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Mechanisms of Different Anticancer Drugs
Published in Anjana Pandey, Saumya Srivastava, Recent Advances in Cancer Diagnostics and Therapy, 2022
Anjana Pandey, Saumya Srivastava
Cancer can evade apoptosis, which is an essential factor for tumor progression and resistance to chemotherapy. In patients of chronic lymphatic leukemia (CLL) and acute myeloid leukemia (AML), leukemic cells have shown a higher level of B-cell lymphoma-2 (Bcl-2) protein. Thus, they can avoid apoptosis (Campos et al., 1993; Konopleva et al., 2006; Lagadinou et al., 2013). Research conducted on specific tumor cell lines have shown that by increasing the expression of intracellular Bax protein (Bcl-2-associated-X), these properties of cells can be reversed. Bax induces the proapoptotic factors release from the mitochondria like cytochrome C and can alert the breast tumor cells to anticancer agents or therapies. Pterostilbene (3,5-dimethoxy-4-hydroxystilbene) is a naturally occurring drug having antioxidant properties. It can inhibit the proliferation of cancer cells and tempt apoptosis in breast cancer cells (Moon et al., 2013).
Transcranial Magnetic and Electric Stimulation
Published in Ben Greenebaum, Frank Barnes, Biological and Medical Aspects of Electromagnetic Fields, 2018
Shoogo Ueno, Masaki Sekino, Tsukasa Shigemitsu
Using a vascular dementia (VaD) rat model, Yang et al. (2015) determined whether low-frequency (1 Hz) 0.5 T rTMS protects pyramidal cell from apoptosis and promotes hippocampal synaptic plasticity. In this study, learning and memory were evaluated via Morris water maze (MWM), and the ultrastructure of hippocampal CA1 neurons was examined by electron microscopy. Hippocampal synaptic plasticity was assessed by long-term potentiation (LTP). The expression of N-methyl-D-aspartic acid receptor 1 (NMDAR1), Bcl-2, and Bax proteins was assessed by Western plot. Bcl-2 promotes cell survival and Bax promotes cell death. LTP is considered essential for cognition and the synaptic plasticity is the cellular basis for memory formation and cognition. Yang et al., applied rTMS for 600 s daily for 10 days during a 2-week period. Rats treated with rTMS had reduced escape latencies, increased swimming time and significantly less synaptic structure damage. The results show that rTMS improves learning and memory, protects the synapse, and increases synaptic plasticity in VaD model rats. In conclusion, increased Bcl-2 expression—upregulation—and reduced Bax expression—downregulation—may be a novel protective mechanism of rTMS treatment for VaD.
First-in-Class Anti-Cancer Nanoparticle Copper(Ii) Phosphorus Dendrimers as Pro-Apoptotic Bax Activators
Published in Anne-Marie Caminade, Cédric-Olivier Turrin, Jean-Pierre Majoral, Phosphorus Dendrimers in Biology and Nanomedicine, 2018
Serge Mignani, Nabil El Brahmi, Thierry Cresteil, Jean-Pierre Majoral
Information collected in these studies suggested that, very interestingly, the pro-apoptotic Bax protein, a central death regulator, was actively translocated to the mitochondrial compartment, allowing the release of apoptosis inducing factor and finally the activation of the caspase-independent apoptotic pathway.
