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Subsequently to the publication of this paper, an interested reader drew to the authors' attention that Figs. 2 and 4, featured on p. 4820 and 4821 respectively, contained apparently matching control β‑actin western blots.

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Melatonin pleiotropically regulates physiological events and has a putative regulatory role in the circadian clock desynchrony-mediated Non-alcoholic fatty liver disease (NAFLD). In this study, we investigated perturbations in the hepatic circadian clock gene, and Nrf2-HO-1 oscillations in conditions of high-fat high fructose (HFHF) diet and/or jet lag (JL)-mediated NAFLD. Melatonin treatment (100 µM) to HepG2 cells led to an improvement in oscillatory pattern of clock genes (Clock, Bmal1, and Per) in oleic acid (OA)-induced circadian desynchrony, while Cry, Nrf2, and HO-1 remain oblivious of melatonin treatment that was also validated by circwave analysis.

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Correction: Melatonin-induced ApoE expression in mouse astrocytes protects endothelial cells from OGD-R induced injuries.

Transl Psychiatry

July 2020

Department of Integrative Medicine, Zhongshan Hospital, Fudan University, 200032, Shanghai, China.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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We studied the effect of a phase shift in circadian rhythms (desynchronosis) on the development of erosive and ulcerative lesions in the gastric mucosa in male Wistar rats with different behavioral activity in the open-field test. The animals kept under conditions of natural or shifted light-dark cycle were untreated or intraperitoneally received physiological saline (1 ml) and melatonin (1 or 2 mg/kg). Desynchronosis induced gastric ulcers in active rats not receiving injections or intraperitoneally injected with physiological saline.

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