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Where Cancer and Bacteria Meet
Published in Ananda M. Chakrabarty, Arsénio M. Fialho, Microbial Infections and Cancer Therapy, 2019
Alexandra Merlos, Ricardo Perez-Tomás, José López-López, Miguel Viñas
These indole-based tambjamine analogs have been used to demonstrate that anion transport induces cell membrane hyperpolarization and cell death in cancer stem cells [91]. The mechanisms responsible for the cytotoxicity of these tambjamine analogs have been studied by one of the authors (Ricardo Pérez-Tomás). The results revealed both a decrease in the intracellular pH (acidification) and the induction of apoptosis through p38 mitogen–activated protein kinase activation [92].
Substrates of Human CYP2D6
Published in Shufeng Zhou, Cytochrome P450 2D6, 2018
CYP2D6, 1A2, 3A4, and 3A5 are the predominant enzymes in the hydroxylation of KR-62980 (a novel and selective peroxisome proliferator-activated receptor-γ agonist) and KR-63198 (Kim et al. 2008). CP-122,721, a novel NK1 antagonist, undergoes O-demethylation and N-dealkylation. In human liver microsomes, O-demethylation is shown to be catalyzed by CYP2D6 with a low Km value, while N-dealkylation is catalyzed primarily by CYP3A4 (Obach et al. 2007). ML3403, a potent inhibitor of p38 mitogen-activated protein kinase, is metabolized by CYP1A2, 2C19, 2D6, and 3A4 (Kammerer et al. 2007). DRF-4367 forms a hydroxy metabolite, DRF-6574 (a novel COX-2 inhibitor), mediated by CYP2D6 and 2C19 enzymes (Muzeeb et al. 2006). UGT1A1, 1A3, and 1A8 show the catalytic activity toward DRF-4367 (Muzeeb et al. 2006). CYP1A2, 3A4, and 2D6 are responsible for the formation of oxidized metabolites, M1, M2, M4, M5, and M9, from RWJ-53050, a novel anxiolytic agent (Wu et al. 2006). In addition, oxybutynin is metabolized by CYP2C9, 2C19, 2D6, 3A4, and 3A5 (Mizushima et al. 2007).
Gene Delivery for Intervertebral Disc
Published in Raquel M. Gonçalves, Mário Adolfo Barbosa, Gene and Cell Delivery for Intervertebral Disc Degeneration, 2018
Gianluca Vadalà, Luca Ambrosio, Vincenzo Denaro
An additional and significant degenerative trigger is inflammation: it has been previously reported that proinflammatory cytokines, such as IL-1, TNF-α, and IL-6 effectively, activate catabolic factors and promote IDD. On the other hand, mechanical stress upregulates p38 mitogen-activated protein kinase (MAPK), which physiologically inhibits the catabolic effect mediated by the aforementioned cytokines (Studer et al. 2007).
Opening eyes to therapeutic perspectives of bioactive polyphenols and their nanoformulations against diabetic neuropathy and related complications
Published in Expert Opinion on Drug Delivery, 2021
Rubiya Khursheed, Sachin Kumar Singh, Sheetu Wadhwa, Monica Gulati, Bhupinder Kapoor, Ankit Awasthi, Arya Kr, Rajan Kumar, Faheem Hyder Pottoo, Vijay Kumar, Harish Dureja, Krishnan Anand, Dinesh Kumar Chellappan, Kamal Dua, K. Gowthamarajan
Yang et al. in 2019 explored the role of quercetin on DNP associated with the P2X4 receptor in the dorsal root ganglia (DRG) of type 2 diabetes mellitus (T2DM) induced rat model. The outcomes revealed that both thermal withdrawal latency and mechanical withdrawal threshold in quercetin treated diabetic rats were increased in contrast to the untreated group. The increased expression of P2X4 was also remarkably suppressed in diabetic rats and also reduced the enhancement in phosphorylated p38 mitogen‐activated protein kinase (p38MAPK) in the DRG. Quercetin remarkably attenuated the P2X4 agonist adenosine triphosphate‐triggered currents in P2X4 receptor transfected HEK293 cells; thus reduced the mechanical and thermal hyperalgesia in diabetic rats [44]. Ji et al. in 2017 reported that single or long-term supplementation of quercetin reduced cold and thermal hyperalgesia dose dependently. Moreover, the symptoms of DNP were reduced by quercetin pre-supplementation. Additionally, quercetin decreased the MAP3K7, and JNK2 phosphorylation in cultured astrocytes. Moreover, quercetin suppressed the NF-κB activity through upregulation of MAP3K7 which was proven by luciferase assay in HEK293 cells. Quercetin also exhibits anti-inflammatory activities and improves DNP via the suppression of Toll-like receptor (TLR) signaling pathway [45]. Moreover, administration of quercetin to diabetic rats prevented neuronal and glial loss in the duodenum; thus, promoted neuroprotective effect [46].
Sevoflurane inhibited inflammatory response induced by TNF-α in human trophoblastic cells through p38MAPK signaling pathway
Published in Journal of Receptors and Signal Transduction, 2020
Li Mo, Shuzhen Hong, Yi Li, Zurong Hu, Baoyi Han, Zaomei Wei, Jie Jia
The p38 mitogen-activated protein kinase (p38MAPK) signaling pathway helps cells to interpret the extracellular signals and respond accordingly. Canonically, MAP2K mediates the phosphorylation of p38MAPK signaling pathway in response of inflammation, stress and growth factors [14]. Study has proved that sevoflurane suppresses the growth and metastasis of lung cancer cells induced by hypoxia via inhibiting hypoxia-inducible factor-1α and down-regulating p38MAPK activity [15]. In addition, it has been verified that preconditioning with sevoflurane suppresses the activation of p38MAPK, and reduces the increase of permeability induced by TNF-α in rat pulmonary microvascular endothelial cells [16]. But the regulatory effects of sevoflurane on p38MAPK signaling pathway in trophoblastic cells remain unclear.
The Effects of Quercetin on the Apoptosis of Human Breast Cancer Cell Lines MCF-7 and MDA-MB-231: A Systematic Review
Published in Nutrition and Cancer, 2022
Roghayeh Molani Gol, Sorayya Kheirouri
The Twist is a basic helix-loop-helix transcription factor, which is observed in various cancer cell lines including breast cancer (121–123). P38 mitogen-activated protein kinases (p38MAPK) play an important role in cell proliferation in many cancers such as breast cancer (124). Recent findings have revealed that p38MAPK stabilizes Twist via phosphorylating it at serine 68 (125). Ranganathan et al. showed that Twist reduced in QT treated MCF-7 cells due to decrease of p38MAPK and suggested that QT acts via p38MAPK. Moreover, QT has ability to downregulate the expression of Twist (77).