Inhibitory potential of prickly pears and their isolated bioactives against digestive enzymes linked to type 2 diabetes and inflammatory response

2019 ◽  
Vol 99 (14) ◽  
pp. 6380-6391 ◽  
Author(s):  
Andrea Gómez‐Maqueo ◽  
Tomás García‐Cayuela ◽  
Rebeca Fernández‐López ◽  
Jorge Welti‐Chanes ◽  
M Pilar Cano
2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Camila Gabriel Kato-Schwartz ◽  
Anacharis Babeto de Sá-Nakanishi ◽  
Ana Carolina Guidi ◽  
Geferson de Almeida Gonçalves ◽  
Fernanda Giacomini Bueno ◽  
...  

2021 ◽  
Author(s):  
Mutiu Kazeem ◽  
Habeeb Bankole ◽  
Olabisi Ogunrinola ◽  
Adedoja Wusu ◽  
Abidemi Kappo

2020 ◽  
Vol 11 ◽  
Author(s):  
Xiaomeng Liu ◽  
Yusong Zhang ◽  
Hongwei Liang ◽  
Yanchao Xu

Background: Type 2 diabetes mellitus (T2DM) is a chronic, hyperglycemia-associated, metabolic disorder. Heart disease is a major complication of T2DM. The present study aimed to explore the effects of miR-216a-3p on cardiomyocyte proliferation, apoptosis, and inflammation in T2DM through the Toll-like receptor (TLR) pathway involving interferon-α2 (IFN-α2) mediation.Methods: T2DM was induced in rats by a high-fat diet, in combination with an intraperitoneal injection of low-dose streptozotocin. ELISAs were conducted to measure inflammatory-related factors in serum. Next, isolated cardiomyocytes were used in loss- and gain-of-function experiments, followed by MTT and flow cytometry assays, conducted to evaluate cell proliferation, cell cycle, and apoptosis.Results: Our results revealed an increase in the inflammatory response in T2DM rat models, accompanied by significantly increased expression of miR-216a-3p and TLR pathway-related genes. However, a decrease in the expression of IFN-α2 was observed. Moreover, the presence of an miR-216a-3p inhibitor and si-IFN-α2 increased the expression of TLR pathway-related genes and cell apoptosis, whereas cell proliferation was significantly decreased in the cardiomyocytes.Conclusion: We found that in T2DM, miR-216a-3p inhibited the proliferation and enhanced the apoptosis of cardiomyocytes and generated an inflammatory response through activation of the TLR pathway and targeting of IFN-α2.


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