Browsing by Author "Ahlatci, Adem"

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Can Zaprinast and Avanafil Induce the Levels of Angiogenesis, Bone Morphogenic Protein 2, 4 and 7 in Kidney of Ovariectomised Rats
(Taylor & Francis Ltd, 2022) Huyut, Zubeyir; Bakan, Nuri; Yildirim, Serkan; Akbay, Halil Ibrahim; Huyut, Mehmet Tahir; Ahlatci, Adem; Ucar, Bunyamin
Objective: This study investigated effects of zaprinast and avanafil on angiogenesis, vascular endothelial growth factor (VEGF), bone morphogenic protein (BMP) 2, 4 and 7. Methods: Female rats were randomly divided into four groups (n = 6). Sham; abdomen was approximately 2 cm opened and closed. Ovariectomised (OVX); abdomen was opened 2 cm and the ovaries were cut. OVX + zaprinast and OVX + avanafil groups; after the same procedure with OVX, 10 mg/kg zaprinast and avanafil were orally administered for 2 month, respectively. Angiogenesis and the levels of VEGF, BMP2, 4 and 7 were determined. Results: VEGF, BMP2, 4 and 7 levels in OVX + zaprinast and especially OVX + avanafil groups were higher than the sham and OVX (p < .05). However, only VEGF and BMP2 levels in OVX + zaprinast group were significant according to sham (p < .05). Also, angiogenesis in OVX + zaprinast and OVX + avanafil groups was dominant according to sham and OVX (p < .05). Conclusions: Zaprinast and avanafil induced BMP2, 4 and 7 levels synergistically with increased VEGF and angiogenesis in renal tissue.
The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the Trpm2 Channel
(Mdpi, 2025) Keles, Omer Faruk; Bayir, Mehmet Hafit; Cicek, Haci Ahmet; Ahlatci, Adem; Yildizhan, Kenan
This study investigated the protective effect of selenium (Se) in a cadmium (Cd)-induced nephrotoxicity model in rats and the role of the TRPM2 channel in this mechanism. For this purpose, Cd (25 mg/kg orally), Se (0.5 mg/kg i.p.), and 2-aminoethoxydiphenyl borate (2-APB), a TRPM2 channel antagonist, (3 mg/kg i.p.) were administered to rats every day for 5 days. At the end of the study, kidney tissues were analysed using histological and biochemical methods. A histopathological examination revealed congestion, tubular degeneration, necrosis, and glomerular adhesion in the Cd group. However, these lesions were significantly reduced in the Cd + Se and Cd + 2-APB groups, while the Cd + Se + 2-APB group showed a histological appearance similar to the control group. Immunohistochemical analysis revealed that Caspase-3, Bax, and TRPM2 expression was higher in the Cd group, while these levels were lower in the Se and 2-APB treatment groups (p < 0.05). Among the groups that received Cd, urea, creatinine, TOS, TNF-alpha, and IL-1 beta levels were at the highest level in the Cd group, while TAS level was at the lowest level (p < 0.05). The Se and 2-APB treatment modulated these parameters; however, Se + 2-APB treatment reduced urea, creatinine, TOS, TNF-alpha, and IL-1 beta levels to the lowest level compared to the Cd groups and brought the TAS level closer to the control group (p < 0.05). These findings indicated that targeting TRPM2 channel inactivation together with the selenium treatment could alleviate Cd-induced nephrotoxicity.
Effect of Selenium Against Doxorubicin-Induced Oxidative Stress, Inflammation, and Apoptosis in the Brain of Rats: Role of Trpm2 Channel
(Natl inst Science Communication-niscair, 2023) Yildizhan, Kenan; Huyut, Zuebeyir; Altindag, Fikret; Ahlatci, Adem
Doxorubicin (DOX) is widely used as an anticancer drug in humans' various solid and haematological tumours. Although many studies on the toxic effect of DOX are used in different organs, its impact on brain tissue has yet to be adequately studied. This study investigated the protective effect of selenium (Se) and the role of transient receptor potential melastatin-2 (TRPM2) channel activation against brain damage caused by DOX administration. Sixty rats were randomly divided into the sham, dimethyl sulfoxide (DMSO), DOX, DOX + Se, DOX + N-(p-amylcinnamoyl) anthranilic acid (ACA), and DOX + Se + ACA groups. The reactive oxygen species (ROS), poly [ADP-ribose] polymerase 1 (PARP1), and TRPM2 channel levels in brain tissues were measured by ELISA. In addition, a histopathological examination was performed in the cerebral cortex and hippocampal areas, and the TRPM2 channel, NF-icB, and caspase-3 expression were determined immunohistochemically. The levels of ROS, PARP1 and TRPM2 channel in the DOX group were higher than in the sham and DMSO groups (P < 0.05). However, these parameters were decreased in the in DOX+Se and DOX+ACA groups by the treatments of Se and ACA (P < 0.05). Also, we determined that Se and ACA treatment decreased the NF-icB, caspase-3, and TRPM2 channel expression in the cerebral cortex and hippocampal areas in the DOX-induced rats. The data showed that Se and/or ACA administration together with DOX administration could be used as a protective agent against DOX-induced brain damage.
Valproic Acid Attenuated Ptz-Induced Oxidative Stress, Inflammation, and Apoptosis in the Sh-Sy5y Cells Via Modulating the Trpm2 Channel
(Springer, 2022) Ahlatci, Adem; Yildizhan, Kenan; Tuluce, Yasin; Bektas, Muhammet
Valproic acid (VPA) is one of the most widely used antiepileptic drugs. The protective role of VPA and the role of the TRPM2 channel in this mechanism in developing neuronal damage due to increased pentylenetetrazol (PTZ)-induced neurotoxicity in SH-SY5Y cells were not clarified. Here, we investigated the role of VPA via modulation of TRPM2 channel on cell death and oxidative neurotoxicity in SH-SY5Y cells. The SH-SY5Y cell toxicity model was constructed by treating SH-SY5Y cells with PTZ. The VPA and TRPM2 channel antagonist N-(p-amylcinnamoyl) anthranilic acid (ACA) were added to prevent neurotoxicity in PTZ-induced SH-SY5Y cells. The role of the VPA and TRPM2 channel was evaluated using an ELISA kit and patch-clamp. Primarily, antioxidant (GSH and GSH-Px) and oxidative stress (MDA and ROS) levels and inflammatory factors (IL-1 beta, IL-6, and TNF-alpha) in cells were determined by ELISA kits. Then, TRPM2 channel activation in cells was detected using both the ELISA kit and patch-clamp methods. In addition, apoptosis and cell viability levels in cells were determined by performing PARP1, caspase-3, caspase-9, and CCK-8 assays by ELISA kits. Our results showed that the TRPM2 channel is vital in damage formation in PTZ-induced cells. Furthermore, we observed that VPA attenuated PTZ-induced neurotoxicity by suppressing cells' oxidative stress and inflammation, and reducing TRPM2 channel activation. In our study, in which the protective effect of VPA and the role of the TRPM2 channel in PTZ-induced SH-SY5Y cells were investigated for the first time, we can conclude that VPA treatment and TRPM2 channel blockade can suppress PTZ-induced neurotoxicity.