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Anticancer Properties of Silver Nanoparticles from Root Extract of Trigonella Foenum-Graecum
Published in Megh R. Goyal, Preeti Birwal, Santosh K. Mishra, Phytochemicals and Medicinal Plants in Food Design, 2022
Ramasamy Harikrishnan, Lourthu Samy S. Mary, Gunapathy Devi, Chellam Balasundaram
A number of proapoptotic fragments of molecules are discharged from the mt through the apoptosis. The mt in the presence of ATP discharged cytochrome c that linked with Apaf-1 in the cytosol encouraging its oligomerization. The apoptosome is produced from oligomeric-Apaf-1 combination and pro-caspase-9, which enhances the stimulation of caspase-9, and in chance triggers the effector caspases-3 and -7 [8]. The exciting outcome from this study was that though ATP concentration declined post-TFAgNPs interaction, the caspase-9 activity was quiet prominent in this experiment.
A Review on Medicinal Plants used in Cardioprotective Remedies in Traditional Medicine
Published in Anne George, Oluwatobi Samuel Oluwafemi, Blessy Joseph, Sabu Thomas, Sebastian Mathew, V. Raji, Holistic Healthcare, 2017
The in vitro and in vivo studies have suggested that DOX induce cardiac toxicity through apoptosis, necrosis and other form of cell death called autophagy. DOX treatment induces apoptosis via an intrinsic and extrinsic pathway. In the extrinsic pathway; caspase 8 was activated by binding of death ligands (FasL, TNF-a, and TRAIL) with their receptors leads to subsequent activation of caspase 3, which results in cell death. The intrinsic pathway is mediated by mitochondrial cytochrome c release (Table 11.4). The cytochrome c forms a complex called apoptosome with the adaptor protein apoptosis protease activator protein-1 (Apaf-1), dATP, and caspase 9 in cytosol. This apoptosome activates caspase 9 results in DNA fragmentation.50 Recent studies have shown that DOX treatment significantly increased the cardiac expression of pro-inflammatory cytokine, inflammatory cell infiltration, and necrosis in rat hearts. The increased generation of ROS leads to mitochondrial calcium accumulation, promotes MPT pore opening, causes mitochondrial swelling and ATP depletion, and hence triggers necrotic cell death.51,52
Applied physiology: neuropathic pain
Published in Peter R Wilson, Paul J Watson, Jennifer A Haythornthwaite, Troels S Jensen, Clinical Pain Management, 2008
Victoria CJ Wallace, Andrew SC Rice
Many forms of nerve injury can also produce death of sensory neurons.96 Apoptosis may be a result of mitochondrial dysfunction97 and has been associated with a number of neuropathies.96,98,99 Mitochondria-dependent apoptosis is activated by a number of factors including reactive oxygen species, ceramide, and nitric oxide,100 which have been implicated in the pathophysiology of neuropathies. These factors cause the release of cytochrome C from mitochondria leading to the formation of the apoptosome complex and subsequent activation of effector caspases. Alternatively, apoptotic pathways can be activated via stimulation of death receptors, such as TNFR1100 which can act via the JNK (c-Jun-N-terminal kinase) pathway to activate effector caspases. In support of this, TNFa is released in response to chemotherapeutic agents that produce painful peripheral neuropathy,101 following direct nerve injury,102 and in response to HIV-gp120 in vitro103 and caspases have been shown to be important in neuropathic responses in various models of neuropathy.20,96,104,105 It is thought that the activation of these pathways may be involved in neuropathic pain even though there may be a prolonged latent phase of apoptosis, before cell death.
