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Öğe A highly bioavailable curcumin formulation ameliorates inflammation cytokines and neurotrophic factors in mice with traumatic brain injury(John Wiley and Sons Inc, 2024) Şakul, Ayşe Arzu; Balçıkanlı, Zeynep; Ateş Özsoy, Nilay; Orhan, Cemal; Şahin, Nurhan; Tuzcu, Mehmet; Juturu, Vijaya; Kılıç, Ertuğrul; Şahin, KazımA novel curcumin formulation increases relative absorption by 46 times (CurcuWIN®) of the total curcuminoids over the unformulated standard curcumin form. However, the exact mechanisms by which curcumin demonstrates its neuroprotective effects are not fully understood. This study aimed to investigate the impact of a novel formulation of curcumin on the expression of brain-derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), a main component of the glial scar and growth-associated protein-43 (GAP-43), a signaling molecule in traumatic brain injury (TBI). Mice (adult, male, C57BL/6j) were randomly divided into three groups as follows: TBI group (TBI-induced mice); TBI + CUR group (TBI mice were injected i.p. curcumin just after TBI); TBI+ CurcuWIN® group (TBI mice were injected i.p. CurcuWIN® just after TBI). Brain injury was induced using a cold injury model. Injured brain tissue was stained with Cresyl violet to evaluate infarct volume and brain swelling, analyzed, and measured using ImageJ by Bethesda (MD, USA). Western blot analysis was performed to determine the protein levels related to injury. While standard curcumin significantly reduced brain injury, CurcuWIN® showed an even greater reduction associated with reductions in glial activation, NF-?B, and the inflammatory cytokines IL-1? and IL-6. Additionally, both standard curcumin and CurcuWIN® led to increased BDNF, GAP-43, ICAM-1, and Nrf2 expression. Notably, CurcuWIN® enhanced their expression more than standard curcumin. This data suggests that highly bioavailable curcumin formulation has a beneficial effect on the traumatic brain in mice.Öğe A novel theanine complex, Mg-L-Theanine improves sleep quality via regulating brain electrochemical activity(Frontiers Media S.A., 2022) Daşdelen, Muhammed Furkan; Er, Sezgin; Kaplan, Berkan; Çelik, Süleyman; Beker, Mustafa Çağlar; Orhan, Cemal; Tuzcu, Mehmet; Şahin, Nurhan; Mamedova, Havakhanum; Sylla, Sarah; Komorowski, James; Ojalvo, Sara PerezL-Theanine is commonly used to improve sleep quality through inhibitory neurotransmitters. On the other hand, Mg2+, a natural NMDA antagonist and GABA agonist, has a critical role in sleep regulation. Using the caffeine-induced brain electrical activity model, here we investigated the potency of L-theanine and two novel Mg-L-theanine compounds with different magnesium concentrations on electrocorticography (ECoG) patterns, GABAergic and serotonergic receptor expressions, dopamine, serotonin, and melatonin levels. Furthermore, we evaluated the sleep latency and duration in the pentobarbital induced sleep model. We herein showed that L-theanine, particularly its various complexes with magnesium increases the expression of GABAergic, serotonergic, and glutamatergic receptors, which were associated with decreased ECoG frequency, increased amplitude, and enhanced delta wave powers. Besides increased dopamine, serotonin, and melatonin; decreased MDA and increased antioxidant enzyme levels were also observed particularly with Mg-complexes. Protein expression analyses also showed that Mg-L-theanine complexes decrease inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) levels significantly. In accordance with these results, Mg complexes improved the sleep latency and duration even after caffeine administration. As a result, our data indicate that Mg-L-theanine compounds potentiate the effect of L-theanine on sleep by boosting slow-brain waves, regulating brain electrical activity, and increasing neurotransmitter and GABA receptor levels.