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    Zinc Ameliorates Nogo-A Receptor and Osteocalcin Gene Expression in Memory-Sensitive Rat Hippocampus Impaired by Intracerebroventricular Injection of Streptozotocin
    (Springernature, 2023) Gumus, Haluk; Baltaci, Saltuk Bugra; Unal, Omer; Gulbahce-Mutlu, Elif; Mogulkoc, Rasim; Baltaci, Abdulkerim Kasim
    Metabolic dysfunction is a critical step in the etiopathogenesis of Alzheimer's disease. In this progressive neurological disorder, impaired zinc homeostasis has a key role that needs to be clarified. The aim of this study was to investigate the effect of zinc deficiency and administration on hippocampal Nogo-A receptor and osteocalcin gene expression in rats injected with intracerebroventricular streptozotocin (icv-STZ). Forty male Wistar rats were divided into 5 groups in equal numbers: Sham 1 group received icy artificial cerebrospinal fluid (aCSF); Sham 2 group received icy a CSF and i.p. saline; STZ group received 3 mg/kg icy STZ; STZ-Zn-deficient group received 3 mg/kg icy STZ and fed a zinc-deprived diet; STZ-Zn-supplemented group received 3 mg/kg icy STZ and i.p. zinc sulfate (5 mg/kg/day). Hippocampus tissue samples were taken following the cervical dislocation of the animals under general anesthesia. Nogo-A receptor and osteocalcin gene expression levels were determined by real-time-PCR method. Zinc supplementation attenuated the increase in hippocampal Nogo-A receptor gene expression, which was significantly increased in zinc deficiency. Again, zinc supplementation upregulated the intrinsic protective mechanisms of the brain by activating osteocalcin-expressing cells in the brain. The results of the study show that zinc has critical effects on Nogo-A receptor gene expression and hippocampal osteocalcin gene expression levels in the memory-sensitive rat hippocampus that is impaired by icv-STZ injection. These results are the first to examine the effect of zinc deficiency and supplementation on hippocampal Nogo-A receptor and osteocalcin gene expression in icv-STZ injection in rats.
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    Zinc Supplementation Improves ZIP14 (SLC39A14) Levels in Cerebral Cortex Suppressed by icv-STZ Injection
    (Turkish Neuropsychiatry Assoc-Turk Noropsikiyatri Dernegi, 2024) Baltaci, Saltuk Bugra; Gumus, Haluk; Unal, Omer; Acar, Gozde; Bayiroglu, Aysenur Feyza
    Introduction: Metabolic dysfunctions are critical in the pathology of Alzheimer's disease. Impaired zinc homeostasis, in particular, is a significant issue in this disease that has yet to be explained. Gene expression of ZIP14 in brain tissue has been previously reported. But to date, only one study has reported reduced ZIP14 levels in aged brain tissue. We investigated how dietary zinc deprivation and supplementation impact ZIP14 levels in the cerebral cortex in rats with sporadic Alzheimer's disease (sAH) produced by intracerebroventricular streptozotocin (icv-STZ). Impaired zinc homeostasis, in particular, is a significant issue with this condition that has yet to be elucidated. Methods: Animals were divided into 5 groups in equal numbers (n=8): Sham 1 group: icv received artificial cerebrospinal fluid (aCSF); Sham 2 group: retrieved icv aCSF and intraperitoneal (ip) saline, STZ group: received 3 mg/kg icv-STZ; STZ-Zn-Deficient group: received 3 mg/ kg icv-STZ and fed a zinc -deprived diet; STZ-Zn-Supplemented: It received 3 mg/kg icv-STZ and ip zinc sulfate (5 mg/kg/day ZIP 14 levels (ng/L) in cortex tissue samples taken from animals sacrificed under general anesthesia were determined by ELISA at the final stage of the experimental applications. Results: Decreased ZIP14 levels in the sporadic Alzheimer's group were severely by zinc deficiency. Zinc supplementation treated the reduction in ZIP14 levels. Conclusion: The results of the current study show that ZIP14 levels in cerebral cortex tissue, which are suppressed in the experimental rat Alzheimer model and are even more critically reduced in zinc deficiency, can be restored by zinc supplementation.