Tropisetron diminishes demyelination and disease severity in an animal model of multiple sclerosis

Protective effects of tropisetron on cerulein-induced acute pancreatitis in mice

“…3A, B) indicating its potent anti-inflammatory aspects. These results confirm different experimental findings revealed tropisetron administration exerts notable protective effects in peripheral and central inflammatory conditions such as experimental inflammatory bowel disease [15], experimental autoimmune encephalomyelitis [19], stroke [17] and beta-amyloid-induced neuroinflammation [18]. The protective actions of tropisetron in AP could be a classical 5-HT 3 receptor dependent effects as recently ondansetron, another 5-HT 3 receptor antagonists, was shown to decrease serum levels of amylase and lipase, cell infiltration and cytokine production in cerulean-induced AP [32].…”

“…Tropisetron, a 5-HT 3 receptor antagonist, is widely used to treat chemotherapy associated emesis [13]. Anti-inflammatory and antioxidant aspects of tropisetron have been shown in various peripheral and central inflammatory settings [14], including experimental colitis [15], cisplatin-induced nephrotoxicity [16], ischemic stroke [17], beta-amyloid-induced neuroinflammation [18] and animal model of multiple sclerosis [19]. Furthermore, in a rat model of cecal ligation and puncture (CLP)-induced sepsis tropisetron administration significantly inhibited TNF-a and IL-6 overproduction in serum [20].…”

Serotonin decreases the production of Th1/Th17 cytokines and elevates the frequency of regulatory CD4+ T‐cell subsets in multiple sclerosis patients

“…In EAE, a study by Aminian et al. demonstrated that selective 5‐HT3 receptor antagonists attenuated disease, and this protective effect was associated with both lower demyelination of the spinal cord and reduced in vitro IL‐6 and IL‐17 production by MOG‐specific CD4 + T cells. By contrast, a recent study published by Chabbi‐Achengli et al.…”

“…This effect can be associated with the ability of this receptor to act as an inotropic ligand-gated ion channel, which is different from other serotonin receptors whose action is mediated via G-proteins [42]. In EAE, a study by Aminian et al [43] demonstrated that selective 5-HT3 receptor antagonists attenuated disease, and this protective effect was associated with both lower demyelination of the spinal cord and reduced in vitro IL-6 and IL-17 production by MOG-specific CD4 + T cells. By contrast, a recent study published by Chabbi-Achengli et al [44], using an experimental rheumatoid arthritis model, demonstrated the ability of serotonin, via the 5-HT2A receptor, to reduce the severity of collagen-induced arthritis in mice.…”

5-HT3 Receptor Antagonists in Neurologic and Neuropsychiatric Disorders: The Iceberg Still Lies beneath the Surface

“…Multiple studies have highlighted the potential neuroprotective properties of ondansetron and tropisetron (Rahimian et al, 2011a(Rahimian et al, , 2013bVenail et al, 2012;Aminian et al, 2013;Dyhrfjeld-Johnsen et al, 2013;Swartz et al, 2013), consistent with their capacity for inhibiting the protein phosphatase calcineurin-involved neurodegenerative cascades (de la Vega et al, 2005;Rahimian et al, 2011b). These results with R-azasetron are consistent with a neuroprotective effect through calcineurin inhibition (Dyhrfjeld-Johnsen, 2016, 2017; Petremann et al, 2017), as is the lack of a protective effect for granisetron since this setron does not inhibit calcineurin (de la Vega et al, 2005;Rahimian et al, 2011b).…”