Sürdürülebilir Kalkınma Amaçları
Yazarlar
- Erten, Fusun(2)
- Abbasoglu Topa, Elif Gulcicek(1)
- Akarca Dizakar, Saadet Özen(1)
- Alim, Ece(1)
- Atalar, Kerem(1)
- Bahcelioglu, Meltem(1)
- Bolay, Hayrunnisa(1)
- Bukan, Neslihan(1)
- Calikusu, Aysen(1)
- Cikim, Ismail Gurkan(1)
- Er, Besir(1)
- Erek, Gozde(1)
- Gok Dagidir, Hale(1)
- Kaplan, Berkan(1)
- Kilic, Ertugrul(1)
- Kursun, Oznur Ece Durmaz(1)
- Orhan, Cemal(1)
- Ozmen, Busra(1)
- Sahin, Kazim(1)
- Sahin, Kazım(1)
- Sahin, Nurhan(1)
- Yabas, Mehmet(1)
Yayınlar
- MakaleAçık Erişim2026Scopus SJRQ1Effects of Melatonin Formulations on Caffeine-Evoked Cortical Activity and Pentobarbital-Induced Sleep in Mice
Sahin, Nurhan; Yabas, Mehmet; Er, Besir; Erten, Fusun; Kursun, Oznur Ece Durmaz; Cikim, Ismail Gurkan; Kaplan, Berkan; Erek, Gozde; Ozmen, Busra; Orhan, Cemal
Melatonin has chronobiotic, antioxidant, anti-inflammatory, and neuromodulatory properties, and its oral effects may vary according to formulation. This study compared conventional melatonin with a lipid-multiparticulate (LMP) formulation in two acute pharmacological mouse paradigms. Eighty-four male BALB/c mice were assigned to caffeine-evoked cortical activity or pentobarbital-induced sedative-hypnotic experiments. Mice received caffeine (7.5 mg/kg, i.p.) alone or with standard or LMP-melatonin (10 or 20 mg/kg, oral). ECoG recorded cortical electrical activity under urethane anaesthesia. In a separate cohort, latency to and duration of pentobarbital-induced loss of the righting reflex were measured. Circulating neurochemical and redox markers, as well as neurotransmitter- and inflammation-related gene and protein expression, were evaluated. Caffeine increased spike frequency and altered ECoG amplitude, together with unfavorable changes in circulating neurochemical and redox markers and in neurotransmitter receptor- and inflammation-related outcomes. Both melatonin formulations attenuated several of these changes in a dose-dependent manner, with the strongest effects generally observed in the high-dose LMP-melatonin group. Compared with conventional melatonin, LMP-melatonin produced greater modulation of ECoG activity, circulating biochemical markers, neurotransmitter-receptor expression, and IL-6 and TNF-α-related outcomes. LMP-melatonin also produced a greater reduction in the latency to and a greater prolongation of the duration of pentobarbital-induced loss of the righting reflex. LMP-melatonin produced greater formulation-dependent effects than conventional melatonin on caffeine-evoked cortical electrical activity, pentobarbital-induced sedative-hypnotic responses, and selected biochemical and molecular outcomes. However, pharmacokinetic exposure, physiological sleep stages, sleep architecture, sleep quality, and direct measures of neuronal injury were not assessed. Therefore, the findings do not directly establish enhanced bioavailability, physiological sleep promotion, or neuroprotection.
- MakaleYayıncıda açık erişim2026Scopus SJRQ1tVNS Mitigates Neuroinflammation and Nociception in a Rodent LPS Endotoxemia Model
Atalar, Kerem; Alim, Ece; Calikusu, Aysen; Abbasoglu Topa, Elif Gulcicek; Gok Dagidir, Hale; Bahcelioglu, Meltem; Bukan, Neslihan; Erten, Fusun; Sahin, Kazım; Akarca Dizakar, Saadet Özen
The vagus nerve plays a modulatory role in the gut-brain axis. Intestinal barrier dysfunction and lipopolysaccharide (LPS) leakage into the systemic circulation are associated with several conditions, such as irritable bowel syndrome (IBS) and migraine headache. This study investigates the impact of non-invasive transauricular vagus nerve stimulation (tVNS) on the neuroinflammatory markers and pain behavior following an acute LPS challenge. Sprague–Dawley rats (n = 28) were given LPS or vehicle and subjected to tVNS or sham intervention in an acute LPS animal model that mimics the systemic consequences of barrier dysfunction. Behaviors were evaluated at the baseline and 6 h later, complemented by testing the levels of serum and brain neuroinflammatory markers. Behavioral analyses revealed that LPS exposure reduced the time spent in the open arm, grooming duration, and periorbital mechanical pain thresholds, and increased freezing duration. The tVNS intervention reversed these behavioral changes induced by LPS. LPS administration triggered elevated serum levels of IL-6, CGRP, haptoglobin, and VE-cadherin. LPS also increased IL-1β, PAR-2, haptoglobin, CGRP, and HMGB1 levels in the brain tissue. The tVNS intervention reversed the effects observed in the brain, but it did not change the elevated levels of inflammatory molecules in the systemic circulation. tVNS has the potential to modulate neuroimmune interactions, with an early impact on the brain during LPS surge. tVNS may have potential therapeutic benefits in managing pain-related disorders associated with LPS endotoxemia.
