Reduction in TNF alpha and oxidative stress by liraglutide: Impact on ketamine-induced cognitive dysfunction and hyperlocomotion in rats

Sedky, Amina Ahmed; Magdy, Yosra

doi:10.1016/j.lfs.2021.119523

Cited by 14 publications

(7 citation statements)

References 67 publications

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“…Therefore, it has also become one of the means for diabetes treatment by inhibiting oxidative stress and inflammatory responses. Sedky and Magdy reported that liraglutide ameliorated cognitive impairment and improved glucose homeostasis in T2DM mice by inhibiting oxidative stress and inflammatory factors . Gao et al reported that bovine α-lactalbumin-derived peptides attenuated TNF-α-induced IR and inflammation in 3T3-L1 adipocytes by inhibiting JNK and NF-κB signaling pathways .…”

Section: Resultsmentioning

confidence: 99%

“…Sedky and Magdy reported that liraglutide ameliorated cognitive impairment and improved glucose homeostasis in T2DM mice by inhibiting oxidative stress and inflammatory factors. 30 Gao et al reported that bovine α-lactalbumin-derived peptides attenuated TNF-αinduced IR and inflammation in 3T3-L1 adipocytes by inhibiting JNK and NF-κB signaling pathways. 25 Our results showed that walnut-derived peptides had good antioxidant and anti-inflammatory effects in T2DM mice.…”

Section: Fraction 3−10 Kda and Lp5 Inhibit Oxidative Stress And Infla...mentioning

confidence: 99%

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Walnut-Derived Peptides Promote Autophagy via the Activation of AMPK/mTOR/ULK1 Pathway to Ameliorate Hyperglycemia in Type 2 Diabetic Mice

Hou

Zhao

et al. 2023

J. Agric. Food Chem.

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Autophagy flux plays a significant protective role in type 2 diabetes mellitus (T2DM). However, the mechanisms by which autophagy mediates insulin resistance (IR) to ameliorate T2DM remain unclear. This study explored the hypoglycemic effects and mechanisms of walnut-derived peptides (fraction 3−10 kDa and LP5) in streptozotocin and high-fat-diet-induced T2DM mice. Findings revealed that walnut-derived peptides reduced the levels of blood glucose and FINS and ameliorated IR and dyslipidemia. They also increased SOD and GSH-P X activities and inhibited the secretion of TNF-α, IL-6, and IL-1β. Additionally, they increased the levels of ATP, COX, SDH, and MMP of liver mitochondria. Western blotting indicated that walnut-derived peptides upregulated LC3-II/LC3-I and Beclin-1 expression, while they down-regulated p62 expression, which may be associated with the activation of the AMPK/mTOR/ULK1 pathway. Finally, the AMPK activator (AICAR) and inhibitor (Compound C) were used to verify that LP5 could activate autophagy through the AMPK/mTOR/ULK1 pathway in IR HepG2 cells.

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Section: Resultsmentioning

confidence: 99%

Section: Fraction 3−10 Kda and Lp5 Inhibit Oxidative Stress And Infla...mentioning

confidence: 99%

Walnut-Derived Peptides Promote Autophagy via the Activation of AMPK/mTOR/ULK1 Pathway to Ameliorate Hyperglycemia in Type 2 Diabetic Mice

Hou

Zhao

et al. 2023

J. Agric. Food Chem.

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“…In addition, stress-induced reinstatement of addictive methamphetamine increased inflammatory cytokines in the prefrontal cortex, leading to changes in neurotransmission, thus, triggering reinstatement of methamphetamine (Karimi-Haghighi et al, 2020). Moreover, the increased pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) were found in addictive psychostimulants including ketamine, methamphetamine, and alcohol (Airapetov et al, 2019;Li et al, 2020;Sedky and Magdy, 2021), suggesting that changes in peripheral markers of inflammation are generally associated with drug abuse. These data raised the possibility that oxytocin participates in social and cognitive functions through interactions with inflammatory processes, and reduction in inflammatory cytokines may play an important role in the reversal effect of oxytocin on ketamineinduced behavioral dysfunctions.…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that ketamine-induced cognitive dysfunction is associated with increased levels of inflammatory cytokines, such as TNF-α (Sedky and Magdy, 2021). In addition, the counts of immune cell neutrophils and monocytes, as well as the neutrophil-lymphocyte ratio (NLR), reliable inflammatory biomarkers for systemic inflammatory response (Gibson et al, 2007;Azab et al, 2011), were found increased in ketamine and psychiatric disorders with a core symptom of impaired social behaviors (Aydin Sunbul et al, 2017;Kayhan et al, 2017;Kido et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Enhancement of Oxytocin in the Medial Prefrontal Cortex Reverses Behavioral Deficits Induced by Repeated Ketamine Administration in Mice