Öğe Allyl isothiocyanate attenuates oxidative stress and inflammation by modulating Nrf2/HO-1 and NF-kappa b pathways in traumatic brain injury in mice(Springer, 2019) Çağlayan, Berrak; Kılıç, Ertuğrul; Dalay, Arman; Altunay, Serdar; Tuzcu, Mehmet; Erten, Füsun; Orhan, Cemal; Günal, Mehmet Yalçın; Yuluğ, Burak; Juturu, Vijaya; Şahin, KazımTraumatic brain injury (TBI) is the leading cause of mortality and morbidity in young adults and children in the industrialized countries; however, there are presently no FDA approved therapies. TBI results in oxidative stress due to the overproduction of reactive oxygen species and overwhelming of the endogenous antioxidant mechanisms. Recently, it has been reported that antioxidants including phytochemicals have a protective role against oxidative damage and inflammation after TBI. To analyze the effects of a naturally occurring antioxidant molecule, allyl isothiocyanate (AITC), on the nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa B (NF-kappa B) signaling pathways in TBI, a cryogenic injury model was induced in mice. Here, we showed that AITC administered immediately after the injury significantly decreased infarct volume and blood-brain barrier (BBB) permeability. Protein levels of proinflammatory cytokines interleukin-1 beta (IL1 beta) and interleukin-6 (IL6), glial fibrillary acidic protein (GFAP) and NF-kappa B were decreased, while Nrf2, growth-associated protein 43 (GAP43) and neural cell adhesion molecule levels were increased with AITC when compared with vehicle control. Our results demonstrated that the antioxidant molecule AITC, when applied immediately after TBI, provided beneficial effects on inflammatory processes while improving infarct volume and BBB permeability. Increased levels of plasticity markers, as well as an antioxidant gene regulator, Nrf2, by AITC, suggest that future studies are warranted to assess the protective activities of dietary or medicinal AITC in clinical studies.Öğe Allyl isothiocyanate enhances brain neuronal plasticity proteins via inhibition of inflammation proteins(Lippincott Williams & Wilkins, 2018) Juturu, Vijaya; Çağlayan, Berrak; Kılıç, Ertuğrul; Dalay, Arman; Tuzcu, Mehmet; Erten, Füsun; Günal, Mehmet Yalçın; Altunay, Serdar; Orhan, Cemal; Şahin, Kazım[Abstract Not Available]Öğe Cinnamon polyphenol extract exerts neuroprotective activity in traumatic brain injury in male mice(Bentham Science Publishers Ltd, 2018) Yuluğ, Burak; Kılıç, Ertuğrul; Altunay, Serdar; Ersavaş, Cenk; Orhan, Cemal; Dalay, Arman; Tuzcu, Mehmet; Şahin, Nurhan; Juturu, Vijaya; Şahin, KazımIntroduction: Cinnamon polyphenol extract is a traditional spice commonly used in different areas of the world for the treatment of different disease conditions which are associated with inflammation and oxidative stress. Despite many preclinical studies showing the anti-oxidative and anti-inflammatory effects of cinnamon, the underlying mechanisms in signaling pathways via which cinnamon protects the brain after brain trauma remained largely unknown. However, there is still no preclinical study delineating the possible molecular mechanism of neuroprotective effects cinnamon polyphenol extract in Traumatic Brain Injury (TBI). The primary aim of the current study was to test the hypothesis that cinnamon polyphenol extract administration would improve the histopathological outcomes and exert neuroprotective activity through its antioxidative and anti-inflammatory properties following TBI. Methods: To investigate the effects of cinnamon, we induced brain injury using a cold trauma model in male mice that were treated with cinnamon polyphenol extract (10 mg/kg) or vehicle via intraperitoneal administration just after TBI. Mice were divided into two groups: TBI+vehicle group and TBI+ cinnamon polyphenol extract group. Brain samples were collected 24 h later for analysis. Results: We have shown that cinnamon polyphenol extract effectively reduced infarct and edema formation which were associated with significant alterations in inflammatory and oxidative parameters, including nuclear factor-KB, interleukin 1-beta, interleukin 6, nuclear factor erythroid 2-related factor 2, glial fibrillary acidic protein, neural cell adhesion molecule, malondialdehyde, superoxide dismutase, catalase and glutathione peroxidase. Conclusion: Our results identify an important neuroprotective role of cinnamon polyphenol extract in TBI which is mediated by its capability to suppress the inflammation and oxidative injury. Further, specially designed experimental studies to understand the molecular cross-talk between signaling pathways would provide valuable evidence for the therapeutic role of cinnamon in TBI and other TBI related conditions.