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Natural Products as an Effective Treatment Option for Depression
Published in Vikas Kumar, Addepalli Veeranjaneyulu, Herbs for Diabetes and Neurological Disease Management, 2018
Yogesh Anant Kulkarni, Kalyani Himanshu Barve, Ginpreet Kaur
Some of the components in rosamarinus like luteolin (Lut), carnosic acid (CA), and rosmarinic acid show anti-depressant effect by regulating gene expression in mice brain like tyrosine hydroxylase (TH), pyruvate carboxylase (PC) and MAPK phosphatase (MKP-1), which are in turn involved in regulating the release of several neurotransmitters (dopamine, norepinephrine, serotonin, and acetylcholine).91 Furthermore compounds contributing to anti-depressant effect of rosemary may be carnosol and betulinic acid.92 A constituent common to many plants also found in rosemary is ursolic acid which shows antidepressant-like effect mediated by an interaction with the dopaminergic system, through the activation of dopamine D1 and D2 receptors.93
Intracellular Signaling Transduction Dysregulation in Depression and Possible Future Targets for Antidepressant Therapy:Beyond the Serotonin Hypothesis
Published in Siegfried Kasper, Johan A. den Boer, J. M. Ad Sitsen, Handbook of Depression and Anxiety, 2003
Andrea Trentani, S. Kuipers, G.J. Ter Horst
Whether or not chronic stress, through its action on neurotrophin expression, is one of the main pathological factors involved in the etiology of depression, this hypothesis provides new targets to improve the efficacy and/or reduce the delay and side effects typical of antidepressants today. These alternative approaches are summarized below, followed by an in-depth discussion of each perspective. Removal or reduction of stress. Reduction of stress refers not only to the reduction of external stressors (psychological or physical stressors), but also to the physiological and/or pathological changes induced by their acute or prolonged exposition (such as increased blood pressure and cortisol levels, changes in releasing factors and/or releasing hormones). The normalization of the physiological parameters and restoration of body homeostasis might enhance the efficacy of antidepressant treatments.BDNF replacement therapy.Direct stimulation or inhibition of selective kinases or phosphatases involved in the neurotrophin transduction system (fluoxetine stimulates the expression of a gene that codifies for a MAPK-phosphatase).Estrogen replacement therapy. Prevention of stress-induced limbic overload.
Chronic Otitis Media
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
George G. Browning, Justin Weir, Gerard Kelly, Iain R.C. Swan
Fbxo11 and Evi1 also interact with the transforming growth factor beta (TGF-² or TGFB) signalling pathway in mice21 and in humans.22 Tateossian et al. 23 identified a further link between TGF-² and COME in mutant TGF-²-induced factor homeobox 1 (Tgif1) mice, highlighting the importance of the TGF-² signalling pathway and its effects on the responses to hypoxia in the chronically inflamed middle ear. There is considerable crosstalk between TGF-² and HIF-1± pathways as both SMAD-3 (which is one of the many mediators of the TGF-² pathway) and HIF-1± are coactivators of VEGF expression.24 Furthermore, TGF-² /SMAD signalling leads to downregulation of p38 by including MAPK phosphatase-1 and the subsequent suppression of the mucin protein MUC5AC,25 resulting in the impaired mucociliary defence. Conversely, NTHi strongly induced upregulation of MUC5AC via activation of the Toll-like receptor 2-MyD88-dependent p38 pathway in a middle ear epithelial cell line.25 In addition, MUC5AC rather than MUC5B or MUC2 was shown to be associated with OME,26 though this has been challenged by Preciado et al. 27 who showed that MUC5B is the predominant mucin in middle ear effusions from children with OME. However, Kerschner et al. 28 showed that the MUC5AC gene was upregulated by more than 150 times in OME samples compared with controls. Either way, the upregulation of mucins, whether by microbial pathogens, cytokines, growth factors, cigarette smoke29 or gastric acid,30 results in overproduction of mucin within the middle ear and the subsequent conductive deafness.
