Treatment with Melatonin Improves Cognitive Behavior and Motor Skills in a Rat Model of Liver Fibrosis

Haeger, Paola; Bouchet, Antoine; Ossandón, Carolina; Bresky, Gustavo

doi:10.5604/01.3001.0012.7867

Cited by 10 publications

(6 citation statements)

References 33 publications

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“…Curiously, a study employed male Sprague−Dawley rats with CCl 4 ‐induced liver fibrosis to evaluate the alterations on behavior and cognitive skills. Higher escape latency and speed were observed when fibrosis was induced, while melatonin administration reduced these parameters, improving the motor skills and cognition of fibrotic rats (Haeger et al, 2019).…”

Section: Resultsmentioning

confidence: 99%

“…Despite the differences in administration route, dosage, and method of fibrosis induction, melatonin is demonstrated to restrain hepatic fibrosis, improving fibrotic markers and histopathology of animal livers (Bona et al, 2018;Chen et al, 2019;Cho et al, 2015;Choi et al, 2015;Colares et al, 2016;Crespo et al, 2015;Czechowska et al, 2015;Das et al, 2017;Esrefoglu et al, 2017;González-Fernández et al, 2017Haeger et al, 2019;Kang et al, 2016;Lebda et al, 2018;D. J. Li et al, 2019;Liao et al, 2020;McMillin et al, 2017;Mortezaee et al, 2017Nalobin et al, 2016;Ostrycharz et al, 2020;Renzi et al, 2011;San-Miguel et al, 2015;Shajari et al, 2015;Stacchiotti et al, 2019;Wang et al, 2018;Wu et al, 2017;Zaitone et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…Although no melatonin measurements in plasma samples have been performed in the included studies, the highest dose employed of melatonin was 30 mg/kg (D. J. Li et al, 2019). Despite the differences in administration route, dosage, and method of fibrosis induction, melatonin is demonstrated to restrain hepatic fibrosis, improving fibrotic markers and histopathology of animal livers (Bona et al, 2018; Chen et al, 2019; Cho et al, 2015; Choi et al, 2015; Colares et al, 2016; Crespo et al, 2015; Czechowska et al, 2015; Das et al, 2017; Esrefoglu et al, 2017; González‐Fernández et al, 2017, 2018; Haeger et al, 2019; Kang et al, 2016; Lebda et al, 2018; D. J. Li et al, 2019; Liao et al, 2020; McMillin et al, 2017; Mortezaee et al, 2017, 2018; Nalobin et al, 2016; Ostrycharz et al, 2020; Renzi et al, 2011; San‐Miguel et al, 2015; Shajari et al, 2015; Stacchiotti et al, 2019; Wang et al, 2018; Wu et al, 2017; Zaitone et al, 2011). In line with this, beneficial properties of melatonin have been broadly reported in several liver pathologies, such as FHF (Laliena et al, 2012) and HCC (Carbajo‐Pescador et al, 2013; Sánchez et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

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Beneficial effects of melatonin on liver fibrosis: A systematic review of current biological evidence

San‐Miguel

Fernández-Palanca

Mauriz

et al. 2022

Journal Cellular Physiology

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Hepatic fibrosis is a reversible response to either acute or chronic cellular injury from a wide variety of etiologies, characterized by excessive deposition of extracellular matrix resulting in liver dysfunction and cirrhosis. Melatonin (N‐acetyl‐5‐methoxytryptamine), the main product secreted by the pineal gland, is a multitasking indolamine with important physiological functions such as anti‐inflammatory and antioxidant actions, modulation of circadian rhythms, and immune system enhancement. Among the numerous biological activities of melatonin, its antifibrotic effects have received increasingly more attention. In this study, we performed a systematic review of publications of the last 10 years evaluating the mechanisms of action of melatonin against liver fibrosis. The study protocol was registered at PROSPERO (CRD42022304744). Literature research was performed employing PubMed, Scopus, and Web of Science (WOS) databases, and after screening, 29 articles were included. Results from the selected studies provided denoted the useful actions of melatonin on the development, progression, and evolution of liver fibrosis. Melatonin antifibrotic effects in the liver involved the reduction of profibrogenic markers and modulation of several cellular processes and molecular pathways, mainly acting as an antioxidant and anti‐inflammatory agent. In addition, the indolamine influenced different molecular processes, such as hepatocyte apoptosis, modulation of autophagy and mitophagy, restoration of circadian rhythms, and modulation of microRNAs, among others. Although some limitations have been found regarding variability in the study design, the findings here summarized display the potential role of melatonin in ameliorating the development of liver fibrosis and its possible progression to liver cirrhosis and hepatocarcinoma.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Beneficial effects of melatonin on liver fibrosis: A systematic review of current biological evidence