Öğe Dose-dependent effect of a new biotin compound in hippocampal remyelination in rats(2025) Yuluğ, Burak; Kılıç, Ertuğrul; Oğuz, Tuba; Orhan, Cemal; Er, Beşir; Tuzcu, Mehmet; Şahin, KazımDemyelination is commonly observed in neurodegenerative disorders, including multiple sclerosis (MS). Biotin supplementation is known to stabilize MS progression. To reduce the effective dose of biotin, we synthesized a new and superior form of biotin, a complex of magnesium ionically bound to biotin (MgB) and compared its dose-dependent effect with biotin alone after inducing demyelination using lysolecithin (LPC) in rats. Myelination was assessed using luxol fast blue staining and immunostaining against MBP protein, revealing that the most significant remyelination occurred in the MgB groups. Additionally, both biotin and MgB-treated animals showed dose-dependent improvements in spatial memory. Moreover, we detected a decrease in inflammatory proteins in both treatment groups, which was more prominent in high-dose MgB-treated animals and correlated with decreased expression of NF-kappa B p65, OP, and MMP-9 proteins. Further analysis of biotin-related proteins demonstrated that both biotin and, notably, MgB reversed the demyelination-dependent reduction of these proteins. Furthermore, biotin, particularly MgB, improved neuronal transmission proteins, Synapsin-1, PSD-93, and PSD-95. Additionally, both treatment groups exhibited increased BDNF, GAP43, and ICAM levels, with significant increments observed in high-dose MgB-treated animals. Increased GFAP, indicative of reactive gliosis, was observed in LPC-treated animals, and this effect was notably reversed by high-dose MgB treatment. The current data emphasize the dose-dependent beneficial effect on the remyelination process. Furthermore, the combination of biotin with Mg resulted in a more potent effect compared to biotin by itself. The strong influence of MgB encourages proof-of-concept studies using MgB in patients with MS.Öğe Enhancement of cisplatin sensitivity in human cervical cancer: Epigallocatechin-3-gallate(Frontiers Media, 2015) Kılıç, Ülkan; Şahin, Kazım; Tuzcu, Mehmet; Başak, Nazlı; Orhan, Cemal; Elibol Can, Birsen; Kılıç, Ertuğrul; Şahin, Fikrettin; Küçük, ÖmerCisplatin is one of the effective chemotherapeutics in the treatment of several types of cancers. However, in addition to the efforts against to its toxicity, the amelioration of cisplatin sensitivity is an important point in treatment of cervical cancer. To do so, additional substances such as epigallocatechin gallate (EGCG), a polyphenol in green tea, have been used in combination with chemotherapeutics. We aimed to investigate the possible molecular pathways to potentiate cervical cancer cell (HeLa) growth inhibition by combination therapy of cisplatin and EGCG. HeLa cells were treated with EGCG (25µM), cisplatin (250 nM), and their combination for 24 h. Cell viability was determined by MTS Assay. We analyzed the expressions of NF-?B p65, COX-2, Nrf2, HO-1, p-mTOR, p-p70S6K1, p-4E-BP1, and p-Akt byWestern blot analysis. Herein, we have demonstrated that EGCG works synergistic with cisplatin in inhibiting growth of cervical cancer cells. EGCG improved efficacy of cisplatin treatment in HeLa cells by regulating NF?B p65, COX-2, p-Akt, and p-mTOR pathways, whereas it increased the expression levels of Nrf2/HO-1 in combined therapy. Our observations revealed that EGCG increases the sensitization of cisplatin to cervical cancer cells by inhibiting cell survival and inducing apoptosis.