Sevelamer arsenite nanoparticle as a Pi-responsive drug carrier and embolic agent for chemoembolization
Published in Drug Delivery, 2022
Qiu-Chen Bi, Jian-Jun Tang, Jun Zhao, Yang-Feng Lv, Zhi-Qiang Deng, Hong Chen, Yu-Hua Xu, Chuan-Sheng Xie, Qing-Rong Liang, Rong-Guang Luo, Qun Tang
Pi deprivation enhances HCC’s sensitivity to anticancer ATO, as we evidenced both in vivo and in vitro tests. Although the mechanism for the enhancement is complex, Pi-triggered apoptosis has been evidenced. Cellular apoptosis can be triggered by the mitochondrial-apoptosome-mediated intrinsic pathway. Pi deprivation stress-induced mitochondrial transmembrane potential drop-down, resulting in higher membrane permeability and cytochrome c release. The released cytochrome c from mitochondria activates caspase-9, eventually initiating caspase cascade reaction and apoptosis, as rationalized by the theory (Hengartner, 2000; Frion-Herrera et al., 2015). The promoter of apoptosis has been proved to sensitize the killing effect of ATO (Szegezdi et al., 2006; Chen et al., 2017).
Potentiality of raloxifene loaded melittin functionalized lipidic nanovesicles against pancreatic cancer cells
Published in Drug Delivery, 2022
Usama A. Fahmy, Shaimaa M. Badr-Eldin, Hibah M. Aldawsari, Nabil A. Alhakamy, Osama A. A. Ahmed, Mohamed F. Radwan, Basma G. Eid, Shaban R. M. Sayed, Gamal A. El Sherbiny, Walaa Abualsunun
Additionally, it has been found that pro-apoptotic proteins such as Bax and pro-inflammatory cytokine TNF-α alter the MMP and alter the permeability transition pore (PTP) responsible for the release of cytochrome c from the outer mitochondrial membrane (Burke, 2017; Iqubal et al., 2019). Once cytochrome c is released from the mitochondrial pore, it associates with Apaf-1 and cascade for apoptosome formation, and caspases such as caspase 3 continues and results in apoptosis (Burke, 2017). Additionally, TNF-α binds with the TNF-α receptors and initiates the mechanism of extrinsic apoptosis via TNF receptor-associated death domain (TRADD) death-inducing signaling complex (DISC). In brief, binding of TNF-α with TNF-α receptor causes activation of procaspase-8 to caspase-8 that in turn convert procaspase-3 produced via Cyt c, Apaf-1, and apoptosome into caspase-3 and hence causes apoptosis (Josephs et al., 2018; Kretz et al., 2018). In the present study, exposure RLX-PL-MEL to the PANC1 cells showed reduced MMP, increased expression of TNF-α and caspase-3 and hence, signifies mitochondrial-mediated apoptosis. It is well established that the apoptotic potency of a drug candidate is validated by the success of an anticancer drug to arrest cycle. In the present study, using RLX-PL-MEL showed cell cycle arrest at the G2-M phase and confirmed the anticancer potential.
Effect of chronic alcohol consumption on myocardial apoptosis in the rat model of isoproterenol-induced myocardial injury and investigation on the cardioprotective role of calpain inhibitor 1
Published in Drug and Chemical Toxicology, 2022
Aysegul Oglakci-Ilhan, Kevser Kusat-Ol, Kubilay Uzuner, Onur Uysal, Ibrahim Sogut, Ferruh Yucel, Gungor Kanbak
High-dose chronic alcohol consumption causes mitochondrial dysfunction, apoptosis, increased reactive oxygen species production, and cellular ATP loss (Bansal et al. 2012). The primary and essential step that initiates the apoptotic pathway is cytochrome c release from mitochondria. Cytochrome c released into the cytosol forms the apoptosome with a protein called Apaf-1 and procaspase 9. Apoptosome activates caspase-9, and this activates caspase-3. Caspase 3 migrates to the nucleus causing DNA fragmentation and cell death there. Cytochrome c is bound to the inner membrane by cardiolipin, an anionic phospholipid. For the release of cytochrome c from mitochondria, it must first be separated from cardiolipin. Cardiolipin peroxidation enables cytochrome c to be released from the inner membrane (Gonzalvez and Gottlieb 2007).