Antidepressant Drugs Modulate Differentially Anti-inflammatory Lithium’s Property: An in Vitro and in Vivo Study (original) (raw)
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The Dual Effect of Lithium on Inflammatory Bowel Disease and Bipolar Disorder: A Review
Madridge Journal of Clinical Research
Lithium has been the gold standard for treatment of bipolar disorder since the mid-20th century. Lithium, at low doses, gained popularity as the first-line treatment of this disorder. Eventually, lithium became part of many successful treatment plans for bipolar and depressed patients, leading to more focused research on basic and applied pharmacological effects of this drug. However, the evidence that lithium can reduce inflammation by inhibiting glycogen synthase kinase 3-beta (GSK3β) enzyme which is linked to autoimmune and inflammatory disorders, and cancer is still emerging. Therefore, this review examines whether inflammatory conditions such as Inflammatory Bowel Disease (IBD) have a higher occurrence rate of mental illness in comparison to the population presenting with IBD without the co-pathology of mental illness. This investigation explored lithium's beneficial effects in IBD when evaluated either in animal models or in IBD patients with or without chronic mental illness. Further research must be conducted to evaluate for significant evidence of its antipsychotic and antiinflammatory effects for IBD patients with chronic mental illness.
Brazilian Journal of Psychiatry
Objective: To evaluate whether an animal model of mania induced by lisdexamfetamine dimesylate (LDX) has an inflammatory profile and whether immune activation by lipopolysaccharides (LPS) has a cumulative effect on subsequent stimuli in this model. We also evaluated the action of lithium (Li) on inflammatory and neurotrophic factors. Methods: Adult male Wistar rats were subjected to an animal model of mania. After the open-field test, they were given LPS to induce systemic immune activation. Subsequently, the animals' blood was collected, and their serum levels of brain-derived neurotrophic factor and inflammatory markers (tumor necrosis factor [TNF]-a, interleukin [IL]-6, IL-1b, IL-10, and inducible nitric oxide synthase [iNOS]) were measured. Results: LDX induced hyperactivity in the animals, but no inflammatory marker levels increased except brain-derived neurotrophic factor (BDNF). Li had no effect on serum BDNF levels but prevented iNOS levels from increasing in animals subjected to immune activation. Conclusion: Although Li prevented an LPS-induced increase in serum iNOS levels, its potential antiinflammatory effects in this animal model of mania were conflicting.