Green synthesized silver nanoparticles with mushroom extracts of Paxina leucomelas and Rhizopogon luteolus induce ROS-Induced intrinsic apoptotic pathway in cancer cells
Published in Inorganic and Nano-Metal Chemistry, 2022
Nazan Gökşen Tosun, Özlem Kaplan, Rizvan Imamoğlu, İbrahim Türkekul, İsa Gökçe, Aykut Özgür
Apoptosis is an important cell death mechanism that mediates the maintenance of cellular homeostasis in normal cells, whereas its dysregulation plays a significant role in the pathogenesis of cancer.[34–37] Apoptosis can be stimulated by multi-signal pathways such as intrinsic and extrinsic pathways. The intrinsic pathway (also known as the mitochondrial pathway) is a critical non-receptor-mediated apoptotic pathway that induces mitochondrial outer membrane permeabilization (MOMP) for releasing cytochrome-c into the cytosol. The pro-apoptotic and anti-apoptotic members of the Bcl-2 regulate apoptosis in a caspase-dependent manner. The anti-apoptotic protein Bcl-2 inhibits cytochrome-c release, whereas the pro-apoptotic protein Bax stimulates its release from mitochondria. Overexpression of Bcl-2 and under-expression of Bax protect human cancer cells from undergoing apoptosis. Therefore, up-regulation of the Bax/Bcl-2 expression ratio seems to be an important parameter in increasing the sensitivity to apoptotic stimuli in cancer cells.[37–41]
Renal damage induced by the pesticide methyl parathion in male Wistar rats
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Victor Hugo Fuentes-Delgado, María Consolación Martínez-Saldaña, María Luisa Rodríguez-Vázquez, Miguel Arturo Reyes-Romero, José Luis Reyes-Sánchez, Fernando Jaramillo-Juárez
TNF-α is a proinflammatory cytokine whose liberation is involved in endothelial cell activation, nitric oxide secretion, increased vascular permeability, and activation of the immune system (Aguillón et al. 2002; Arango Duque and Descoteaux 2014). Further, TNF-α induces cytotoxicity of the glomerular, mesangial, and epithelial cells and produces renal damage (McCarthy, Sharma, and Sharma 1998). Inhibition of TNF-α production might reduce or generate modifications in all these processes. BAX is a proapoptotic molecule, triggering caspase activation and mitochondrial cytochrome C, termed mitochondrial outer membrane permeabilization (Westphal et al. 2011). Decreased or inhibited expression levels of BAX indicate diminished gene transcription might be linked to a lower apoptotic role in tissue damage process. Therefore, proximal cell death might be related to a necrotic process. The results of densitometry analyzes are compatible with a recovery process from AKI.
Ginkgo biloba modulates ET-I/NO signalling in Lead Acetate induced rat model of endothelial dysfunction: Involvement of oxido-inflammatory mediators
Published in International Journal of Environmental Health Research, 2023
Jerome Ndudi Asiwe, Godwin D. Yovwin, Nwoke Enekabokom Ekene, Simon Irikefe Ovuakporaye, Anthony Chibuzor Nnamudi, Eze Kingsley Nwangwa
Inflammation has been associated with increased oxidative stress in several studies (Aimo et al. 2020). Innate immune cells are drawn to lead acetate which generate inflammatory mediators such as TNF-α and IL-6. Also, during the inflammatory reaction, ROS are produced causing tissue and cell damage (Conti et al. 2020). Endothelial dysfunction has previously been connected to the interplay between cytokines and nuclear factor-kappa B (NF-кB), a complex cytoplasmic protein that is involved in p50 and p65 dimer activation (2021). Our findings revealed that lead induced endothelial inflammation, which manifested in the significant increase in IL-6 and TNF-α levels and that treatment with GBE suppresses these cytokine levels in the endothelium, supporting Ginkgo biloba anti-inflammatory impact in rat endothelium. Furthermore, increased oxidative stress and apoptosis have been linked to a variety of disease conditions (Paithankar et al. 2021). During the apoptotic process, however, Bax releases cytochrome-C from mitochondria, which sets off a chain of events that leads to caspase activation and cell death. Stress stimuli such as DNA damage or reactive oxygen species activate caspase-9, the initiator caspase, resulting in the formation of an Apaf-1/procaspase-9 apoptosome, which then activates caspase-3 and caspase-7, the cell’s downstream effectors (Shakeri et al. 2021; Kolawole et al. 2022). Nonetheless, by suppressing the release of cytochrome-C by Bax, Bcl-2 prevents the downstream activation of apoptotic machinery (Shakeri et al. 2021; Kolawole et al. 2022). Lead-exposed rats showed considerably lower endothelial Bcl-2 protein expression in this study, indicating that apoptosis is linked to toxic effect of lead acetate exposure. Following treatment with Ginkgo biloba (50 and 100 mg), Bcl-2 protein expression was enhanced significantly, indicating that the extract had anti-apoptotic properties.