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1.
ACS Omega ; 9(1): 1183-1195, 2024 Jan 09.
Artigo em Inglês | MEDLINE | ID: mdl-38222665

RESUMO

Biocompatible and bioactive carbon-based nanocomposites are ingeniously designed and fabricated with the aim of enhancing drug delivery applicability in breast cancer treatment. Reduced graphene oxide (rGO) and multiwalled carbon nanotubes (MWCNTs) are utilized as nanocarriers for increasing penetrability into cells and the loading capacity. What sets our study apart is the strategic incorporation of the two different complexes of silver (AgL2) and palladium (PdL2) with the carboxamide-based ligand C9H7N3OS (L), which have been synthesized and decorated on nanocarriers alongside doxorubicin (DOX) for stabilizing DOX by π-π interactions and hydrogen bonding. Although DOX is a well-known cancer therapy agent, the efficacy of DOX is hindered owing to drug resistance, poor internalization, and limited site specificity. Aside from stabilizing DOX on nanocarriers, our carbon-based nanocarriers are tailored to act as a precision-guided missile, strategically by adorning with target-sensitive complexes. Based on the literature, carboxamide ligands can connect to overexpressed receptors on cancerous cells and inhibit them from proliferation signaling. Also, the complexes have an antibacterial activity that can control the infection caused by decreasing white blood cells and necrosis of cancerous cells. A high-concentration cytotoxicity assay revealed that decorating PdL2 on a DOX-containing nanocarrier not only increased cytotoxicity to breast cancerous cell lines (MDA-MB-231 and MCF-7) but also revealed higher cell viability on a normal cell line (MCF-10A). The drug release screening results showed that the presence of PdL2 led to 72 h correlate release behavior in acidic and physiological pH profiles, while the AgL2-containing nanocomposite showed an analogue behavior for just 6 h and the release of DOX continued and after about 100 h hit the top.

2.
Biomed Pharmacother ; 168: 115811, 2023 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-37922652

RESUMO

Currently, cancer is one of the main research topics, due to its high incidence and drug resistance to existing anti-cancer drugs. Formononetin, a natural product with phytoestrogenic properties and diverse biological functions, has attracted the attention of researchers working on anticancer drugs. Formononetin emerges as an intriguing bioactive substance compared to other isoflavones as it exhibits potent chemotherapeutic activity with less toxicity. Formononetin effectively plays a significant role in inhibiting cell proliferation, invasion, and metastatic abilities of cancer cells by targeting major signaling pathways at the junction of interconnected pathways. It also induces apoptosis and cell cycle arrest by modulating mediator proteins. It causes upregulation of key factors such as p-AKT, p38, p21, and p53 and downregulation of NF-κB. Furthermore, formononetin regulates the neoplastic microenvironment by inactivating the ERK1/2 pathway and lamin A/C signaling and has been reported to inactivate JAK/STAT, PKB or AKT, and mitogen-activated protein kinase pathways and to suppress cell migration, invasion, and angiogenesis in human cancer cells. To assist researchers in further exploring formononetin as a potential anticancer therapeutic candidate, this review focuses on both in vitro and in vivo proof of concept studies, patents, and clinical trials pertinent to formononetin's anticancer properties. Overall, this review discusses formononetin from a comprehensive perspective to highlight its potential benefits as an anticancer agent.


Assuntos
Antineoplásicos , Isoflavonas , Neoplasias , Humanos , Proteínas Proto-Oncogênicas c-akt/metabolismo , Linhagem Celular Tumoral , Transdução de Sinais , Proliferação de Células , Isoflavonas/farmacologia , Isoflavonas/uso terapêutico , Apoptose , Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Neoplasias/tratamento farmacológico
3.
Toxics ; 11(5)2023 May 22.
Artigo em Inglês | MEDLINE | ID: mdl-37235286

RESUMO

Pesticide exposure can pose a serious risk to nontarget animals. Cartap is being broadly used in agricultural fields. The toxic effects of cartap on the levels of hepatotoxicity and neurotoxicity have not been properly studied in mammalian systems. Therefore, the present work focused on the effect of cartap on the liver and brain of Wistar rats and made an assessment of the ameliorating potential of A. vera. The experimental animals were divided into 4 groups, comprising six rats in each: Group 1-Control; Group 2-A. vera; Group 3-Cartap; and Group 4-A. vera + Cartap. The animals orally given cartap and A. vera were sacrificed after 24 h of the final treatment and histological and biochemical investigations were conducted in liver and brain of Wistar rats. Cartap at sublethal concentrations caused substantial decreases in CAT, SOD, and GST levels in the experimental rats. The activity levels of transaminases and phosphatases in cartap group were also found to be substantially altered. The AChE activity was recorded as decreasing in RBC membrane and brain of the cartap-treated animals. The TNF-α and IL-6 level in serum were increased expressively in the cartap challenged groups. Histological investigation of liver showed disorganized hepatic cords and severely congested central veins due to cartap. However, the A. vera extract was observed to significantly protect against the effects of cartap toxicity. The protective impact of A. vera against cartap toxicity may be due to the existence of antioxidants in it. These findings suggest that A. vera may be developed as a potential supplement to the appropriate medication in the treatment of cartap toxicity.

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