ABSTRACT
[This corrects the article DOI: 10.1016/j.apsb.2022.08.024.].
ABSTRACT
In situ and real-time monitoring of responsive drug release is critical for the assessment of pharmacodynamics in chemotherapy. In this study, a novel pH-responsive nanosystem is proposed for real-time monitoring of drug release and chemo-phototherapy by surface-enhanced Raman spectroscopy (SERS). The Fe3O4@Au@Ag nanoparticles (NPs) deposited graphene oxide (GO) nanocomposites with a high SERS activity and stability are synthesized and labeled with a Raman reporter 4-mercaptophenylboronic acid (4-MPBA) to form SERS probes (GO-Fe3O4@Au@Ag-MPBA). Furthermore, doxorubicin (DOX) is attached to SERS probes through a pH-responsive linker boronic ester (GO-Fe3O4@Au@Ag-MPBA-DOX), accompanying the 4-MPBA signal change in SERS. After the entry into tumor, the breakage of boronic ester in the acidic environment gives rise to the release of DOX and the recovery of 4-MPBA SERS signal. Thus, the DOX dynamic release can be monitored by the real-time changes of 4-MPBA SERS spectra. Additionally, the strong T2 magnetic resonance (MR) signal and NIR photothermal transduction efficiency of the nanocomposites make it available for MR imaging and photothermal therapy (PTT). Altogether, this GO-Fe3O4@Au@Ag-MPBA-DOX can simultaneously fulfill the synergistic combination of cancer cell targeting, pH-sensitive drug release, SERS-traceable detection and MR imaging, endowing it great potential for SERS/MR imaging-guided efficient chemo-phototherapy on cancer treatment.
ABSTRACT
Objective To study the effect of cisplatin on the hepatocellular carcinoma HepG2 cells by Atomic Force Microscopy (AFM), then analysis the changes of ultrastructural in HepG2 cells during apoptosis induced by cisplatin at nanoscale level. Methods HepG2 cells were treated with cisplatin for 24h and 48h. The ultrastructural change of cell surface was detected by AFM , the inhibitory rate and apoptotic rate of cell were examined by MTT and fow cytometry. Results AFM images showed that with the prolongation of cisplatin-inducing, the deformation change of HepG2 cells varying degree. The cells appeared larger pore size of cell membrane, the value of cell membrane particle sizes, Rp-v, Ra, Rq and Meant Ht were significant increased. The inhibitory rate and apoptotic rate were significant increased. Conclusions Cisplatin induced shrinkage in cell morphology, pore formation and roughness increasing in cell membrane, thereby inducing apoptosis in HepG2 cells.