Öğe Impact of a novel valerian extract on sleep quality, relaxation, and gaba/serotonin receptor activity in a murine model(2024) Şahin, Kazım; Gençoğlu, Hasan; Korkusuz, Ahmet Kayhan; Orhan, Cemal; Aldatmaz, İsmail Ertuğ; Erten, Füsun; Er, Beşir; Morde, Abhijeet; Padigaru, Muralidhara; Kılıç, ErtuğrulInsomnia is a major global health issue, highlighting the need for treatments that are both effective and safe. Valerian extract, a traditional remedy for sleep problems, offers potential therapeutic options. This research examined the potential sleep-enhancing effects of VA (Valerian Pdr%2) in mice. The study evaluated sleep quality by comparing the impact of the VA extract against melatonin on brain activity, using electrocorticography (ECoG) to assess changes in brain waves. For this purpose, the study utilized two experimental models on BALB/c mice to explore the effects of caffeine-induced insomnia and pentobarbital-induced sleep. In the first model, 25 mice were assigned to five groups to test the effects of caffeine (caffeine, 7.5 mg/kg i.p) alone, caffeine with melatonin (2 mg/kg), or caffeine with different doses of valerian extract (100 or 300 mg/kg) given orally on brain activity, assessed via electrocorticography (ECoG) and further analyses on the receptor proteins and neurotransmitters. In the second model, a different set of 25 mice were divided into five groups to examine the impact of pentobarbital (42 mg/kg) alone, with melatonin, or with the valerian extract on sleep induction, observing the effects 45 min after administration. The study found that ECoG frequencies were lower in groups treated with melatonin and two doses of valerian extract (100 and 300 mg/kg), with 300 mg/kg showing the most significant effect in reducing frequencies compared to the caffeine control group, indicating enhanced sleep quality (p < 0.05). This was supported by increased levels of serotonin, melatonin, and dopamine and higher levels of certain brain receptors in the melatonin and valerian extract groups (p < 0.05). Modulatory efficacy for the apoptotic markers in the brain was also noted (p < 0.05). Additionally, melatonin and both doses of VA increased sleep duration and reduced sleep onset time compared to the pentobarbital control, which was particularly notable with high doses. In conclusion, the findings suggest that high doses (300 mg/kg) of valerian extract enhance both the quantity and quality of sleep through the GABAergic pathway and effectively increase sleep duration while reducing the time to fall asleep in a pentobarbital-induced sleep model in mice.Öğe Protective effects of magnesium biotinate on propionic acid-induced autistic features in rats(Wiley, 2020) Komorowski, James; Ojalvo, Sara; Orhan, Cemal; Erten, Füsun; Şahna, Engin; Kılıç, Ertuğrul; Şahin, KazımObjective This study investigated the protective effects of magnesium biotinate (MgB) on propionic acid (PPA)-induced autistic features in rats. Background Biotin is involved in energy metabolism and various immune and nerve functions. MgB is a novel biotin complex that has enhanced absorption. Compared to D-Biotin, MgB has superior tissue uptake and anti-inflammatory effects. Neurological problems can occur in biotin-deficient individuals. Supplementation with MgB may prevent or reduce neurodevelopmental disorders such as those seen in autism spectrum disorder. Design/Methods Thirty-five male Wistar rats (3 weeks old) were randomized into the following five groups; 1: Control (received saline), 2: PPA alone, 3: PPA + 10 mg human equivalent dose (HED) MgB, 4: PPA + 100 mg HED MgB, 5: PPA + 500 mg HED MgB. Animals were fed a standard diet, with or without MgB, for 35 days and on day 30, rats were administered PPA (500 mg/kg BW/day) by subcutaneous injection for 5 days. Neurobehavioral tests were then performed for two days. Serum and tissue samples were then collected for analysis. Results Social interaction deficits and signs of brain toxicity, including higher brain levels of inflammatory and oxidative stress markers, were observed in PPA alone rats. Brain levels of inflammatory markers were lower in all MgB groups compared to PPA alone (p<0.05). Oxidative stress markers were lower and antioxidant markers were higher in the 100 mg and 500 mg HED MgB groups compared to PPA alone (p<0.05). These effects were most significant in the 500 mg HED MgB group. Sociability and social preference scores were greater in the 100 and 500 mg HED MgB treatment groups compared to PPA alone (p<0.05). The 500 mg HED MgB dose improved social preference score to the extent that it did not differ from normal controls. Conclusions Pre-treatment with MgB significantly reduced brain toxicity and improved autistic features induced by PPA.