RESUMO
Prostate cancer treatment poses significant challenges due to its varying aggressiveness, potential for metastasis, and the complexity of treatment options. Balancing the effectiveness of therapies, minimizing side effects, and personalizing treatment strategies are ongoing challenges in managing this disease. Significant advances in the use of nanotechnology for the treatment of prostate cancer with high specificity, sensitivity, and efficacy have recently been made. This study aimed to synthesize and characterize a novel Cu/Fe layer double hydroxide (LDH) nanocomposite for use as an anticancer agent to treat prostate cancer. Cu/Fe LDH nanocomposites with a molar ratio of 5:1 were developed using a simple co-precipitation approach. FT-IR, XRD, SEM, TEM, TGA, and zeta potential analyses confirmed the nanocomposite. Moreover, the MTT cell viability assay, scratch assay, and flow cytometry were utilized to examine the prospective anticancer potential of Cu/Fe LDH on a prostate cancer (PC-3) cell line. We found that Cu/Fe LDH reduced cell viability, inhibited cell migration, induced G1/S phase cell cycle arrest, and triggered apoptotic effect in prostate cancer cells. The findings also indicated that generating reactive oxygen species (ROS) formation could improve the biological activity of Cu/Fe LDH. Additionally, Cu/Fe LDH showed a good safety impact on the normal lung fibroblast cell line (WI-38). Collectively, these findings demonstrate that the Cu/Fe LDH nanocomposite exhibited significant anticancer activities against PC-3 cells and, hence, could be used as a promising strategy in prostate cancer treatment.
RESUMO
Rheumatoid arthritis (RA) is a long-term autoimmune disease. As nanotechnology has advanced, a growing number of nanodrugs have been used in the treatment of RA due to their unique physical and chemical properties. The purpose of this study was to assess the therapeutic potential of a novel zeolite/vitamin B12 nanocomposite (Nano ZT/Vit B12) formulation in complete Freund's adjuvant (CFA)-induced arthritis. The newly synthesized Nano ZT/Vit B12 was fully characterized using various techniques such as XRD, FT-IR, BET analysis, HERTEM, SEM, practical size, zeta potential, XRF, and EDX. The anti-arthritic, anti-inflammatory, and antioxidant activities as well as the immunomodulation effect of Nano ZT/Vit B12 on the CFA rat model of arthritis were examined. Histopathologic ankle joint injuries caused by CFA intrapedal injection included synovium hyperplasia, inflammatory cell infiltration, and extensive cartilage deterioration. The arthritic rats' Nano ZT/Vit B12 supplementation significantly improved these effects. Furthermore, in arthritic rats, Nano ZT/Vit B12 significantly reduced serum levels of RF and CRP, as well as the levels of IL-1ß, TNF-α, IL-17, and ADAMTS-5, while increasing IL-4 and TIMP-3 levels. Nano-ZT/Vit B12 significantly declined the LPO level and increased antioxidant activities, such as GSH content and GST activity, in the arthritic rats. In arthritic rats, Nano ZT/Vit B12 also reduced TGF-ß mRNA gene expression and MMP-13 protein levels. Collectively, Nano ZT/Vit B12 seems to have anti-arthritic, anti-inflammatory, and antioxidant properties, making it a promising option for RA in the future.
RESUMO
Nanotechnology holds great promise for the development of treatments for deadly human diseases, such as hepatocellular carcinoma (HCC). In the current study, we compared the hepatoprotective effects of naringin-dextrin nanoparticles (NDNPs) against HCC in male Wistar rats with those of pure naringin and investigated the underlying cellular and molecular mechanisms. HCC was induced by intraperitoneal injection of diethylnitrosamine (DEN, 150 mg/kg body weight (b.w.) per week) for two weeks, followed by oral administration of 2-acetylaminofluorene (2AAF, 20 mg/kg b.w.) four times per week for three weeks. DEN/2AAF-administered rats were divided into three groups that respectively received 1% carboxymethyl cellulose (as vehicle), 10 mg/kg b.w. naringin, or 10 mg/kg b.w. NDNP every other day by oral gavage for 24 weeks. Both naringin and NDNP significantly attenuated the harmful effects of DEN on liver function. Both compounds also suppressed tumorigenesis as indicated by the reduced serum concentrations of liver tumor markers, and this antitumor effect was confirmed by histopathological evaluation. Additionally, naringin and NDNP prevented DEN-induced changes in hepatic oxidative stress and antioxidant activities. In addition, naringin and NDNP suppressed inflammation induced by DEN. Moreover, naringin and NDNP significantly reduced the hepatic expression of Bcl-2 and increased Bax, p53, and PDCD5 expressions. Naringin and NDNP also reduced expression of IQGAP1, IQGAP3, Ras signaling, and Ki-67 while increasing expression of IQGAP2. Notably, NDNP more effectively mitigated oxidative stress and inflammatory signaling than free naringin and demonstrated improved antitumor efficacy, suggesting that this nanoformulation improves bioavailability within nascent tumor sites.
