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Öğe Morphine Induces Apoptosis, Inflammation, and Mitochondrial Oxidative Stress via Activation of TRPM2 Channel and Nitric Oxide Signaling Pathways in the Hippocampus(Springer, 2020) Osmanloglu, Omer; Yldirim, Mustafa Kemal; Akyuva, Yener; Yildizhan, Kenan; Naziroglu, MustafaMorphine as an opioid is an important drug in the treatment of moderate to severe pain. Several stress factors via generation of nitric oxide (NO) and oxidative stress (OS) are responsible for the adverse effects of morphine-induced analgesia, addiction, and antinociceptive tolerance, including altered Ca(2+)concentration, inflammation, OS, and release of apoptotic factors. TRPM2 is a Ca2+-permeable cation channel and it is activated by OS and NO. Hence, adverse effect of morphine addiction may occur via the OS and NO-induced TRPM2 activation. Because of the unclear etiology of morphine-induced adverse effects in the hippocampus, investigating the involvement of TRPM2 and NO synthetase (NOS) activations in the treatment of morphine-induced OS, apoptosis, and neuroinflammation is a major challenge. The hippocampal neuron of TRPM2 wild-type (TRPM2-WT) and knockout (TRPM2-KO) mice were divided into control, morphine, NOS inhibitor (L-NAME) + morphine, and TRPM2 channel blockers (ACA and 2-APB) + morphine. The morphine-induced increases of apoptosis, neuron death, OS, lipid peroxidation, caspase-3 and caspase-9, neuroinflammatory cytokines (IL-1 beta, TNF-alpha, IL-6), and Ca(2+)levels in the hippocampal neuron of TRPM2-WT mouse were decreased by the L-NAME, ACA, and 2-APB treatments, although cell viability, neuron count, and reduced glutathione and glutathione peroxidase levels were increased by the treatments. However, the effects of morphine were not observed in the hippocampus of TRPM2-KO mice. Taken together, our data show that neurodegeneration adverse effects of morphine were induced by activation of TRPM2, and excessive generations of NO and OS. Thus, inhibition of TRPM2 may modulate morphine-induced neurodegeneration in the hippocampus.Öğe Morphine Induces Apoptosis, Inflammation, and Mitochondrial Oxidative Stress via Activation of TRPM2 Channel and Nitric Oxide Signaling Pathways in the Hippocampus (vol 17, pg 313, 2020)(Springer, 2020) Osmanlioglu, Haci Omer; Yildirim, Mustafa Kemal; Akyuva, Yener; Yildizhan, Kenan; Naziroglu, Mustafa[Abstract Not Available]Öğe Protective effects of Urtica dioica L. seed extract on liver tissue injury and antioxidant capacity in irradiated rats(Univ Sao Paulo, Conjunto Quimicas, 2020) Yildizhan, Kenan; Demirtas, Omer Can; Uyar, Ahmet; Huyut, Zubeyir; Cakir, Tahir; Keles, Omer Faruk; Yener, ZabitRadiotherapy is often used for the treatment of cancer. However, it causes some side effects in patients. This study aimed to determine the hepatoprotective effects of Urtica dioica L. seed-extract (UDSE) in radiation-induced liver injury. Thirty-two male rats were randomly divided into 4 groups (n=8): control(C) group: no action was taken; radiation (R) group: irradiation was administrated at 5Gy single-fraction, radiation with UDSE(R+UDSE) group: irradiation was administrated at 5 Gy single-fraction and animals were fed pellets with 30 mL UDSE/kg; UDSE group: animals were fed pellets with 30 mL UDSE/kg. All of the experiments were performed in all of the groups over 10 days. Malondialdehyde (MDA) and reduced-glutathione (GSH) levels and superoxide-dismutase (SOD), catalase (CAT), glutathione-peroxidase (GSH-Px), aspartate-transaminase (AST), and alanine-aminotransferase (ALT) activities were detennined. Histopathological findings were also evaluated in liver tissues. SOD, CAT and GSH-Px activities and GSH levels in the serum and liver were significantly increased, while MDA levels decreased in the R+UDSE group compared with the R group (P<0.05). Moreover, AST and ALT serum activities in the R+UDSE group were lower than those in the R group (P<0.05). In addition, radiation induced degenerative/necrotic changes in the R group were significantly compensated in the R+UDSE group. The results showed that radiation increased oxidative stress and decreased antioxidant capacity, as well as degeneration in the liver. However, UDSE attenuated these degenerative changes.Öğe Selenium prevents interferon-gamma induced activation of TRPM2 channel and inhibits inflammation, mitochondrial oxidative stress, and apoptosis in microglia(Springer/Plenum Publishers, 2021) Akyuva, Yener; Naziroglu, Mustafa; Yildizhan, KenanMicroglia as the primary immune cells of brain act protective effects against injuries and infections in the central nervous system. Inflammation via excessive Ca(2+)influx and oxygen radical species (ROS) generation is a known factor in many neurodegenerative disorders. Importantly, the Ca(2+)permeable TRPM2 channel is activated by oxidative stress. Thus, TRPM2 could provide the excessive Ca(2+)influx in the microglia. Although TRPM2 expression level is high in inflammatory cells, the interplay between mouse microglia and TRPM2 channel during inflammation is not fully identified. Thus, it is important to understand the mechanisms and factors involved in order to enhance neuronal regeneration and repair. The data presented here indicate that TRPM2 channels were activated in microglia cells by interferon-gamma (IFN gamma). The IFN gamma treatment further increased apoptosis (early and late) and cytokine productions (TNF-alpha, IL-1 beta, and IL-6) which were due to increased lipid peroxidation and ROS generations as well as increased activations of caspase -3 (Casp-3) and - 9 (Casp-9). However, selenium treatment diminished activations of TRPM2, cytokine, Casp-3, and Casp-9, and levels of lipid peroxidation and mitochondrial ROS production in the microglia that were treated with IFN gamma. Moreover, addition of either PARP1 inhibitors (PJ34 or DPQ) or TRPM2 blockers (2-APB or ACA) potentiated the modulator effects of selenium. These results clearly suggest that IFN gamma leads to TRPM2 activation in microglia cells; whereas, selenium prevents IFN gamma-mediated TRPM2 activation and cytokine generation. Together the interplay between IFN gamma released from microglia cells is importance in brain inflammation and may affect oxidative cytotoxicity in the microglia.
