ABSTRACT

Dengue virus (DENV) infection triggers significant inflammatory responses in human hepatocytes, contributing to endothelial dysfunction, vascular permeability, and tissue remodeling. The regulation of key inflammatory markers, such as PAI-1, CASP-1, and TGF-β1, plays a crucial role in the pathogenesis of dengue, influencing coagulation and immune response. While current treatments focus on managing symptoms, there is a need for therapeutic strategies targeting the inflammatory pathways involved in severe dengue cases. This study investigates the effects of crude and methylated extracts on the expression levels of these inflammatory markers in DENV-infected human hepatocytes. Human hepatocytes were infected with DENV for 24 hours, followed by treatment with crude and methylated extracts. The expression levels of PAI-1, CASP-1, and TGF-β1 were measured using quantitative PCR, and fold change values were calculated relative to uninfected controls. The results showed that DENV infection led to significant upregulation of all three markers. The crude extract caused a mild upregulation of PAI-1 and slight downregulation of CASP-1 and TGF-β1, while the methylated extract induced mild downregulation of TGF-β1 and a slight upregulation of CASP-1. These findings suggest that both extracts exert subtle effects on inflammatory pathways, offering potential as therapeutic agents to modulate inflammation and fibrosis in dengue.

Keywords: Dengue virus, human hepatocytes, inflammatory markers, PAI-1, TGF-β1
https://doi.org/10.57180/llaw7591