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| Luteolin can improve cognitive dysfunction in septic mice by regulating HMGB1 |
| Hits 630 Download times 451 Received:February 22, 2022 |
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| DOI
10.11656/j.issn.1673-9043.2022.03.19 |
| Key Words
sepsis associated encephalopathy;luteolin;cognitive dysfunction;high mobility group box 1 protein;mouse |
| Author Name | Affiliation | | ZHANG Lian | Department of Critical Care Medicine, Deyang People's Hospital of Sichuan Province, Deyang 618000, China | | WANG Maojuan | Department of Critical Care Medicine, Deyang People's Hospital of Sichuan Province, Deyang 618000, China | | ZHOU Rong | Department of Traditional Chinese Medicine, Deyang People's Hospital of Sichuan Province, Deyang 618000, China | | JIANG Fan | Department of Critical Care Medicine, Deyang People's Hospital of Sichuan Province, Deyang 618000, China |
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| Abstract
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| [Objective] To investigate the effect of luteolin on cognitive dysfunction in sepsis associated encephalopathy mice by regulating high mobility group box 1 protein (HMGB1).[Methods] Mice with sepsis induced by cecal ligation and puncture were randomly divided into 6 groups:Sham group, model group, luteolin low, medium and high dose group and dexamethasone group. The open field test and Morris water maze were used to detect the activity exploration, learning and cognition of mice. Brain injury was detected by HE staining. TUNNEL staining was used to detect neuronal apoptosis. Levels of interleukin-6(IL-6), interleukin-1β(IL-1β), tumor necrosis factor(TNF-α) were detected by ELISA. The contents of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) were detected by the kit. Western blotting was used to detect HMGB1 protein expression.[Results] Compared with model group, luteolin medium, high dose group and dexamethasone group significantly increased survival rate of mice (P<0.05), total distance and a significant rise in the central area residence time (P<0.05), the escape latency time significantly reduced (P<0.05), a significant rise in target quadrant time, through the regional times (P<0.05), the hippocampus tissue pathological damage, nerve cells apoptosis rate was significantly lower (P<0.05);IL-6, IL-1β, TNF-α were significantly reduced(P<0.05);SOD and GSH contents increased significantly(P<0.05);MDA content decreased significantly (P<0.05), and HMGB1 protein level decreased significantly (P<0.05). The addition of HMGB1 inhibitor glycyrrhizin reversed the effect of luteolin on the sepsis associated encephalopathy mice model.[Conclusion] Luteolin can improve cognitive dysfunction in sepsis associated encephalopathy mice by regulating HMGB1. |
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