ReferenceID 2012
Harmine Ameliorates Cognitive Impairment by Inhibiting NLRP3 Inflammasome Activation and Enhancing the BDNF/TrkB Signaling Pathway in STZ-Induced Diabetic Rats
Front Pharmacol
Diabetes mellitus (DM) is considered a risk factor for cognitive dysfunction. Harmine not only effectively improves the symptoms of DM but also provides neuroprotective effects in central nervous system diseases. However
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Record Fields
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- Reference Id
- 2012
- Evidence Id
- 18602
- Core Evidence Id
- 18602
- Source Reference Id
- 4033
- Herb2 Reference Id
- HBREF004830
- Subject Paper Key
- HBIN028803_32425784
- Pubmed Id
- 32425784
- Doi
- 10.3389/fphar.2020.00535
- Paper Title
- Harmine Ameliorates Cognitive Impairment by Inhibiting NLRP3 Inflammasome Activation and Enhancing the BDNF/TrkB Signaling Pathway in STZ-Induced Diabetic Rats
- Paper Abstract
- Diabetes mellitus (DM) is considered a risk factor for cognitive dysfunction. Harmine not only effectively improves the symptoms of DM but also provides neuroprotective effects in central nervous system diseases. However, whether harmine has an effect on diabetes-induced cognitive dysfunction and the underlying mechanisms remain unknown. In this study, the learning and memory abilities of rats were evaluated by the Morris water maze test. Changes in the nucleotide-binding oligomerization domain-containing protein (NOD)-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome and brain-derived neurotrophic factor (BDNF)/TrkB signaling pathway were determined in both streptozotocin (STZ)-induced diabetic rats and high glucose (HG)-treated SH-SY5Y cells by western blotting and histochemistry. Herein, we found that harmine administration significantly ameliorated learning and memory impairment in diabetic rats. Further study showed that harmine inhibited NLRP3 inflammasome activation, as demonstrated by reduced NLRP3, ASC, cleaved caspase-1, IL-1beta, and IL-18 levels, in the cortex of harmine-treated rats with DM. Harmine was observed to have similar beneficial effects in HG-treated neuronal cells. Moreover, we found that harmine treatment enhanced BDNF and phosphorylated TrkB levels in both the cortex of STZ-induced diabetic rats and HG-treated cells. These data indicate that harmine mitigates cognitive impairment by inhibiting NLRP3 inflammasome activation and enhancing the BDNF/TrkB signaling pathway. Thus, our findings suggest that harmine is a potential therapeutic drug for diabetes-induced cognitive dysfunction.
- Journal
- Front Pharmacol
- Publish Year
- 2020
- Experiment Subject
- rat; hg-treated cells; hg-treated neuronal cells; high glucose (hg)-treated sh-sy5y cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Diabetes Mellitus; Cognitive Dysfunction; Cognitive Impairment; Diabetes-induced Cognitive Dysfunction; Memory Impairment; Diabetic; Central Nervous System Diseases
- Paper Title Cn
- Paper Title En
- Harmine Ameliorates Cognitive Impairment by Inhibiting NLRP3 Inflammasome Activation and Enhancing the BDNF/TrkB Signaling Pathway in STZ-Induced Diabetic Rats
- Bilingual Status
- semi_complete