Inflammation-induced behavioral changes is driven by alterations in Nrf2-dependent apoptosis and autophagy in mouse hippocampus: Role of fluoxetine

Ghosh, Sayan; Choudhury, Sumana; Chowdhury, Olivia; Mukherjee, Sudeshna; Das, Ankur; Sain, Arindam; Gupta, P. C. Sen; Adhikary, Arghya; Chattopadhyay, Sreya

doi:10.1016/j.cellsig.2019.109521

Cited by 37 publications

(24 citation statements)

References 83 publications

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“…Existing data verify that adriamycin reduces the protein expression of Nrf2, but the expression of keap1 does not change with that of Nrf2. p62 is the specific autophagy receptor of Keap1 ( Ghosh et al, 2020 ). P62 binds to Keap1 and combines with other ubiquitinated protein polymers for degradation and cause cell apoptosis ( Zheng et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV Attenuates the Myocardial Injury Caused by Adriamycin by Inhibiting Autophagy

et al. 2021

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Astragaloside IV (ASIV) is the main active component of Astragalus, and can ameliorate cardiomyocyte hypertrophy, apoptosis and fibrosis. In this experiment, we studied how ASIV reduces the cardiotoxicity caused by adriamycin and protects the heart. To this end, rats were randomly divided into the control, ADR, ADR + ASIV and ASIV groups (n = 6). Echocardiography was used to observe cardiac function, HE staining was used to observe myocardial injury, TUNEL staining was used to observe myocardial cell apoptosis, and immunofluorescence and Western blotting was used to observe relevant proteins expression. Experiments have shown that adriamycin can damage heart function in rats, and increase the cell apoptosis index, autophagy level and oxidative stress level. Further results showed that ADR can inhibit the PI3K/Akt pathway. ASIV treatment can significantly improve the cardiac function of rats treated with ADR and regulate autophagy, oxidative stress and apoptosis. Our findings indicate that ASIV may reduce the heart damage caused by adriamycin by activating the PI3K/Akt pathway.

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Section: Discussionmentioning

confidence: 99%

Astragaloside IV Attenuates the Myocardial Injury Caused by Adriamycin by Inhibiting Autophagy

et al. 2021

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“…13 An increasing number of studies also indicate the relationship between autophagy and apoptosis. 14,15 It has been accepted that increased hippocampal neuron apoptosis plays an important role in the pathogenesis of diabetes-related depression. 10,16 In addition, various evidence suggested that abnormally elevated glutamate levels had a particularly negative effect on memory, due to the excessive release of excitatory amino acids and the activation of their receptors.…”

Section: Introductionmentioning

confidence: 99%

The molecular mechanism underlying mitophagy‐mediated hippocampal neuron apoptosis in diabetes‐related depression

Liu

Han

et al. 2021

J Cellular Molecular Medi

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“…17,18 Inflammatory conditions involving the hippocampus are thought to be one of the causes of depressive behavior. 19 Of note, glial activation and proinflammatory cytokine expression have been described in the hippocampus of animal models of diabetes. 20,21 Thus, it is predicted that minocycline will improve diabetes-related depression through the inhibition of inflammatory glial activation.…”

Section: Introductionmentioning

confidence: 99%

“…Several studies have indicated that the depressive behavior commonly observed in neurodegenerative diseases relates to hippocampal lesions 17,18 . Inflammatory conditions involving the hippocampus are thought to be one of the causes of depressive behavior 19 . Of note, glial activation and proinflammatory cytokine expression have been described in the hippocampus of animal models of diabetes 20,21 .…”

Section: Introductionmentioning

confidence: 99%

Minocycline prevents depression‐like behavior in streptozotocin‐induced diabetic mice

et al. 2020

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Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia. Diabetic patients are known to have a higher prevalence and a higher risk of depression compared with the general population. The pathogenesis of diabetes-related depression is unclear, and the treatment is not well-established. Therefore, the prevention of diabetes-related depression is important for improving the quality of life of diabetic patients. Minocycline, a secondgeneration tetracycline antibiotic, has recently gained attention as a new agent for depression. In this study, we investigated the effect of minocycline on diabetes-related depression in a streptozotocin-induced mouse model of diabetes. Eight-week-old male C57BL/6 mice were injected with streptozotocin (200 mg/kg, i.p.). Seven days after injection, the mice received minocycline treatment through drinking water. We compared these mice with vehicle-treated control mice and diabetic mice not receiving minocycline treatment. On day 34, depression-like behavior was investigated using the forced swim test. On the following day, brain samples were collected, and formalin-fixed, paraffin-embedded specimens were prepared for immunohistochemistry. Compared with the control group, the diabetic mice not receiving minocycline treatment showed a prolonged duration of immobility in the forced swim test, the observation being interpreted as a depression-like behavior. Immunohistochemistry revealed an increase in microglia with an activated morphology in the diabetic mice without minocycline treatment. The expression of tumor necrosis factor alpha in microglia was increased. In addition, a decrease in the number of doublecortin-positive immature neurons was found in the hippocampus of diabetic mice. Minocycline treatment of diabetic animals prevented the depression-like behavior and microglial activation; however, minocycline did not reverse impaired hippocampal neurogenesis. These results indicate that minocycline has a preventive effect on diabetes-related depression. Inhibition of microglial activation would be a critical target for the antidepressant mechanism of minocycline. Impaired hippocampal neurogenesis was observed in diabetic mice; however, this may not be involved in the pathogenesis of depression.

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Inflammation-induced behavioral changes is driven by alterations in Nrf2-dependent apoptosis and autophagy in mouse hippocampus: Role of fluoxetine

Cited by 37 publications

References 83 publications

Astragaloside IV Attenuates the Myocardial Injury Caused by Adriamycin by Inhibiting Autophagy

Astragaloside IV Attenuates the Myocardial Injury Caused by Adriamycin by Inhibiting Autophagy

The molecular mechanism underlying mitophagy‐mediated hippocampal neuron apoptosis in diabetes‐related depression

Minocycline prevents depression‐like behavior in streptozotocin‐induced diabetic mice

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