et al. 2021

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Ketamine is a popular recreational substance of abuse that induces persistent behavioral deficits. Although disrupted oxytocinergic systems have been considered to modulate vulnerability to developing drugs of abuse, the involvement of central oxytocin in behavioral abnormalities caused by chronic ketamine has remained largely unknown. Herein, we aimed to investigate the potential role of oxytocin in the medial prefrontal cortex (mPFC) in social avoidance and cognitive impairment resulting from repeated ketamine administration in mice. We found that ketamine injection (5 mg/kg, i.p.) for 10 days followed by a 6-day withdrawal period induced behavioral disturbances in social interaction and cognitive performance, as well as reduced oxytocin levels both at the periphery and in the mPFC. Repeated ketamine exposure also inhibited mPFC neuronal activity as measured by a decrease in c-fos-positive cells. Furthermore, direct microinjection of oxytocin into the mPFC reversed the social avoidance and cognitive impairment following chronic ketamine exposure. In addition, oxytocin administration normalized ketamine-induced inflammatory cytokines including TNF-α, IL-6, and IL-1β levels. Moreover, the activation of immune markers such as neutrophils and monocytes, by ketamine was restored in oxytocin-treated mice. Finally, the reversal effects of oxytocin on behavioral performance were blocked by pre-infusion of the oxytocin receptor antagonist atosiban into the mPFC. These results demonstrate that enhancing oxytocin signaling in the mPFC is a potential pathway to reverse social avoidance and cognitive impairment caused by ketamine, partly through inhibition of inflammatory stimulation.

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“…Ketamine has also been shown to impair spontaneous alterations as a function of spatial working memory [ 74 , 75 ]. Moreover, ketamine can exert anxiety-like behavior [ 76 , 77 ], altered social behavior [ 78 , 79 ], hyperlocomotion [ 66 , 80 ], and impaired sensorimotor gating [ 81 , 82 ].…”

Section: Pharmacological Modelsmentioning

confidence: 99%

Advantages and Limitations of Animal Schizophrenia Models

Białoń

Wąsik

2022

IJMS

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Mental illness modeling is still a major challenge for scientists. Animal models of schizophrenia are essential to gain a better understanding of the disease etiopathology and mechanism of action of currently used antipsychotic drugs and help in the search for new and more effective therapies. We can distinguish among pharmacological, genetic, and neurodevelopmental models offering various neuroanatomical disorders and a different spectrum of symptoms of schizophrenia. Modeling schizophrenia is based on inducing damage or changes in the activity of relevant regions in the rodent brain (mainly the prefrontal cortex and hippocampus). Such artificially induced dysfunctions approximately correspond to the lesions found in patients with schizophrenia. However, notably, animal models of mental illness have numerous limitations and never fully reflect the disease state observed in humans.

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Reduction in TNF alpha and oxidative stress by liraglutide: Impact on ketamine-induced cognitive dysfunction and hyperlocomotion in rats

Cited by 14 publications

References 67 publications

Walnut-Derived Peptides Promote Autophagy via the Activation of AMPK/mTOR/ULK1 Pathway to Ameliorate Hyperglycemia in Type 2 Diabetic Mice

Walnut-Derived Peptides Promote Autophagy via the Activation of AMPK/mTOR/ULK1 Pathway to Ameliorate Hyperglycemia in Type 2 Diabetic Mice

Enhancement of Oxytocin in the Medial Prefrontal Cortex Reverses Behavioral Deficits Induced by Repeated Ketamine Administration in Mice

Advantages and Limitations of Animal Schizophrenia Models

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