The mechanism of miR-363-3p/DUSP10 signaling pathway involved in the gastric mucosal injury induced by clopidogrel
Published in Toxicology Mechanisms and Methods, 2021
Jiang Zongdan, Lu Yuyu, Wang Zhibing, Li Chao, Zhang Zhenyu, Sun Weihao
Our recent study (Wu et al. 2013) had concluded that attenuated expression of the TJ proteins occludin and ZO-1 in human gastric epithelial cells could be involved in clopidogrel-induced gastric mucosal injury through activation of the p38 MAPK pathway. P38 is a kinase that regulates multiple cellular functions, including cell apoptosis, differentiation, stress response, proliferation, and so on (Cuenda and Sanz-Ezquerro 2017). Negative regulation of MAPK activity is mediated by MAPK phosphatase (MKP) (Farooq and Zhou 2004). The dual-specificity phosphatase 10 (DUSP10) also called MKP5 was identified as a phosphatase that selectively inactivates JNK and p38 MAPK (Tanoue et al. 1999). Interestingly, different groups have described how the DUSP10 gene is negatively regulated by miRNAs, which are induced in different diseases and cancers. In hepatocellular cancer and pancreatic cancer, miR-181 and miR-92a, respectively, negatively regulate the DUSP10 expression, affecting the proliferation and migration of tumorigenic cells (Song et al. 2013; He et al. 2014).
Advances with glucocorticoids in the treatment of asthma: state of the art
Published in Expert Opinion on Pharmacotherapy, 2020
Josuel Ora, Luigino Calzetta, Maria Gabriella Matera, Mario Cazzola, Paola Rogliani
The secretion of anti-inflammatory proteins, such as mitogen-activated protein kinase (MAPK) phosphatase, is increased by GCR activation, with the final result of inhibiting MAPK signaling pathways [11]. Less commonly, histone deacetylases promote a process that packs DNA into an inactivated chromatin structure which prevents transcriptional activity of several genes and this is also linked to the drug’s side effects, such as inhibition of osteocalcin, involved in bone synthesis [18,19]. GCs also have a post-transcriptional effect on some proinflammatory genes. Inflammatory mediators stabilize unstable messenger RNA while GCs reverse this process, accelerating its degradation [20]. In asthmatic inflammation, a reduced production of pathogenic asthma interleukins (ILs) such as IL-4, IL-5, and IL-13 mitigates the airway inflammatory activity [21].
Exploitation of receptor tyrosine kinases by viral-encoded growth factors
Published in Growth Factors, 2018
The unique receptor profile of ORFV VEGF-E variants has been exploited to dissect VEGFR2 signalling pathways in endothelial cells. Selective activation by VEGF-E demonstrated the role of VEGFR2 in activation of ERK, Akt, PLCγ and endothelial cell proliferation and tube formation (Kawamura et al., 2008; Grummer et al., 2009; Cudmore et al., 2012). The role of VEGFR2 in eNOS expression, NO release, and vessel vasodilation was also demonstrated with VEGF-E (Kroll & Waltenberger, 1999; Ahmad et al., 2006; Cudmore et al., 2006). VEGF-E-induced pro-urokinase-type plasminogen activator expression, urokinase receptor trafficking and fibrinolytic activity confirmed a role for VEGFR2 in endothelial cell migration (Prager et al., 2004; Poettler et al., 2012). Studies with VEGF-E also illustrated that VEGFR2 activation of MAPK phosphatase-1 leads to dephosphorylation of ERK and p38MAPK and suppression of endothelial cell migration (Kinney et al., 2008). As selected VEGF-E variants bind NRP1, they have also proved useful in defining the influence of this co-receptor on VEGFR2-mediated activities. Activation of the VEGFR2-NRP1 complex has highlighted the role of NRP1 in sprouting angiogenesis in embryonic stem cells, formation of branching pericyte-coated vessels in subcutaneous matrigel plugs in mice and sprouting of intersegmental vessels in zebrafish (Kawamura et al., 2008). The endothelial signalling pathways induced by the other PPV VEGF-Es and megalocytivirus VEGFs have not yet been examined.