An overview of the research progress on Mylabris: entomology, active ingredients, traditional use, pharmacology, clinical application, pharmacokinetics, toxicity and detoxification strategies

Abstract

Mylabris, a traditional Chinese medicine (TCM), is derived from the dried forms of Mylabris phalerata Pallas or Mylabris cichorii Linnaeus. It was recorded in Shennong Bencaojing in Han Dynasty and used for the treatment of psoriasis, facial paralysis, amenorrhea, and carbuncle. As a key component in antitumor formulations, Mylabris contains numerous bioactive compounds, including organic acids, terpenoids, amino acids and their conjugates, metal complexes, cantharimide dimers and peptides and proteins. Traditionally, Mylabris has been employed in the treatment of malaria, suppurative infectious diseases, and lymph node tuberculosis. Pharmacological studies have demonstrated its antitumor, anti-inflammatory, leukocytosis-inducing, and immune function-enhancing activities, as well as its pest resistance and skin blistering effects. Clinical prescriptions containing Mylabris have been used in the treatment of cancer and skin diseases. However, strong penetration and rapid absorption in all tissues contribute to multi-organ toxicity on the liver, kidney, heart, nerves and reproduction and gastrointestinal systems. Therefore, traditional processing methods and targeted drug delivery systems have been designed for increasing efficacy and decreasing toxicity. Here, we provide a comprehensive overview of Mylabris in terms of entomology, active ingredients, traditional use, pharmacology, clinical application, pharmacokinetics, toxicity, and detoxification strategies to provide a rational application in the future.

Keywords: Active ingredients and activity; Entomology; Mylabris; Toxicology; Traditional and clinical uses.

Fig. 1

The distinctive characteristics of Mylabris phalerata Pallas and Mylabris cichorii Linnaeus

Fig. 2

Active compounds in Mylabris. A: Sesquiterpenoids and their analogs, B: Volatile components, C: Other compounds

Fig. 3

The antitumor mechanisms of Mylabris. A: CTD, B: Other active ingredients. (CTD Cantharidin, DKK3 Dickkopf-3, EphB4 Eph receptor B4, JAK2 Janus kinase 2, STAT3 Signal transducer and activator of transcription 3, PI3K Phosphatidylinositol-4,5-bisphosphate 3-kinase, Akt Protein kinase B, MMP2/9 Matrix metalloproteinases 2 and 9, PP2A/5 Protein phosphatases 2A/5, NF‑κB Nuclear factor‑κB, IKKα NF‑κB kinase subunit α, IκBα NF‑κB inhibitor α, JNK c-Jun N-terminal kinase, CHOP Enhancer-binding protein homologous protein, MAPK Mitogen-activated protein kinase, ERK Extracellular signal-regulated kinase, PKM2 Pyruvate kinase M2, GLUT1 Glucose transporter 1, PKC Protein kinase C, CCAT1 Colon cancer associated transcript 1, C-MYC Myelocytomatosis viral oncogene homolog CDK1/4/6 Cyclin-dependent kinase 1/4/6, PARP Poly ADP-ribose polymerase, LC3 Microtubule-associated protein 1 light chain 3)

Fig. 4

The toxicity mechanisms of Mylabris. (MAPK Mitogen-activated protein kinase, PERK Protein kinase RNA-like endoplasmic reticulum kinase, CHOP Enhancer-binding protein homologous protein, AMPK AMP-activated protein kinase; HIF-1 Hypoxia-inducible factor-1, NLRP3 Nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3, TN-T Troponin T, VEGF Vascular endothelial growth factor, PI3K Phosphatidylinositol-4,5-bisphosphate 3-kinase, Akt Protein kinase B, COX-2 Cyclooxygenase-2)

Fig. 5

New targeted delivery systems of CTD. A: Schematic of metal–organic framework-based platforms integrating Fenton reaction and photothermal therapy. B: Schematic of biomimetic nano-drug delivery systems with tellurium and cancer cell membrane-derived nanocarriers. C: Schematic of redox-sensitive polymeric micelles modified with glycyrrhetinic acid. D: Schematic of mPEG-PLGA micelles. E: Schematic of GA and FA modified CTD loaded solid lipid nanoparticles. F: Schematic of carbonic anhydrase IX antibody and BR2 peptide modification dual-functional liposomes. G: Schematic of thermal-sensitive liposomes coated with gold nanoparticles. H: Schematic of GL-based liposome. I: Schematic of dual-modified CTD/baicalin co-loaded liposomes. (CTD Cantharidin, GL Glycyrrhizic acid, GA Glycyrrhetinic acid, FA Folate)