The effect of cilostazol on hippocampal memory and oxidative stress biomarkers in rat model of diabetes mellitus

Rababa’h, Abeer; Mardini, Afrah N.; Alzoubi, Karem H.; Ababneh, Mera A.; Athamneh, Rabaa Y.

doi:10.1016/j.brainres.2019.03.025

Cited by 21 publications

(14 citation statements)

References 30 publications

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“…The obtained findings of this research study confirm that diosgenin administration to STZ-diabetic rats could improve learning and memory disturbances through appropriate modulation of NF-κB/TLR4/Nrf2 and attenuation of astrogliosis biomarker, restoration of cholinergic function, and mitigation of oxidative and inflammatory responses in addition to its neuroprotective potential. DM-associated cognitive deficits have already been reported, as shown by the poor performance of diabetic animals in the passive avoidance test, Y-maze [39], radial arm maze [40, 41], and novel object discrimination tasks [42] which is also consistent with our obtained behavioral data.…”

Section: Discussionsupporting

confidence: 92%

Diosgenin Attenuates Cognitive Impairment in Streptozotocin-Induced Diabetic Rats: Underlying Mechanisms

et al. 2020

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Objective: Prolonged diabetes mellitus causes impairments of cognition and attentional dysfunctions. Diosgenin belongs to a group of steroidal saponins with reported anti-diabetic and numerous protective properties. This research aimed to assess the effect of diosgenin on beneficially ameliorating learning and memory decline in a rat model of type 1 diabetes caused by streptozotocin (STZ) and to explore its modes of action including involvement in oxidative stress and inflammation.Methods:Rats were assigned to one of four experimental groups, comprising control, control under treatment with diosgenin, diabetic, and diabetic under treatment with diosgenin. Diosgenin was given daily p.o. (40 mg/kg) for 5 weeks. Results: The administration of diosgenin to the diabetic group reduced the deficits of functional performance in behavioral tests, consisting of Y-maze, passive avoidance, radial arm maze, and novel object discrimination tasks (recognitive). Furthermore, diosgenin treatment attenuated hippocampal acetylcholinesterase activity and malondialdehyde, along with improvement of antioxidants such as superoxide dismutase and glutathione. Meanwhile, the hippocampal levels of inflammatory indicators, namely interleukin 6, nuclear factor-κB, toll-like receptor 4, tumor necrosis factor α, and astrocyte-specific biomarker glial fibrillary acidic protein, were lower and, on the other hand, tissue levels of nuclear factor (erythroid-derived 2)-related factor 2 were elevated upon diosgenin administration. Besides, the mushroom-like spines of the pyramidal neurons of the hippocampal CA1 area decreased in the diabetic group, and this was alleviated following diosgenin medication. Conclusions: Taken together, diosgenin is capable of ameliorating cognitive deficits in STZ-diabetic animals, partly due to its amelioration of oxidative stress, inflammation, astrogliosis, and possibly improvement of cholinergic function in addition to its neuroprotective potential.

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Section: Discussionsupporting

confidence: 92%

Diosgenin Attenuates Cognitive Impairment in Streptozotocin-Induced Diabetic Rats: Underlying Mechanisms

et al. 2020

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“…Multiple factors, such as hyperglycemia, vascular disease, hypoglycemia, and insulin resistance, are well known to play significant roles in diabetes‐associated complications as well as in cognitive dysfunction in relation to diabetes (Kodl & Seaquist, 2008). Substantial evidence suggests that the hippocampus is vulnerable to damage caused by hyperglycemia‐induced oxidative stress and cell apoptosis (Kahya et al., 2017; Rababa'h et al., 2019). We observed that t‐AUCB markedly ameliorated oxidative stress according to immunofluorescence staining and reduced apoptosis levels in the hippocampus of diabetic mice.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of soluble epoxide hydrolase (sEH) protects hippocampal neurons and reduces cognitive decline in type 2 diabetic mice

Fan

Zhao

et al. 2021

Eur J of Neuroscience

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Diabetes mellitus is a metabolic disorder that can lead to cognitive dysfunction. The hippocampus plays an important role in the cognitive function. Research has identified correlations between hippocampal impairment and diabetes, yet their intermediate remains unclear. Soluble epoxide hydrolase (sEH) is an enzyme that degrades epoxyeicosatrienoic acids (EETs), which have multiple protective effects by suppressing inflammation, apoptosis and oxidative stress. In this study, under diabetic conditions both hippocampal injury and cognitive decline are accompanied by upregulation of sEH. Moreover, the sEH inhibitor trans‐4‐[4‐(3‐adamantan‐1‐y1‐ureido)‐cyclohexyloxy]‐benzoic acid (t‐AUCB) prevents cognitive dysfunction and decreased ROS accumulation and apoptosis in the diabetic hippocampus. t‐AUCB treatment restored neuronal synaptic plasticity by restoring the expression of the postsynaptic proteins Postsynaptic density protein‐95 (PSD95) and N‐methyl‐d‐aspartate receptor subunit 2B (NR2B), the levels of which were positively correlated with Proline‐rich tyrosine kinase 2 (Pyk2) levels under diabetic conditions. Thus, we suggest that hippocampal protection via sEH inhibition might be a potential therapeutic approach to attenuate the progression of cognitive decline in diabetes.

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“…Moreover, one study using a diabetes mellitus-induced rat model and another evaluating the effects of cilostazol on hippocampal memory and oxidative stress also did not provide any information as to how the hippocampal tissues were resected (14). In another study that investigated the effects of tramadol administration on hippocampal cell apoptosis, learning, and memory and investigated the neuroprotective effects of crocin in adult rats (1), no surgical procedures were described as to how to dissect hippocampal tissues (1).…”

Section: █ Discussionmentioning

confidence: 99%

Practical performance of hippocampal tissue resection in rats in pharmacomolecular research

Yılmaz

Karaarslan²,

Özbek³

2020

Turkish Neurosurgery

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AIM: To explain how to resect hippocampal tissue in rats used as live mammalian subjects for the resection of fresh cerebral tissue in laboratories. MATERIAL and METHODS:Adult male Wistar-Albino rats (n=50) were used for this purpose. RESULTS:The average bodyweight of the rats was 316.4 ± 11.71 g, and the average weight of the resected hippocampal tissues was 1.01 ± 0.03 g; however, there were no statistically significant differences between the body weights and the hippocampal tissue weights (p>0.05). The hippocampal tissues to be used in the study were excised practically by preserving the original anatomical configuration without injury to the tissue. CONCLUSION:This paper elucidates a simple, step-by-step methodology for performance in the laboratory in order to improve the standardization of hippocampal tissue dissection.

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The effect of cilostazol on hippocampal memory and oxidative stress biomarkers in rat model of diabetes mellitus

Cited by 21 publications

References 30 publications

Diosgenin Attenuates Cognitive Impairment in Streptozotocin-Induced Diabetic Rats: Underlying Mechanisms

Diosgenin Attenuates Cognitive Impairment in Streptozotocin-Induced Diabetic Rats: Underlying Mechanisms

Inhibition of soluble epoxide hydrolase (sEH) protects hippocampal neurons and reduces cognitive decline in type 2 diabetic mice

Practical performance of hippocampal tissue resection in rats in pharmacomolecular research

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