The neuroprotective effect and action mechanism of polyphenols in diabetes mellitus-related cognitive dysfunction

2019 ◽  
Vol 59 (4) ◽  
pp. 1295-1311 ◽  
Author(s):  
Shenshen Zhang ◽  
Ran Xue ◽  
Ruizhe Hu
Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 323
Author(s):  
Subrat Kumar Bhattamisra ◽  
Hui Min Koh ◽  
Shin Yean Lim ◽  
Hira Choudhury ◽  
Manisha Pandey

Catalpol isolated from Rehmannia glutinosa is a potent antioxidant and investigated against many disorders. This review appraises the key molecular pathways of catalpol against diabetes mellitus and its complications. Multiple search engines including Google Scholar, PubMed, and Science Direct were used to retrieve publications containing the keywords “Catalpol”, “Type 1 diabetes mellitus”, “Type 2 diabetes mellitus”, and “diabetic complications”. Catalpol promotes IRS-1/PI3K/AKT/GLUT2 activity and suppresses Phosphoenolpyruvate carboxykinase (PEPCK) and Glucose 6-phosphatase (G6Pase) expression in the liver. Catalpol induces myogenesis by increasing MyoD/MyoG/MHC expression and improves mitochondria function through the AMPK/PGC-1α/PPAR-γ and TFAM signaling in skeletal muscles. Catalpol downregulates the pro-inflammatory markers and upregulates the anti-inflammatory markers in adipose tissues. Catalpol exerts antioxidant properties through increasing superoxide dismutase (sod), catalase (cat), and glutathione peroxidase (gsh-px) activity in the pancreas and liver. Catalpol has been shown to have anti-oxidative, anti-inflammatory, anti-apoptosis, and anti-fibrosis properties that in turn bring beneficial effects in diabetic complications. Its nephroprotective effect is related to the modulation of the AGE/RAGE/NF-κB and TGF-β/smad2/3 pathways. Catalpol produces a neuroprotective effect by increasing the expression of protein Kinase-C (PKC) and Cav-1. Furthermore, catalpol exhibits a cardioprotective effect through the apelin/APJ and ROS/NF-κB/Neat1 pathway. Catalpol stimulates proliferation and differentiation of osteoblast cells in high glucose condition. Lastly, catalpol shows its potential in preventing neurodegeneration in the retina with NF-κB downregulation. Overall, catalpol exhibits numerous beneficial effects on diabetes mellitus and diabetic complications.


2021 ◽  
pp. 1-9
Author(s):  
Guizhen Liu ◽  
Yuchuan Sun ◽  
Fei Liu

<b><i>Objective:</i></b> The purpose of this study was to explore the role of curcumin (Cur) in isoflurane (ISO)-induced learning and memory dysfunction in Sprague-Dawley rats and further elucidate the mechanism of the protective effect produced by Cur. <b><i>Methods:</i></b> Rat models of cognitive impairment were established by inhaling 3% ISO. The Morris water maze test was used to assess the cognitive function of rats. ELISA and qRT-PCR were used to analyze the protein levels of pro-inflammatory cytokines and expression levels of miR-181a-5p, respectively. <b><i>Results:</i></b> Cur significantly improved the ISO-induced cognitive dysfunction in rats and alleviated the ISO-induced neuroinflammation. miR-181a-5p was overexpressed in ISO-induced rats, while Cur treatment significantly reduced the expression of miR-181a-5p. Overexpression of miR-181a-5p promoted the cognitive impairment and the release of inflammatory cytokines and reversed the neuroprotective effect of Cur. <b><i>Conclusion:</i></b> Cur has a protective effect on ISO-induced cognitive dysfunction, which may be achieved by regulating the expression of miR-181a-5p.


2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
S. W. Seto ◽  
G. Y. Yang ◽  
H. Kiat ◽  
A. Bensoussan ◽  
Y. W. Kwan ◽  
...  

Diabetes mellitus (DM) is a metabolic disorder affecting a large number of people worldwide. Numerous studies have demonstrated that DM can cause damage to multiple systems, leading to complications such as heart disease, cancer, and cerebrovascular disorders. Numerous epidemiological studies have shown that DM is closely associated with dementia and cognition dysfunction, with recent research focusing on the role of DM-mediated cerebrovascular damage in dementia. Despite the therapeutic benefits of antidiabetic agents for the treatment of DM-mediated cognitive dysfunction, most of these pharmaceutical agents are associated with various undesirable side-effects and their long-term benefits are therefore in doubt. Early evidence exists to support the use of traditional Chinese medicine (TCM) interventions, which tend to have minimal toxicity and side-effects. More importantly, these TCM interventions appear to offer significant effects in reducing DM-related complications beyond blood glucose control. However, more research is needed to further validate these claims and to explore their relevant mechanisms of action. The aims of this paper are (1) to provide an updated overview on the association between DM and cognitive dysfunction and (2) to review the scientific evidence underpinning the use of TCM interventions for the treatment and prevention of DM-induced cognitive dysfunction and dementia.


2019 ◽  
Vol 104 (6) ◽  
pp. 2239-2249 ◽  
Author(s):  
Anna Shalimova ◽  
Beata Graff ◽  
Dariusz Gąsecki ◽  
Jacek Wolf ◽  
Agnieszka Sabisz ◽  
...  

2016 ◽  
Vol 15 (10) ◽  
pp. 2173 ◽  
Author(s):  
Jian-Xin Zhang ◽  
Zhi-Ying Li ◽  
Liang Zhao ◽  
Gang Li ◽  
Gui-Lin Cao ◽  
...  

2020 ◽  
Vol 11 (5) ◽  
pp. 4416-4427 ◽  
Author(s):  
Chu-Wen Li ◽  
Min-Zhen Deng ◽  
Zhi-Jie Gao ◽  
Yuan-Ye Dang ◽  
Guo-Dong Zheng ◽  
...  

The metabolite of ginsenosides, compound K improves memory and cognitive dysfunction in diabetes mellitus mice.


2019 ◽  
Vol 29 (5) ◽  
pp. 339-351
Author(s):  
Tingting Liu ◽  
Jung Eun Lee ◽  
Jing Wang ◽  
Song Ge ◽  
Changwei Li

Although cognitive dysfunction is related to type 2 diabetes mellitus (T2DM), the concept has not yet been well defined. The purpose of this study was to define the concept of cognitive dysfunction in persons with T2DM and examine its defining attributes, antecedents, and consequences. Literature was retrieved from 2008 to 2018 by systematically searching the PubMed, CINAHL, and PsycINFO databases. Based on 37 included studies, three defining attributes were identified: cognitive dysfunction is a recognized or unrecognized symptom, is characterized by a subtle decline in one or more cognitive domains, and is accompanied by pronounced structural changes observed in brain imaging. One major antecedent was diabetes-related or diabetes-specific pathological changes. Consequences included interference with diabetes self-management, nonadherence to recommended self-management behaviors, and a higher risk of having hypoglycemic events. The concept analysis provides a theoretical foundation that can be used to guide evaluations and interventions related to cognitive dysfunction in individuals with T2DM.


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