PCR and Western blotting analyses validated the mRNA and protein expression of key target genes.

Bioinformatics analysis identified 473 unique genes common to OA and OP. Network pharmacology analysis identified 30 intersecting genes as the principal target genes for anti-OA and anti-OP effects. Ten hub genes were identified using protein-protein interaction as potential therapeutic targets. These genes were related to transcription regulation and enriched in certain signaling pathways, such as interleukin-17 and tumor necrosis factor. Molecular docking analysis revealed danshenxinkun B to exhibit a strong affinity for Ptgs2, Fos, and Tnfaip3, while miltirone displayed a strong affinity for Ptgs2. The experimental results have been verified using cellular experiments.

This study showed Ptgs2, Fos, and Tnfaip3 to be mainly enriched in interleukin-17 and tumor necrosis factor signaling pathways. Moreover, danshenxinkun B and miltirone significantly modulated the expression levels of these genes.

This study has demonstrated that danshenxinkun B and miltirone may be pivotal agents in treating OA and OP by down-regulating the expressions of Ptgs2, Fos, and Tnfaip3.

Hepatitis C virus (HCV) remains a major global health challenge, driving chronic hepatitis C (CHC) progression to severe liver diseases, including hepatocellular carcinoma (HCC). Direct-acting antivirals (DAAs) have transformed HCV treatment by achieving high sustained virological response (SVR) rates. However, limitations such as resistance, reinfection, and restricted accessibility emphasize the urgent need for novel therapeutic approaches. Among HCV therapeutic targets, the NS3/4A protease is critical for viral replication and immune evasion, positioning it as a prime focus for innovative drug discovery.

A comprehensive computational approach was adopted to evaluate flavonoids, natural compounds with known antiviral and anticancer properties, as potential inhibitors of the HCV NS3/4A protease. A curated flavonoid library was subjected to virtual screening using molecular docking techniques. Top-ranked flavonoids were further assessed based on binding affinity, dissociation constants, and key protein-ligand interactions. Pharmacokinetic profiling, molecular dynamics simulations, MM/PBSA energy calculations, and principal component analysis were performed to validate the most promising candidate.

The top ten scoring flavonoids demonstrated strong binding affinities and stable interactions with key catalytic residues of the NS3/4A protease. CID 100943380 emerged as the most promising candidate, exhibiting favorable pharmacokinetic properties and sustained stability throughout molecular dynamics simulations. MM/PBSA and PCA analyses further confirmed its robust binding and conformational stability.

The findings highlight flavonoids as promising inhibitors of NS3/4A protease, supporting their potential for further antiviral development.

This investigation identifies 10 flavonoids with high potential as NS3/4A protease inhibitors, providing a basis for future biological validation and safer drug development.