# Network pharmacology mechanisms and experimental verification of Hedyotis Diffusae Herba-Scutellariae Barbatae Herba drug pair extract in the treatment of nasopharyngeal carcinoma

## TL;DR

This study explores how a traditional Chinese herb pair may treat nasopharyngeal cancer by identifying key compounds and biological pathways involved.

## Contribution

The study combines network pharmacology and experiments to reveal the mechanism of a herb pair in treating NPC.

## Key findings

- HDH-SBH contains 36 bioactive components targeting 155 genes linked to NPC.
- Quercetin, luteolin, wogonin, and β-sitosterol are key components interacting with AKT1, TP53, and BCL2.
- HDH-SBH inhibits NPC cell growth and migration while promoting apoptosis via pathway modulation.

## Abstract

Nasopharyngeal carcinoma (NPC) represents the predominant head-neck malignancy in China. While the Hedyotis Diffusae Herba-Scutellariae Barbatae Herba (HDH-SBH) herb pair shows antitumor potential, its mechanism against NPC remains unclear.

This network pharmacology study integrated with experimental validation identified NPC-related targets through GEO database and disease databases (OMIM, GeneCards, TTD). Active components of HDH-SBH and their targets were retrieved from Traditional Chinese Medicine Systems Pharmacology Database (TCMSP). Common targets were analyzed via STRING, with functional enrichment using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Core components were validated through molecular docking and in vitro experiments using HDH-SBH-treated 5-8F and CNE2 cells.

We identified 36 bioactive components and 155 shared targets, with quercetin, luteolin, wogonin, and β-sitosterol emerging as core components. KEGG analysis highlighted PI3K/AKT pathway inhibition (P<0.05). Molecular docking confirmed strong binding between core components and key targets (AKT1, TP53, BCL2). In vitro validation showed HDH-SBH significantly inhibited NPC cell proliferation/migration while inducing apoptosis through downregulating BCL2, upregulating TP53, and suppressing AKT1 phosphorylation.

Based on the network pharmacology approach, we predicted the potential mechanism of HDH-SBH for the treatment of NPC, which provided a new idea for further research on its pharmacological mechanism.