Immunotherapy has become an increasingly pivotal approach in the management of uterine (endometrial) and cervical malignancies. Immune checkpoint inhibitors, particularly pembrolizumab and dostarlimab, have demonstrated remarkable improvements in overall survival, predominantly among patients exhibiting deficient mismatch repair (dMMR), microsatellite instability-high (MSI-H) status, or elevated PD-L1 expression. In cervical carcinoma, integrating checkpoint inhibitors with concurrent chemoradiotherapy has yielded enhanced therapeutic outcomes in high-risk populations, while antibody–drug conjugates such as tisotumab vedotin have broadened the therapeutic landscape. Although challenges including therapeutic resistance and immune-related adverse events remain, recent international clinical trials substantiate that immunotherapy is redefining current standards of care and paving the way for the advancement of precision oncology.

Background: The long-term use of conventional anti-inflammatory drugs is associated with significant adverse effects, necessitating the search for safer alternatives from natural sources. The genus Clerodendrum is widely used in traditional medicine, but the specific anti-inflammatory potential of Clerodendrum thomsoniae Balf.f. remains underexplored. This study aimed to identify the major phytochemicals in an alcoholic leaf extract of C. thomsoniae and evaluate their potential as Cyclooxygenase-2 (COX-2) inhibitors using a computational approach.

Methods: An alcoholic extract of C. thomsoniae leaves was prepared and subjected to Gas Chromatography-Mass Spectrometry (GC-MS) for phytochemical profiling. The major identified compounds were then evaluated for their anti-inflammatory potential via molecular docking studies against the COX-2 enzyme using PyRx software. Rofecoxib was used as a standard reference drug. Furthermore, the Absorption, Distribution, Metabolism, Excretion, and Toxicity (ADMET) properties of the top-performing compounds were predicted using the SwissADME online server to assess their drug-likeness.

Results: The GC-MS analysis successfully identified 15 distinct phytochemicals in the extract, with Verbenone, Linalool, and Eucalyptol being the most abundant. The molecular docking results revealed that Verbenone exhibited the highest binding affinity of -8.5 kcal/mol, which was superior to that of the standard drug Rofecoxib (-7.9 kcal/mol). The analysis of the binding pose showed strong hydrogen bond and hydrophobic interactions between Verbenone and the key amino acid residues in the COX-2 active site.

Conclusion: The findings suggest that Clerodendrum thomsoniae is a rich source of bioactive compounds with significant anti-inflammatory potential. Verbenone, identified as the major component, shows great promise as a selective COX-2 inhibitor and warrants further in-vitro and in-vivo validation as a lead compound for developing novel anti-inflammatory therapies.

Non-alcoholic fatty liver disease (NAFLD) is a multifactorial condition characterized by complex interactions between metabolic dysfunction, lipid accumulation, inflammation, and progressive fibrosis. Molecular mechanisms underlying these processes increasingly highlight the role of receptor genes involved in lipid transport and oxidative stress regulation. The present study aimed to investigate the association between the expression levels of LRP1, LDLR, and LOX1 receptor genes and key morphometric and non-invasive indicators of hepatic involvement in NAFLD. A cohort of patients with varying degrees of steatosis and fibrosis underwent molecular-genetic analysis, elastographic assessment of liver stiffness (Young’s modulus), and evaluation of the Fatty Liver Index (FLI).

The results demonstrated that decreased expression of LRP1 and LDLR was significantly associated with higher FLI values, indicating a potential contribution of impaired receptor-mediated lipid uptake to the

amplification of hepatic steatosis. These findings may reflect reduced hepatic clearance of circulating lipoproteins and altered lipid handling within hepatocytes, promoting intracellular lipid overload. In contrast, LOX1 expression showed a weak but statistically significant positive correlation with liver stiffness measurements, suggesting that oxidative stress and oxLDL-mediated signaling may participate in the early development of fibrosis. LOX1-dependent pathways are known to activate pro-inflammatory cascades, endothelial dysfunction, and extracellular matrix remodeling—mechanisms that could influence fibrogenesis in NAFLD.

Collectively, the obtained data indicate that alterations in the expression profiles of LRP1, LDLR, and LOX1 may serve as molecular indicators of steatosis severity and early fibrotic changes. These genes may represent promising biomarkers for identifying patients at risk of progressive liver injury and developing personalized therapeutic strategies aimed at modifying lipid metabolism and oxidative stress. Further studies with larger cohorts and longitudinal follow-up are required to clarify the causal relationships and determine their potential as predictive markers in clinical practice.