Öğe Schiff base-poloxamer p85 combination prevents prostate cancer progression in c57/bl6 mice(Wiley, 2016) Do?an, Ayşegül; Demirci, Selami; Başak Türkmen, Neşe; Çağlayan, Ahmet Burak; Aydın, Safa; Telci, Dilek; Kılıç, Ertuğrul; Şahin, Kazım; Orhan, Cemal; Tuzcu, Mehmet; Doğan Ekici, Asiye Işın; Şahin, FikrettinBACKGROUNDProstate cancer which is the second most common cause of death among men has a high incidence in recent years. Current therapeutic regimens should be improved to overcome drug resistance. At the metastatic stage, tumors become refractory to established chemotherapeutic treatments and cause serious problems at the clinics. Development of new drug molecules that are able to transport through the membrane easily and kill tumor cells rapidly is of great interest. METHODIn the current study, a novel Heterodinuclear copper(II)Mn(II) Schiff base complex combined with P85 was used for prostate cancer treatment in vivo. Tramp-C1 cells injected animals were subjected to chemotherapeutic formulation treatment and results were analyzed by toxicology analysis, tumor volume measurements, and histopathological analysis. 0.5mg/kg Schiff base was selected and combined with 0.05% P85 according to the toxicology analysis showing the enzyme levels, blood parameters, and multiple organ toxicity. RESULTSResults demonstrated that Heterodinuclear copper(II)Mn(II) complex-P85 combination decreased tumor formation and tumor volume steadily over the course of experiments. CONCLUSIONSOverall, Heterodinuclear copper(II)Mn(II) complex-P85 exerted remarkable anti-cancer activity in vivo in C57/B16 mice. Prostate 76:1454-1463, 2016.Öğe The effect of a novel theanine complex (JDS-MT-003) on sleep in a caffeine-induced insomnia mouse model(Wiley, 2020) Komorowski, James; Ojalvo, Sara; Sylla, Sarah; Mamedova, Havakhanum; Orhan, Cemal; Tuzcu, Mehmet; Şahin, Kazım; Kılıç, Ertuğrul[Abstract Not Available]Öğe The effect of a novel theanine complex (JDS-MT-003) on sleep in a pentobarbital-induced sleep model in mice(Wiley, 2020) Sylla, Sarah; Ojalvo, Sara; Komorowski, James; Orhan, Cemal; Tuzcu, Mehmet; Şahin, Nurhan; Kılıç, Ertuğrul; Şahin, Kazım[Abstract Not Available]Öğe The effect of water-soluble alpinia galanga extract on sleep and the activation of the gabaaergic/serotonergic pathway in mice(2024) Şahin, Kazım; Korkusuz, Ahmet Kayhan; Şahin, Emre; Orhan, Cemal; Er, Beşir; Morde, Abhijeet; Kılıç, ErtuğrulBackground/Objectives: With increasing interest in plant-based compounds that can enhance sleep quality without the side effects of caffeine, Alpinia galanga (AG) has emerged as a promising herbal supplement for improving mental alertness. This study assessed the impact of water-soluble AG extract on sleep quality; the activity of GABAergic, glutamatergic, and serotonergic receptors; and concentrations of dopamine and serotonin in the brains of mice. Methods: The study employed two experimental models using BALB/c mice to examine the impact of pentobarbital-induced sleep and caffeine-induced insomnia. In the first model, a set of 20 mice was assigned to four groups to assess the effects of pentobarbital (42 mg/kg) or pentobarbital with AG extract on sleep induction, with observations made 45 min post-administration. In the second model, 20 mice were divided into four groups to evaluate the impact of caffeine (25 mg/kg) alone or caffeine with varying doses of AG extract (61.25 or 205.50 mg/kg administered orally) on brain activity along with additional analyses on receptor proteins and neurotransmitters. Results: A higher dose of AG extract (205.50 mg/kg) significantly increased total deep sleep duration compared to the caffeine group (p < 0.0001). Furthermore, this dose extended sleep latency and suppressed GABAergic and glutamatergic receptor activity compared to the lower AG dose (p < 0.05). Additionally, the 205.50 mg/kg dose elevated serotonin and dopamine levels compared to caffeine (p < 0.0001), suggesting improved sleep quality alongside enhanced wakefulness. Conclusions: Our data indicate that a higher dose of AG extract improved sleep latency and duration by regulating GABAergic and glutamatergic receptors through the GABAergic/serotonergic pathway in mice.
