ABSTRACT
Methicillin-resistant Staphylococcus aureus (MRSA) has evolved vast antibiotic resistance. These strains contain numerous virulence factors facilitating the development of severe infections. Considering the costs, side effects, and time duration needed for the synthesis of novel drugs, seeking efficient alternative approaches for the eradication of drug-resistant bacterial agents seems to be an unmet requirement. Nickel nanoparticles (NiNPs) have been applied as prognostic and therapeutic cheap agents to various aspects of biomedical sciences. Their antibacterial effects are exerted via the disruption of the cell membrane, the deformation of proteins, and the inhibition of DNA replication. NiNPs proper traits include high-level chemical stability and binding affinity, ferromagnetic properties, ecofriendliness, and cost-effectiveness. They have outlined pleomorphic and cubic structures. The combined application of NiNPs with CuO, ZnO, and CdO has enhanced their anti-MRSA effects. The NiNPs at an approximate size of around 50 nm have exerted efficient anti-MRSA effects, particularly at higher concentrations. NiNPs have conferred higher antibacterial effects against MRSA than other nosocomial bacterial pathogens. The application of green synthesis and low-cost materials such as albumin and chitosan enhance the efficacy of NPs for therapeutic purposes.
ABSTRACT
OBJECTIVES: Owing to inefficiency of chemotherapy towards cancer treatment, formulation and application of herbal drug compounds will open new avenues with this regard. In this study, the anticancer effects of itexin, cinobufacini, and Physalis alkekengi (P. alkekengi) were assessed. METHODS: Herein, synergistic effects of vitexin, cinobufacini, and P. alkekengi hydroalcoholic extract were assessed against estrogen-receptor (EGFR2)-positive breast cancer mouse model. Sixty ER + breast cancer BALB/c mice (six groups each including ten members) were included. The anticancer effects of P. alkekengi hydroalcoholic extract, vitexin, and cinobufacini were administered against EGFR2 cancerous cells for 14 days. The tumor size, cytotoxic effects, and expression of Beclin-1, LC3-II, and ATG5 autophagy-related genes were investigated using RT-qPCR technique. The data was analyzed using chi-square, ANOVA, and multinomial logistic regression tests. KEY FINDINGS: The 50% lethal dose (LD50) of P. alkekengi and vitexin against the breast cancer cells included 12 mg/kg, respectively, while cinobufacini LD50 was 24 mg/kg but had no toxicity against CRL7242 breast normal cells. Furthermore, 24 mg/kg of the P. alkekengi, vitexin, and cinobufacini significantly increased the ATG5, Beclin-1, and LC3-II gene expression. CONCLUSION: Considering anticancer effects of P. alkekengi, vitexin, and cinobufacini against breast cancer through induction of the autophagy pathway, the compound formulations can be applied as anticancer therapies.
