[Exploring therapeutic mechanism of Compound Pien Tze Huang Tablets for adenoid hypertrophy in children based on network pharmacology and animal experiments].
The study combined network-pharmacology predictions with an ovalbumin/lipopolysaccharide-induced rat model, reporting that Compound Pien Tze Huang Tablets reduced inflammatory and Th2-associated markers, symptoms, and nasopharyngeal lymphoid hyperplasia related to adenoid hypertrophy.
Open original publication →What the AI sees
The study combined network-pharmacology predictions with an ovalbumin/lipopolysaccharide-induced rat model, reporting that Compound Pien Tze Huang Tablets reduced inflammatory and Th2-associated markers, symptoms, and nasopharyngeal lymphoid hyperplasia related to adenoid hypertrophy.
Research significance
The animal evidence supports an anti-inflammatory effect associated with reduced Th2 cytokines, TNF-α, IL-6, IgE, and histamine; it is inferred—but not directly established—that PZHT acts through coordinated TNF and PI3K-Akt pathway modulation and could benefit children with adenoid hypertrophy. No pediatric anticancer hypothesis is tested.
Source abstract
This study aimed to systematically predict and elucidate the potential therapeutic targets and molecular mechanisms of Compound Pien Tze Huang Tablets(PZHT) in the treatment of adenoid hypertrophy(AH) in children by integrating network pharmacology with animal experiments. Chemical components of PZHT were retrieved from the TCMSP, HERB 2.0, and SwissADME databases, which identified 276 putative bioactive components with favorable pharmacokinetic properties. A total of 1 266 potential targets corresponding to these components were predicted. Meanwhile, 943 AH-related targets were retrieved from the GeneCards and OMIM databases. Intersection analysis yielded 316 common targets between PZHT and AH. The protein-protein interaction(PPI) network analysis further identified 10 core targets, including BCL2, ESR1, interleukin(IL)-6, GSK3B, EGFR, PARP1, KDR, MMP2, HSP90AA1, and SRC. GO functional annotation and KEGG pathway enrichment analyses suggested that PZHT might exert therapeutic effects mainly through inflammation-and immunity-related pathways, such as the tumor necrosis factor(TNF) and PI3K-Akt signaling pathways. On the basis of network pharmacology predictions, a rat model of AH was induced by ovalbumin(OVA) combined with lipopolysaccharide(LPS) for experimental validation. The results demonstrated that compared with the model group, PZHT groups at different doses showed significantly reduced frequencies of nasal rubbing and sneezing, with the middle-dose exhibiting the most pronounced improvement. In addition, the PZHT groups showed significant declines in the serum levels of inflammatory cytokines TNF-α and IL-6, as well as Th2-type immune response-related cytokines IL-4, IL-5, and IL-13, and the levels of allergy-related indicators, including OVA-specific immunoglobulin E(sIgE) and histamine. Histopathological examinations revealed that PZHT alleviated nasal mucosal injury, goblet cell hyperplasia, edema, and inflammatory infiltration, and suppressed abnormal lymphoid hyperplasia in the nasopharyngeal region. In conclusion, by combining network pharmacology analysis with animal experimental validation, this study demonstrates that PZHT exerts therapeutic effects on AH in children through multi-target and multi-pathway regulation. The mechanism may involve coordinated modulation of Th2-type immune responses and key inflammatory signaling pathways, which leads to attenuation of local inflammation and abnormal lymphoid tissue proliferation. These findings provide experimental evidence and a theoretical basis for the clinical application of PZHT in the treatment of AH in children.