scholarly journals Berberine Ameliorates Spatial Learning Memory Impairment and Modulates Cholinergic Anti-Inflammatory Pathway in Diabetic Rats

2019 ◽  
Vol 10 ◽  
Author(s):  
Kaifu Wang ◽  
Qingjie Chen ◽  
Ninghua Wu ◽  
Yong Li ◽  
Ruyi Zhang ◽  
...  
Neuroscience ◽  
2017 ◽  
Vol 344 ◽  
pp. 39-47 ◽  
Author(s):  
Rui Wang ◽  
Yu Zhang ◽  
Jianguo Li ◽  
Ce Zhang

2021 ◽  
Vol 25 (Suppl 2) ◽  
pp. S72-80
Author(s):  
Jae-Min Lee ◽  
Jongmin Park ◽  
Joo-Hee Lee ◽  
Min Kyung Song ◽  
Youn-Jung Kim

Purpose: Silent information regulator 1 (SIRT1) in the brain is essential for maintaining cellular homeostasis and plays a neuroprotective role in cerebral ischemia and neurodegenerative disorders. The effect of preischemic treadmill exercise on chronic cerebral hypoperfusion (CCH)-induced spatial learning memory impairment, microvascular injury, and blood-brain barrier (BBB) disruption in relation with SIRT1 expression was evaluated.Methods: Prior to bilateral common carotid artery occlusion (BCCAO) surgery, the rats in the exercise groups performed low-intensity treadmill running for 30 minutes once daily during 8 weeks. BCCAO surgery was performed on male Wistar rats at 12 weeks of age. Spatial learning memory was measured using the Morris water maze test. Neuronal nuclear antigen, SIRT1, and rat endothelial cells antigen 1 were determined by immunohistochemistry and platelet-derived growth factor receptor beta was determined by immunofluorescence.Results: Preischemic treadmill exercise ameliorated spatial learning memory impairment and enhanced SIRT1 expression in the BCCAO rats. Preischemic treadmill exercise ameliorated BCCAO-induced damage to microvasculature and pericytes that make up the BBB. The effect of preischemic treadmill exercise was lost with sirtinol treatment.Conclusions: These results can apply treadmill exercise prior to cerebral ischemia as a rational preventive and therapeutic intervention strategy to improve cognitive dysfunction in CCH patients.


2020 ◽  
Vol 394 ◽  
pp. 112814 ◽  
Author(s):  
Arman Keymoradzadeh ◽  
Mojtaba Hedayati Ch ◽  
Mahmood Abedinzade ◽  
Rohollah Gazor ◽  
Mohammad Rostampour ◽  
...  

Planta Medica ◽  
2021 ◽  
Author(s):  
Dingkun Wang ◽  
Yanlin Ren ◽  
Wei Sun ◽  
Jing Gong ◽  
Xin Zou ◽  
...  

AbstractBerberine is an isoquinoline derivative alkaloid extracted from Chinese herbs. Recent studies have demonstrated the therapeutic effect of berberine on glucose metabolic disorders. However, its specific mechanism is still unclear. Our study aimed to research the glucose-lowering effect of berberine in diabetic rats and to reveal the possible role of the cholinergic anti-inflammatory pathway. Diabetic rats induced by administration of a high-calorie diet and streptozocin tail vein injection were assessed by the oral glucose tolerance test. Then, the diabetic rats were divided into two groups, those with or without the alpha7 nicotinic acetylcholine receptor gene downregulated, respectively, followed by treatment including berberine for 6 weeks. Results of this study show that the administration of berberine downregulated levels of fasting blood glucose and fasting insulin, and ameliorated insulin resistance in diabetic rats. Treatment with berberine inhibited acetylcholinesterase activity, and upregulated acetylcholine levels in the serum and alpha7 nicotinic acetylcholine receptor gene expression in the liver tissue. Meanwhile, berberine reversed elevated expression of cytokines interleukin-1β and TNF-α in the serum and downregulated nuclear factor κB expression. However, berberine administration showed no glucose-lowering or anti-inflammatory effect in diabetic rats in which alpha7 nicotinic acetylcholine receptor gene expression was downregulated, and acetylcholinesterase activity was also significantly inhibited. In conclusion, berberine may ameliorate glucose metabolism by activating the alpha7 nicotinic acetylcholine receptor-mediated cholinergic anti-inflammatory pathway.


