apigenin

Overview

Apigenin is a naturally occurring plant flavone, a subclass of flavonoids widely distributed in edible and medicinal plants. In biomedical research, it is commonly studied for its antioxidant, anti-inflammatory, and cytoprotective properties, as well as for its ability to participate in multi-component phytochemical systems and nanomedicine formulations. Across the recent studies provided here, apigenin appears as a bioactive constituent of herbal extracts and formulations, and also as a building block in carrier-free nanoparticle assemblies.

Biologically, apigenin is being investigated in relation to inflammatory signaling, oxidative stress, cardiovascular protection, and tissue injury responses. The recent literature contexts specifically connect it with pathways and targets such as NLRP3, Caspase-1, Gasdermin D, FOXO1/PDK4 signaling, and broader polyphenol-based therapeutic platforms that also involve tannic acid, Cu2+ ions, cannabidiol, kaempferol, quercetin, salidroside, naringenin, and related phytochemicals.

Focus of Latest Publications

Recent publications have examined apigenin mainly as a bioactive flavonoid with potential anticancer, anti-inflammatory, cardioprotective, and neuroprotective roles. In a diethylnitrosamine-induced hepatocellular carcinoma rat model, apigenin was tested alone and in combination with chrysin after tumor induction. The study reported that DEN-treated rats showed activation of tumor-promoting signaling markers, including survivin, annexin-V, smoothened, sonic hedgehog, jagged1, and notch1, together with reduced caspase-3 expression. Apigenin treatment was associated with marked reductions in fibrosis and inflammation, and the apigenin group showed the most pronounced effects among the treatment groups based on biochemical and histopathological findings.

Computational work has also highlighted apigenin as a candidate anticancer compound. In a breast cancer study using network pharmacology, molecular docking, and molecular dynamics simulations, apigenin was identified from Scutellaria barbata as one of three flavonoids with favorable drug-likeness, bioavailability, and predicted safety. The analyses pointed to Akt1, IL6, and TNF as central hub targets, with enrichment in the PI3K-Akt, MAPK, and TNF signaling pathways. Apigenin showed strong predicted binding to Akt1 and the apigenin-Akt1 complex was reported to be relatively stable over 100 ns of simulation, supporting further investigation of its effects on oncogenic signaling.

Other recent studies placed apigenin within multi-component natural product systems. In Achillea arabica extract, apigenin was among the major flavonoids detected by UHPLC-QTOF-MS2, and ADMET predictions suggested favorable pharmacokinetic and safety profiles for apigenin alongside naringenin. In dandelion extract, apigenin was one of the quantified bioactive compounds under optimized ultrasound-assisted extraction conditions. In a rheumatoid arthritis study of the “Tianyu” formulation, apigenin was one of the major compounds identified by UHPLC-Q Exactive HFX, and docking suggested that it bound well to NLRP3, Caspase-1, and Gasdermin D, consistent with the formulation’s reported suppression of NLRP3/Caspase-1/GSDMD-mediated pyroptosis in cells and rats.

Apigenin also appeared in studies focused on non-oncologic therapeutic applications. In a post-myocardial infarction heart failure rat model, apigenin was identified as one of the active constituents of Yangxinshi Tablet in an OGD-induced H9c2 cell injury model, alongside senkyunolide H, astragaloside IV, and astragaloside VII. The formulation improved cardiac function, reduced inflammatory infiltration and collagen deposition, and was reported to act through inhibition of FOXO1/PDK4 signaling and restoration of energy metabolism. In an ischemic stroke nanoparticle study, apigenin was incorporated into a multifunctional biomimetic nanoformulation together with cannabidiol and polysaccharide components; the resulting system reduced brain tissue damage, neuroinflammation, and neuronal apoptosis in a middle cerebral artery occlusion rat model, with effects linked to inhibition of NLRP3/NF-κB signaling.