scholarly journals Treatment with Gaoziban Tablet Ameliorates Depression by Promoting GSK-3β Phosphorylation to Enhance the Wnt/β-catenin Activation in the Hippocampus of Rats

2021 ◽  
Vol 000 (000) ◽  
pp. 000-000
Author(s):  
Xin-Shuang Zou ◽  
Hai-Long Yin ◽  
Lei Shi ◽  
Hai-Ping Li ◽  
Meng-Heng Wang ◽  
...  
Keyword(s):  
Gsk 3Β

Inhibition of GSK-3β Prevents Experimental BPD

2017 ◽  
Author(s):  
Ruben Vaidya ◽  
Julia Hummler ◽  
Jawahar Jagarapu ◽  
Karen Young ◽  
Shu Wu ◽  
...  
Keyword(s):  
Gsk 3Β

Role of GSK-3β in hepatocellular carcinoma cell migration

2010 ◽  
Vol 30 (1) ◽  
pp. 28-32
Author(s):  
Jian-fei WANG ◽  
Ying HOU ◽  
Rui-liang GE ◽  
Yi-zheng WANG ◽  
Feng SHEN ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Migration ◽  
Carcinoma Cell ◽  
Hepatocellular Carcinoma Cell ◽  
Gsk 3Β

The Roles of GSK-3β in Regulation of Retinoid Signaling and Sorafenib Treatment Response in Hepatocellular Carcinoma

2019 ◽  
Author(s):  
Shuaishuai Zhang ◽  
Weiwei Gao ◽  
Juan Tang ◽  
Huaifang Zhang ◽  
Yuqi Zhou ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Treatment Response ◽  
Sorafenib Treatment ◽  
Retinoid Signaling ◽  
Gsk 3Β

Pharmacological Inhibition of Transient Receptor Potential Melastatin 2 (TRPM2) Channels Attenuates Diabetes-induced Cognitive Deficits in Rats: A Mechanistic Study

2020 ◽  
Vol 17 (3) ◽  
pp. 249-258 ◽  
Author(s):  
Pavan Thapak ◽  
Mahendra Bishnoi ◽  
Shyam S. Sharma
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Deficits ◽  
Ache Activity ◽  
Transient Receptor Potential ◽  
Mrna Level ◽  
Receptor Potential ◽  
Transient Receptor Potential Melastatin ◽  
Trpm2 Channels ◽  
Transient Receptor ◽  
Gsk 3Β

Background: Diabetes is a chronic metabolic disorder affecting the central nervous system. A growing body of evidence has depicted that high glucose level leads to the activation of the transient receptor potential melastatin 2 (TRPM2) channels. However, there are no studies targeting TRPM2 channels in diabetes-induced cognitive decline using a pharmacological approach. Objective: The present study intended to investigate the effects of 2-aminoethoxydiphenyl borate (2-APB), a TRPM2 inhibitor, in diabetes-induced cognitive impairment. Methods: Streptozotocin (STZ, 50 mg/kg, i.p.) was used to induce diabetes in rats. Animals were randomly divided into the treatment group, model group and age-matched control and pre se group. 2-APB treatment was given for three weeks to the animals. After 10 days of behavioural treatment, parameters were performed. Animals were sacrificed at 10th week of diabetic induction and the hippocampus and cortex were isolated. After that, protein and mRNA expression study was performed in the hippocampus. Acetylcholinesterase (AchE) activity was done in the cortex. Results: : Our study showed the 10th week diabetic animals developed cognitive impairment, which was evident from the behavioural parameters. Diabetic animals depicted an increase in the TRPM2 mRNA and protein expression in the hippocampus as well as increased AchE activity in the cortex. However, memory associated proteins were down-regulated, namely Ca2+/calmodulin-dependent protein kinase II (CaMKII-Thr286), glycogen synthase kinase 3 beta (GSK-3β-Ser9), cAMP response element-binding protein (CREB-Ser133), and postsynaptic density protein 95 (PSD-95). Gene expression of parvalbumin, calsequestrin and brain-derived neurotrophic factor (BDNF) were down-regulated while mRNA level of calcineurin A/ protein phosphatase 3 catalytic subunit alpha (PPP3CA) was upregulated in the hippocampus of diabetic animals. A three-week treatment with 2-APB significantly ameliorated the alteration in behavioural cognitive parameters in diabetic rats. Moreover, 2-APB also down-regulated the expression of TRPM2 mRNA and protein in the hippocampus as well as AchE activity in the cortex of diabetic animals as compared to diabetic animals. Moreover, the 2-APB treatment also upregulated the CaMKII (Thr-286), GSK-3β (Ser9), CREB (Ser133), and PSD-95 expression and mRNA levels of parvalbumin, calsequestrin, and BDNF while mRNA level of calcineurin A was down-regulated in the hippocampus of diabetic animals. Conclusion: : This study confirms the ameliorative effect of TRPM2 channel inhibitor in the diabetes- induced cognitive deficits. Inhibition of TRPM2 channels reduced the calcium associated downstream signaling and showed a neuroprotective effect of TRPM2 channels in diabetesinduced cognitive impairment.

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