Figure 7 - uploaded by Yener Akyuva
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Light microscopy images in brain cortex. A. CSF+NS. Brain cortex. Normal histological appearance. Neuronal nuclei (arrows), glial cells' nuclei (arrowheads). H&E. Scale 100 μm. B. CSF+APO. Brain cortex. Histological appearance is very similar to normal. Neuronal nuclei (arrows), glial cells' nuclei (arrowheads). H&E. Scale 100 μm. C. STZ+SF. Brain cortex. STZ induced neuronal damage. Pyknotic, heterochromatic, disorganized neuronal nuclei (arrows), increased glial cells (arrowheads). H&E. Scale 100 μm. D. STZ+SF. STZ induced neuronal damage. Senile plaque formation in the brain cortex (arrow). H&E. Scale 100 μm. E. STZ+APO. Brain cortex. STZ induced damage is partially reversed by APO. Pyknotic, heterochromatic, neuronal nuclei (arrows). H&E. Scale 100 μm.
Source publication
Scope: We investigated the potential beneficial effect of Apocynin (APO) on motor and cognitive functions in experimental Alzheimer's disease (AD). Materials and Methods: Experimental AD was induced in rats by intraventricular streptozotocin (STZ) injection. Sham group received artificial cerebrospinal fluid (CSF). Both groups were randomly divided...
Contexts in source publication
Context 1
... microscopy examina- tion of CSF+NS group was normal in histological appearance. Cortical layers were easily indefinable, neuronal nuclei were euchromatic and had clear contours ( Figure 7A). Neuronal/glia ratio was normal. ...
Context 2
... was an observable neurofilament web between glial cells and the neurons. The H-E and TEM findings of the CSF-APO group were similar to that of CSF-NS ( Figure 7B). ...
Context 3
... microscopy revealed numerous neurons with heterochromatic and irregularly shaped nuclei in STZ+NS group ( Figure 7C and D). Neuron/glia ratio was decreased in the cortical areas. ...
Citations
... Experimental and clinical studies are present about reducing OFR in I/R injury (9,10,11). Antioxidants (vitamin E, ascorbic acid, glutathione etc.) and various enzymes (catalase, superoxide dismutase, glutathione peroxidase etc.) were tested in these studies (10,11,12). The results of the drugs, which stand out with their antioxidant properties, are promising especially in experimental studies. ...
The Neuroprotective effect of carvacrol, which has anti-inflammatory and antioxidant effects, on infarcted cerebral tissue is present in literature,
but this contribution was not sufficiently clarified in terms of biochemistry. It is aimed to investigate the effect of orally administered carvacrol
on plasma and intraparenchymal levels of TBARS, GSH, SOD, CAT, GSH-Px, IL-1β, IL-4, and TNF-α after the formation of global ischemia in
cerebral tissue. Four groups were formed, each containing ten Wistar albino rats. After anesthesia and analgesia, bilateral carotid communis
arteries of rats in the first two groups were clamped for 15 minutes with aneurysm clips. Oral 50 mg/kg/day carvacrol was administered for 15
days to the first group (I/R+CRV) of these two groups in which cerebral ischemia-reperfusion (I/R) was established. On the other hand, %0,01
carboxymethylcellulose (CMC), which is a solvent of carvacrol, at a same volume of first group was administered orally for the same duration to
the other group in which also I/R was established (I/R+CMC). In the other two groups in which ischemia was not induced, only carotid artery
dissections were made and sutured again. In these two groups, 50 mg/kg/day of carvacrol was administered to the first group (CRV). The Same
dose of CMC was administered to the second group (control group). After all these treatments, plasma was collected, and brain tissue was dissected
from all groups at the end of the 15th day. Carvacrol can be included in the possible treatment regimen of cerebral stroke with the help of other
studies that can be supported on this topic
Aim:The aim of this study was to evaluate Paraoxonase (PON), total antioxidant status (TAS), total oxidant status (TOS), high-density lipoproteins (HDL), CRP, AST, ALT, GGT, ALP levels in patients with head and multiple organ traumas.
Material and Methods:The study included 29 male patients undergoing treatment for head and multiple organ traumas. Blood sample analysis was performed on the first, third, and seventh days after trauma.
Results:The mean age, duration of hospitalization in the intensive care unit, and intubation period of the study sample was 45 years (range: 9 to 81 years), 4.29 days, and 2.94 days, respectively. One patient died, and 13 underwent surgical intervention. Comparison of PON, TAS, TOS, and CRP levels showed statistically significant differences between the first day and the third and seventh days, although no such differences were seen in HDL levels. A moderately positive correlation was observed between CRP/AST, CRP/ALT and between CRP/GGT, while a moderately negative correlation was seen between CRP/ALP.
Conclusion:The findings of this study suggest that some oxidative parameters may play a significant role in the prognosis and follow-up of intensive care patients. Moreover, biochemical markers can provide important information about patient response to trauma.
The mycotoxin fumonisin b1 (Fb1) is produced by fusarium verticillioides , which commonly infects corn and other agricultural products. Fb1 found to be a source of vast range of toxic effects like hepatotoxicity, neurotoxicity and carcinogenicity in a number of animal species. However, the information available currently regarding neurotoxic effects exerted by Fb1 is scanty. Hence, the present study was aimed to evaluate the neurotoxic effects of Fb1 and the possible mechanisms of toxicity in mice and as well as the role of cytotoxic, oxidative stress and apoptosis in neuroblastoma (SH-SY5Y) cell line. In this context, the toxicity of Fb1 was examined in male albino mice. Apocynin with 25,50,100mg/kg b/wt was pretreated for 7 days oral administration. Fb1 6.75 mg/kg b/wt was injected subcutaneously for 5 days. A significant elevation of 5-HT was observed in mice treated with Fb1 in whole brain showed biogenic amines may reflect Fb1 neurotoxicity which was attenuated by pretreatment of apocynin. Fb1 treatment increased oxidative damage in the brain, as evidenced by a decrease in GSH level along with significant increases in ROS, lipid peroxidation, protein carbonyl. Apocynin supplementation significantly ameliorated these biological parameter changes. In addition, apocynin pretreatment normalized the degenerative changes in histology studies. The cytotoxicity of Fb1 was evaluated by MTT and LDH assay showed that, Fb1 induced dose-dependent cell death in SH-SY5Y cells and IC 50 value was determined as 150µM. Fb1 showed elevated reactive oxygen species, depolarized mitochondrial membrane potential and TEM observation showed vacuolation in SH-SY5Y cells. Further, apoptotic changes revealed in DAPI staining and DNA damage in comet assay. To overcome these toxicological effects, apocynin was pretreated followed by Fb1 exposure for 24 h. Pretreatment with apocynin resulted in significant increase in cell viability, restored membrane integrity, reactive oxygen species level was maintained and neutralized apoptotic changes. The protein expression CAT, GPx downregulated with Fb1 treatment and apoptotic markers caspase-3 and caspase-8 was upregulated. Pretretment with apocynin restored the antioxidant enzymes and overexpressed apocynin markers also altered. Collectively, these results suggest that ROS is the main upstream signal leading to increased Fb1 mediated neurotoxicity in mice and SH-SY5Y cells. Use of an antioxidant apocynin reversed the toxin-induced oxidative stress and apoptosis by its antioxidant potency.
