Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice

Hemmati, Ali Asghar; Alboghobeish, Soheila; Ahangarpour, Akram

doi:10.4196/kjpp.2018.22.3.257

Cited by 46 publications

(32 citation statements)

References 67 publications

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“…Further, diabetic mice of both genotypes (WT and KO) showed decrease in movement velocity and the number of arm entries at 8 weeks post-MLDS injection, which might be associated with diabetes-induced motor impairments. In line with our findings, several studies have shown a reduction in the number of total arm entries of diabetic mice compared with non-diabetic controls (59–61). Likewise, another study has found a marked reduction in speed and traveling distance of diabetic mice, indicating impairment of exploratory behavior and motor activity (62).…”

Section: Resultssupporting

confidence: 93%

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

et al. 2019

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Diabetic encephalopathy is a severe diabetes-related complication in the central nervous system (CNS) that is characterized by degenerative neurochemical and structural changes leading to impaired cognitive function. While the exact pathophysiology of diabetic encephalopathy is not well-understood, it is likely that neuroinflammation is one of the key pathogenic mechanisms that cause this complication. Lipocalin-2 (LCN2) is an acute phase protein known to promote neuroinflammation via the recruitment and activation of immune cells and glia, particularly microglia and astrocytes, thereby inducing proinflammatory mediators in a range of neurological disorders. In this study, we investigated the role of LCN2 in multiple aspects of diabetic encephalopathy in mouse models of diabetes. Here, we show that induction of diabetes increased the expression of both Lcn2 mRNA and protein in the hippocampus. Genetic deficiency of Lcn2 significantly reduced gliosis, recruitment of macrophages, and production of inflammatory cytokines in the diabetic mice. Further, diabetes-induced hippocampal toxicity and cognitive decline were both lower in Lcn2 knockout mice than in the wild-type animals. Taken together, our findings highlight the critical role of LCN2 in the pathogenesis of diabetic encephalopathy.

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Section: Resultssupporting

confidence: 93%

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

et al. 2019

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“…Concerning the direct effects of phenolic acids on the central nervous system, it has been demonstrated that hydroxycinnamic acids and their esters may exert beneficial effects toward cognitive functions by improving neuronal cell antioxidant activity against oxidative stress [ 47 , 48 ], through various signaling pathways including Nrf2/HO-1 pathway [ 49 ]. Moreover, hydroxycinnamic acids have been shown to rescue memory deficits in animal models of diabetes induced by streptozotocin through the reduction of oxidative stress and the positive modulation of the PI3-kinase pathway [ 50 , 51 ]. Among hydroxybenzoic acids, gallic acid has been shown to reverse impaired learning and memory in a rodent model of Alzheimer’s disease through simultaneous elevation of α-secretase and reduction of β-secretase activity and, most importantly, activation of metalloproteinase domain-containing protein 10 [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

Dietary Phenolic Acids and Their Major Food Sources Are Associated with Cognitive Status in Older Italian Adults

et al. 2021

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Background: Life expectancy is increasing along with the rising prevalence of cognitive disorders. Among the factors that may contribute to their prevalence, modifiable risk factors such as diet may be of primary importance. Unarguably, plant-based diets rich in bioactive compounds, such as polyphenols, showed their potential in decreasing risk of neurodegenerative disorders. Therefore, the aim of the present study is to investigate whether exposure to components of plant-based diets, namely phenolic acids, may affect cognitive status in older Italian adults. Methods: The demographic, lifestyle and dietary habits of a sample of individuals living in southern Italy were analyzed. Dietary intake was assessed through food frequency questionnaires (FFQs). Data on the phenolic acids content in foods were estimated using the Phenol-Explorer database. Cognitive status was evaluated using The Short Portable Mental Status Questionnaire. Multivariate logistic regression analyses were used to assess the associations. Results: The mean intake of phenolic acids was 346.6 mg/d. After adjustment for potential confounding factors, individuals in the highest quartile of total phenolic acid intake were less likely to have impaired cognitive status (OR = 0.36 (95% CI: 0.14, 0.92)); similarly, the analysis for subclasses of phenolic acids showed the beneficial effect toward cognitive status of greater intake of hydroxycinnamic acids (OR = 0.35 (95% CI: 0.13, 0.91)). Among individual compounds, only higher intake of caffeic acid was inversely associated with impaired cognitive status (OR = 0.32 (95% CI: 0.11, 0.93)); notably, the association with ferulic acid intake was significant only when adjusting for background characteristics, and not for adherence to the Mediterranean diet. Conclusions: This study revealed that greater intakes of dietary phenolic acids were significantly inversely associated with impaired cognition, emphasizing the possible role of phenolic acids in the prevention of cognitive disorders.

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“…The study was approved by the UCLouvain Ethical Committee (Brussels, Belgium; permit number: 2015/UCL/MD/07) and was conducted in accordance with the Practice Guidelines for Laboratory Animals of Belgium. NMRI mice are a well-known mice model for streptozotocin-induced T1D [16–18]. Moreover, the multiple low-dose STZ-induced diabetes mice model is a model widely used to demonstrate the effect of drug treatment or knockdown in type 1 diabetic mice.…”

Section: Methodsmentioning

confidence: 99%

Early Treatment with Empagliflozin and GABA Improves β-Cell Mass and Glucose Tolerance in Streptozotocin-Treated Mice

Daems¹,

Welsch²,

Boughaleb³

et al. 2019

Journal of Diabetes Research

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While the autoimmune character of T1D (type 1 diabetes) is being challenged, it is currently recognized that inflammation plays a key role in its development. We hypothesized that glucotoxicity could contribute to β-cell mass destruction through participation in islet inflammation. We evaluated the potential of empagliflozin (EMPA) and GABA (gamma-aminobutyric acid) to protect β-cell mass against glucotoxicity and to increase β-cell mass after diagnosis of T1D. Empagliflozin is a SGLT2 (sodium-dependent glucose cotransporter) inhibitor which thereby blocks glucose recapture by the kidney and promotes glucose excretion in urine. GABA is an inhibitory neurotransmitter, which stimulates α-to-β cell transdifferentiation. In streptozotocin-treated mice, empagliflozin and/or GABA were delivered for a period of five days or three weeks. As compared to untreated T1D mice, EMPA-treated T1D mice had decreased FFA (free fatty acid) levels and improved glucose homeostasis. EMPA-treated T1D mice had higher islet density, with preserved architecture, compared to T1D mice, and EMPA-treated T1D mice also differed from T1D mice by the total absence of immune cell infiltration within islets. Islets from EMPA-treated mice were also less subjected to ER (endoplasmic reticulum) stress and inflammation, as shown by qPCR analysis. Glucose homeostasis parameters and islet area/pancreas area ratio improved, as compared to diabetic controls, when T1D mice were treated for three weeks with GABA and EMPA. T1D EMPA+GABA mice had higher glucagon levels than T1D mice, without modifications of glucagon area/islet area ratios. In conclusion, empagliflozin and GABA, used in monotherapy in streptozotocin-induced diabetic mice, have positive effects on β-cell mass preservation or proliferation through an indirect effect on islet cell inflammation and ER stress. Further research is mandatory to evaluate whether empagliflozin and GABA may be a potential therapeutic target for the protection of β-cell mass after new-onset T1D.

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Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice

Cited by 46 publications

References 67 publications

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

Dietary Phenolic Acids and Their Major Food Sources Are Associated with Cognitive Status in Older Italian Adults

Early Treatment with Empagliflozin and GABA Improves β-Cell Mass and Glucose Tolerance in Streptozotocin-Treated Mice

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