2020
DOI: 10.1007/s11033-020-05696-w
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Minocycline attenuates depressive-like behaviors in mice treated with the low dose of intracerebroventricular streptozotocin; the role of mitochondrial function and neuroinflammation

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Cited by 16 publications
(8 citation statements)
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“…Due to the rich lipid contents in the membrane of brain cells, excessive ROS destroys the structure and function of the phospholipid bilayer of brain cells through lipid peroxide, alters the permeability of the BBB, and ultimately exacerbates neuroinflammation [ 71 ]. Therefore, antidepressant effects could theoretically be exerted by reducing OS and neuroinflammatory responses; this is in agreement with the reports of the study by Nouri et al [ 79 ] and Mozafari et al [ 73 ].…”
Section: Relationship Between Inflammation and Depressionsupporting
confidence: 92%
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“…Due to the rich lipid contents in the membrane of brain cells, excessive ROS destroys the structure and function of the phospholipid bilayer of brain cells through lipid peroxide, alters the permeability of the BBB, and ultimately exacerbates neuroinflammation [ 71 ]. Therefore, antidepressant effects could theoretically be exerted by reducing OS and neuroinflammatory responses; this is in agreement with the reports of the study by Nouri et al [ 79 ] and Mozafari et al [ 73 ].…”
Section: Relationship Between Inflammation and Depressionsupporting
confidence: 92%
“…Cerebral neuroinflammation, in addition to being associated with peripheral immunity, is also related to oxidative stress (OS) [ 70 , 71 ], mitochondrial dysfunction [ 72 , 73 ], energy metabolism disorders, nitroenergy system [ 74 , 75 ], eating habits [ 76 , 77 ], sleep quality [ 78 ], etc., to some extent.…”
Section: Relationship Between Inflammation and Depressionmentioning
confidence: 99%
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“…It seems that an increase in ROS levels subsequently leads to oxidative damage and pathogenesis of transient cerebral ischemia or stroke. The elevation in ROS production stimulated interaction with macromolecules and activation of cell death signaling pathways [ 21 , 37 ].…”
Section: Discussionmentioning
confidence: 99%
“…Hyperactivated microglia secrete excessive pro‐inflammatory mediators, including tumor necrosis factor‐alpha (TNF‐α), interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6), and reactive oxygen species (ROS) (Cherry et al, 2014), which are toxic for neurons. In addition, the transcription level of inducible nitric oxide synthase (iNOS) increases in activated microglia, resulting in the excessive synthesis of downstream nitric oxide (NO), which can induce neuronal death (Anjomshoa et al, 2020; Haj‐Mirzaian et al, 2019; Hassanipour et al, 2016; Lorigooini et al, 2021; Mozafari et al, 2020). The hyperactivation and dysregulation of microglia contribute heavily to cognitive dysfunction in AD (Calsolaro & Edison, 2016).…”
Section: Introductionmentioning
confidence: 99%