Journal of Pineal Research最新文献

RETRACTION: S. Cuzzocrea, G. Costantino, E. Mazzon, and A. P. Caputi, “Regulation of Prostaglandin Production in Carrageenan-Induced Pleurisy Melatonin,” Journal of Pineal Research 27, no. 1 (1999): 9-14, https://doi.org/10.1111/j.1600-079X.1999.tb00591.x.

The above article, published online on 30 January 2007 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Gianluca Tosini; and John Wiley & Sons Ltd. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, the sample shown in Figure 3A has been identified as being used in a different scientific context in another article from the same author group, which was submitted concurrently. The data provided by the corresponding author upon request was insufficient to address the concerns. The article is retracted as the editors have lost trust in the accuracy and integrity of the overall body of data presented in the article and consider its conclusions invalid.

RETRACTION: S. Cuzzocrea, B. Zingarelli, G. Costantino, and A. R. Caputi, “Protective Effect of Melatonin in a Non-Septic Shock Model Induced by Zymosan in the Rat,” Journal of Pineal Research 25, no. 1 (1998): 24–33, https://doi.org/10.1111/j.1600-079X.1998.tb00382.x.

The above article, published online on 30 January 2007 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Gianluca Tosini; and John Wiley & Sons Ltd. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, there is evidence of image duplication between Figures 6A and 6C, indicating that the same biological sample has been utilized to represent two distinct experimental conditions. The article is retracted as the editors have lost trust in the accuracy and integrity of the overall body of data presented in the article and consider its conclusions invalid.

RETRACTION: R. D'Emmanuele Di Villa Bianca, S. Marzocco, R. Di Paola, G. Autore, A. Pinto, S. Cuzzocrea, and R. Sorrentino, “Melatonin Prevents Lipopolysaccharide-induced Hyporeactivity in Rat,” Journal of Pineal Research 36, no. 3 (2004): 146-154, https://doi.org/10.1046/j.1600-079X.2003.00111.x.

The above article, published online on 8 March 2004 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Gianluca Tosini; and John Wiley & Sons Ltd. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, there is evidence of image duplication between Figures 6A and 8A, indicating that the same biological sample has been utilized to represent two distinct experimental conditions. The article is retracted as the editors have lost trust in the accuracy and integrity of the overall body of data presented in the article and consider its conclusions invalid.

The identification of protective agents for the treatment of neurodegenerative diseases is the mainstay therapeutic goal to modify the disease course and arrest the irreversible disability progression. Pharmacological therapies synergistically targeting multiple pathogenic pathways, including oxidative stress, mitochondrial dysfunction, and inflammation, are prime candidates for neuroprotection. Combination or synergistic therapy with melatonin, whose decline correlates with altered sleep/wake cycle and impaired glymphatic “waste clearance” system in neurodegenerative diseases, has a great therapeutic potential to treat inflammatory neurodegenerative states. Despite the protective outcomes observed in preclinical studies, mild or poor outcomes were observed in clinical settings, suggesting that melatonin combinations promoting synergistic actions at appropriate doses might be more suitable to treat multifactorial neurodegenerative disorders. In this review, we first summarize the key melatonin actions and pathways contributing to cell protection and its therapeutic implication in Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). We remark the major controversies in the field, mostly generated by the lack of a common consensus for the optimal dosing, molecular targets, and toxicity. Then, we review the literature investigating the efficacy of melatonin combinations with approved or investigational neuroprotective agents and of melatonin-containing hybrid molecules, both in vitro and in animal models of AD, PD, and MS, as well as the efficacy of add-on melatonin in clinical settings. We highlight the rationale for such melatonin combinations with a focus on the comparison with single-agent treatment and on the assays in which an additive or a synergistic effect has been achieved. We conclude that a better characterization of the mechanisms underlying such melatonin synergistic actions under neuroinflammation at appropriate doses needs to be tackled to advance successful clinical translation of neuroprotective melatonin combination therapies or melatonin-based hybrid molecules.

Metabolic dysfunction-associated steatotic liver disease (MASLD) affects two billion people worldwide and is currently mostly treatable via lifestyle interventions, such as exercise training. However, it is unclear whether the positive effects of exercise are restricted to unique circadian windows. We therefore aimed to study whether the timing of exercise training differentially modulates MASLD development. Twenty weeks old male APOE*3-Leiden.CETP mice were fed a high fat-high cholesterol diet to induce MASLD and treadmill-trained for 1 h five times per week for 12 weeks either early (ZT13; E-RUN) or late (ZT22; L-RUN) in the dark phase while corresponding sedentary groups (E-SED and L-SED) did not. Late, but not early exercise training decreased the MASLD score, body weight, fat mass, and liver triglycerides, accompanied by an altered composition of the gut microbiota. Specifically, only late exercise training increased the abundance of short-chain fatty acid-producing bacterial families and genera, such as Akkermansia, Lachnospiraceae, and Rikenella. To assess the role of the gut microbiota in training-induced effects, the study was repeated and trained (ZT22 only, RUN) or sedentary mice (SED) served as fecal donors for sedentary recipient mice (RUN FMT and SED FMT). Fecal microbiota transplantation reduced liver weight and plasma triglycerides in RUN FMT compared to SED FMT and tended to lower the MASLD score and liver triglycerides. Timing of exercise training is a critical factor for the positive effect on MASLD in this preclinical model, and the effect of late exercise is partially mediated via the gut-liver axis.

The dried root of Peucedanum praeruptorum is often used medicinally and has high pyran- and furanocoumarin content. Although exogenous melatonin (MT) impacts the regulation of plant growth, stress responses, secondary metabolism, etc., it remains unclear whether MT regulates the vegetative growth and development of P. praeruptorum. Thus, the aim of the current study is to characterize the effects of different exogenous MT concentrations on the physiological functions, photosynthesis, antioxidant systems, hormone induction, and coumarin synthesis of P. praeruptorum. Different MT concentrations exert distinct regulatory effects on P. praeruptorum growth and the expression of genes related to coumarin synthesis. Treatment of P. praeruptorum with low concentrations of MT increases photosynthesis and leaf growth compared to the control, while high concentrations reduce root vitality and elongation and decrease the expression of photosynthetic system genes. Low concentrations of MT also significantly increase antioxidant enzyme activity and photosynthetic pigment content and modulate the levels of IAA, gibberellic acid, salicylic acid, jasmonic acid, abscisic acid, and endogenous MT. Moreover, MT increases the activity of the MT synthesis enzymes tryptophan decarboxylase, tryptophan hydroxylase, tryptamine-5-hydroxylase, serotonin N-acetyltransferase, acetylserotonin O-methyltransferase, and caffeic acid O-methyltransferase, and promotes the accumulation of isoscopoletin, scopoletin, peucedanocoumarin II, praeruptorin A, praeruptorin B, and praeruptorin E. MT also upregulates most genes associated with coumarin synthesis, including PAL1, C4H, 4CL-3, C3H-1, F6H-1, CCoAMT, OMT-1, CYP71AJ1, CYP84A1-1, S8H-1, PT-1, and COSY-1. These findings demonstrate that MT may improve P. praeruptorum growth and development while promoting the synthesis of coumarin components.