San‐Miguel

Fernández-Palanca

Mauriz

et al. 2022

Journal Cellular Physiology

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“…These treatments result in hyperammonemia, 89,91 hyperpermeability of the BBB, 91 increased neuroinflammatory signals, 88‐90 microglia/glial cell activation 88,89 and increased GABA signaling 88 . In rats, CCl 4 administration (0.1‐0.2 mL/kg twice per week; ip for up to 5 months) 87,92,93 results in hyperammonemia, 87,92 impaired memory acquisition as determined using the Morris Water Maze 87,93 and a decrease in hippocampal neurogenesis 87…”

Section: Current Animal Models Of Hementioning

confidence: 99%

2021 ISHEN guidelines on animal models of hepatic encephalopathy

DeMorrow

Cudalbu

Davies

et al. 2021

Liver International

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This working group of the International Society of Hepatic Encephalopathy and Nitrogen Metabolism (ISHEN) was commissioned to summarize and update current efforts in the development and characterization of animal models of hepatic encephalopathy (HE). As defined in humans, HE in animal models is based on the underlying degree and severity of liver pathology. Although hyperammonemia remains the key focus in the pathogenesis of HE, other factors associated with HE have been identified, together with recommended animal models, to help explore the pathogenesis and pathophysiological mechanisms of HE. While numerous methods to induce liver failure and disease exist, less have been characterized with neurological and neurobehavioural impairments. Moreover, there still remains a paucity of adequate animal models of Type C HE induced by alcohol, viruses and non‐alcoholic fatty liver disease; the most common etiologies of chronic liver disease.

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“…Melatonin is secreted by the pineal gland and plays a cyto-protective role in the regulation of oxidative stress, apoptosis-related factors and signaling pathways (3). Melatonin is beneficial during the treatment of insomnia, obesity, type 2 diabetes and liver fibrosis (4)(5)(6) and can inhibit hormone-dependent or hormone-independent tumors (7). notably, melatonin was found to exert its anticancer activity through various biological processes including chemosensitivity, reduced drug resistance and anti-proliferative effects in ovarian, breast, prostate, oral, gastric and colorectal cancers (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Melatonin suppresses epithelial‑to‑mesenchymal transition in the MG‑63 cell line

et al. 2019

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epithelial-to-mesenchymal transition (eMT) is a major process involved in tumor progression and metastasis. Melatonin is secreted by the pineal gland and has been documented as a potential therapeutic agent for multiple tumors. However, the effects of melatonin on eMT during osteosarcoma (oa) development remain undefined. The present study explored the biological functions and effects of melatonin on eMT induced by transforming growth factor β1 (TGF-β1) and its underlying mechanisms in MG-63 cells. using western-blotting and immunofluorescence, it was found that the switch in e-cadherin/n-cadherin and vimentin expression was induced by TGF-β1, which was reversed by melatonin through the suppression of Snail and matrix metalloproteinase 9 (MMP-9), through hypoxia-inducible factor 1α (HiF-1α) inhibition. These findings demonstrated that the anticancer effects of melatonin against oa MG-63 cells is through the suppression of eMT via HiF-1α/Snail/MMP-9 signaling.

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Treatment with Melatonin Improves Cognitive Behavior and Motor Skills in a Rat Model of Liver Fibrosis

Cited by 10 publications

References 33 publications

Beneficial effects of melatonin on liver fibrosis: A systematic review of current biological evidence

Beneficial effects of melatonin on liver fibrosis: A systematic review of current biological evidence

2021 ISHEN guidelines on animal models of hepatic encephalopathy

Melatonin suppresses epithelial‑to‑mesenchymal transition in the MG‑63 cell line

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