2018 ◽  
Vol Volume 12 ◽  
pp. 89-98 ◽  
Author(s):  
Hongxia Zhang ◽  
Yanlan Yang ◽  
Yanqin Wang ◽  
Baodong Wang ◽  
Rongshan Li

2016 ◽  
Vol 7 (6) ◽  
pp. 512-520 ◽  
Author(s):  
Chengrui An ◽  
Xiaoyan Jiang ◽  
Hongjian Pu ◽  
Dandan Hong ◽  
Wenting Zhang ◽  
...  

Author(s):  
Archita C. Joshi ◽  
Chetna R. Patel ◽  
Naresh D. Kantharia

Background: Diabetes mellitus is known to cause cognitive impairment that can be possibly attributed to deficient levels of leptin in diabetic animals. This study was undertaken to study the effect of administration of leptin on spatial learning, memory and blood glucose levels in diabetic rats.Methods: Rats were divided into three groups. The first group was the control group. Diabetes was induced in groups 2 and 3 by streptozotocin (STZ) injection (60 mg/kg) intraperitoneally. Group 2 received saline while group 3 received leptin (0.1 mg/kg) subcutaneously for 10 days from 4th day of STZ administration. Behavioural assessment was done in T maze after 21 days of the last injection of leptin. Blood glucose levels were also analysed.Results: The number of correct arm entries decreased while time spent being immobile and time spent to reach the correct arm increased in the diabetic group when compared to the control group and correct arm entries increased while time spent immobile and time spent to reach the correct arm decreased with leptin treatment when compared to the diabetic control rats. Blood glucose levels increased in the diabetic rats while leptin administration reduced blood glucose levels in the group 3.Conclusions: Our study suggests that leptin can improve learning and memory while also producing a slight reduction in the blood glucose levels in diabetic rats.


2020 ◽  
Author(s):  
Li Kong ◽  
Yue Liu ◽  
Yu-Meng Zhang ◽  
Yu Li ◽  
Zhuang-Zhuang Tang ◽  
...  

Abstract Background: Sarsasapogenin (Sar), a natural steroidal compound, shows neuroprotective, promoting cognition, anti-inflammatory, anti-thrombosis effects, etc. However, whether Sar can ameliorate diabetes-associated cognitive impairment and whether it is related to the anti-inflammatory and anti-thrombosis effects of Sar, it remains unknown. Methods: Streptozotocin-induced diabetic rats were treated orally with Sar (20 and 60 mg/kg), and normal rats was orally administrated of Sar (60 mg/kg). Cognitive tests were performed using Morris water maze. Nucleotide-binding domain and leucine-rich repeat containing protein 1 (NLRP1) inflammasome (NLRP1, cleaved caspase 1, IL-1β, and IL-18), as well as thrombin and its receptor protease-activated receptor 1 (PAR-1) pathway and advanced glycation endproducts (AGEs) and its receptor RAGE axis were examined in the brain of diabetic rats. Meanwhile high glucose-cultured human SH-SY5Y cells were used to further investigate the effects of Sar (0.2, 1, 5 μM) on central neurons and deeply explore the mechanism. Results: Sar markedly increased numbers of crossing platform and percentage of time spent in the target quadrant in Morris water maze tests in diabetic rats, accompanied by inhibitions of NLRP1 inflammasome, PAR-1 upregulation, and AGEs/RAGE axis in cerebral cortex. Moreover, Sar mitigated neuronal damages, NLRP1 inflammasome activation, and PAR-1 upregulation in high glucose-cultured SH-SY5Y cells, and the effects were similar to those of the PAR-1 inhibition with a selective PAR-1 antagonist vorapaxar. But Sar also did not affect thrombin activity in the brain of diabetic rats and high glucose-cultured SH-SY5Y cells. Further studies indicated that the key molecules of NLRP1 inflammasome and the phosphorylated NF-kappaB p65 were remarkably decreased in SH-SY5Y cells cultured with high glucose after PAR-1 knockdown by using F2R (the gene symbol of PAR-1) shRNA, and these effects were confirmed by using Sar addition in such condition. Conclusions: These findings demonstrated that Sar could improve memory impairment caused by diabetes, which was achieved through suppressing neuroinflammation from the activated NLRP1 inflammasome and NF-kappaB mediated by thrombin/PAR-1 activation in brain. Moreover, Sar was proved to be a pleiotropic neuroprotective agent and memory enhancer.


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