Synthesis of Cu(Ⅱ) complex based on 3,5-dibromosalicylaldehyde-4-aminoantipyrine Schiff base and its anticancer activity evaluation

ObjectiveTo design and synthesize a novel Cu(Ⅱ) complex based on 3,5-dibromosalicylaldehyde-4-aminoantipyrine Schiff base (CuL₂), and evaluate its anticancer activity.

MethodsA novel Schiff base ligand, 3,5-dibromosalicylalde-4-aminoantipyrine (HL), was synthesized by condensation reaction of 3,5-dibromosalicylalde and 4-aminoantipyrine.The CuL₂ was synthesized by solvothermal method with HL and Cu(Ac)₂·H₂O.The CuL₂ was characterized by X-ray single crystal diffraction, polycrystaline powder X-ray diffraction (PXRD), Fourier transform infrared spectroscopy (FT-IR) and thermogravimetric analysis (TGA-DSC).The in vitro anticancer activity of HL and CuL₂ on MDA-MB-231, SMMC-7721, CNE-2Z and A-549 cells was determined by MTT assay.The effect of CuL₂ on apoptosis and cell cycle of MDA-MB-231 cells was analyzed by flow cytometry (FCM).

ResultsX-ray single crystal diffraction analysis showed that CuL₂ was a mononuclear metal complex, belonging to the monoclinic crystal system, with space group of C2/c and 4-coordination micro-torsion square structure; PXRD showed that the crystallinity of CuL₂ was good, and the crystal structure accorded with the results of single crystal test; the FT-IR characteristic peaks were consistent with the molecular structures of ligand and complex; TGA-DSC analysis showed that CuL₂ had good thermal stability below 270 ℃.The MTT assay results showed that when HL forms a complex with Cu (Ⅱ), CuL₂ had better anticancer activity than HL, and its inhibitory activity on MDA-MB-231 cells and SMMC-7721 cells was stronger, which was slightly lower than that of cisplatin.The FCM analysis results showed that CuL₂ could induce apoptosis in MDA-MB-231 cells (P < 0.05), and induce cell cycle arrest in G₀/G₁ and S phases in MDA-MB-231 cells (P < 0.05).

ConclusionsThe CuL₂ is synthesized, which can inhibit the activity of MDA-MB-231 and SMMC-7721 cells, and induce cell cycle arrest and apoptosis in MDA-MB-231 cells.