Regular ArticleLithium Induces Apoptosis in Immature Cerebellar Granule Cells but Promotes Survival of Mature Neurons
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Pyrvinium pamoate ameliorates cyclosporin A- induced hepatotoxicity via the modulation of Wnt/β-catenin signaling and upregulation of PPAR-γ
2022, International ImmunopharmacologyCitation Excerpt :These findings supported the conclusions of a previous experimental investigation on a NASH model where PP decreased the hepatic FZD-7 expression. In some cells, an increased expression or stability of β-catenin has been observed to promote apoptosis [11,31]. CsA generated a considerable increase in hepatic β-catenin expression in this study, which was also seen in earlier cardiotoxicity research [65].
Patients receiving lithium therapy have a reduced prevalence of neurological and cardiovascular disorders
2016, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :A variety of evidence from in vitro and animal studies suggests that lithium has neurotrophic and cytoprotective properties. Recent research studies have reported that lithium can inhibit neuronal apoptosis (D'Mello et al., 1994; Nonaka et al., 1998), protects against neuronal death from a variety of injurious agents (Bijur et al., 2000; Centeno et al., 1998; Inouye et al., 1995; Xu et al., 2003; Zhong et al., 2006), and can enhance neuronal growth (Chen et al., 2000; Hellwey et al., 2002; Williams et al., 2004; Yasuda et al., 2009). Moreover, lithium has been demonstrated to improve brain function following brain injury.
Posterior cerebellar vermal deficits in bipolar disorder
2013, Journal of Affective DisordersChronic lithium impairs skin tolerance to ischemia in random-pattern skin flap of rats
2011, Journal of Surgical ResearchCitation Excerpt :Lithium is a mainstay for treatment of manic-depressive disorders, which was introduced into psychiatry in 1949 for the treatment of mania [4]. However, it took decades until newer properties of this drug were recognized [5, 6]. The potent biological properties of lithium in inhibiting programmed cell death attracted considerable interest to this drug in the field of reperfusion injury as well as neurodegenerative disorders such as Alzheimer's disease [7].
Molecular actions and therapeutic potential of lithium in preclinical and clinical studies of CNS disorders
2010, Pharmacology and TherapeuticsCitation Excerpt :Although AP-1 activation may be either anti-apoptotic or pro-apoptotic depending on the nature of AP-1 binding components and the target genes induced (Karin, 1998; Mummery, 1975), it has been suggested that m3-muscarinic receptors and the DNA binding activities of AP-1 and CREB play prominent roles in regulating cell viability. Earlier pioneering studies noted that lithium promotes survival of gamma aminobutyric acid-releasing (GABAergic) neurons (Volonte et al., 1994) and mature CGCs (D'Mello et al., 1994), and accumulating evidence from various laboratories supports the view that lithium protects against diverse forms of death insults, suggesting that it is a multifunctional neuroprotectant. Glutamate-induced excitotoxicity in discrete brain areas has been implicated in a variety of neurodegenerative diseases such as stroke, Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), brain trauma, cerebellar degeneration, spinal cord injury, and possibly Alzheimer's disease (AD) and Parkinson's disease (PD) (Friedlander, 2003; Mattson & Kroemer, 2003; Yuan & Yankner, 2000).
Protective role of lithium during aluminium-induced neurotoxicity
2010, Neurochemistry International