Nageen Sharma
Craniosacral therapy
Federal Hostels , Faisalabad, Punjab, Pakistan, 38000
Years of experience 3

Total years in practice: 3

Published Date
May 31, 2015
Abstract Authors
Xiao-Ling Li, Yum-Shing Wong, Gang Xu, Juliana C N Chan
Abstract Source
Eur J Nutr. 2015 Jun ;54(4):509-22. Epub 2014 Aug 12. PMID: 25112514
Abstract Affiliation
Xiao-Ling Li
Study Type
Research
Conditions
Diabetes: Type I
Therapies
Functional Medicine, Naturopathic Medicine
Reference
Abstract Content
PURPOSE: Human islet amyloid polypeptide (hIAPP) aggregation is linked to loss of pancreatic beta cells in type 2 diabetes, in part due to oxidative stress. Currently, little is known about the effects of selenium-enriched Spirulina on beta cells with the presence of hIAPP. In this study, INS-1E rat insulinoma cells were used as a model to evaluate in vitro protective effects of Se-enriched Spirulina extract (Se-SE) against hIAPP-induced cell death, as well as the underlying mechanisms.
METHODS:
Flow cytometric analysis was used to evaluate cell apoptosis, mitochondrial membrane potential (??m) and ROS generation. Caspase activity was measured using a fluorometric method. Western blotting was applied to detect protein expression.
Results:
Our results showed that exposure of INS-1E cells to hIAPP resulted in cell viability loss, LDH release and appearance of sub-G peak. However, cytotoxicity of hIAPP was significantly attenuated by co-treatment with Se-SE. Se-SE also inhibited hIAPP-induced activation of caspase-3, -8 and -9. Additionally, hIAPP-induced accumulation of ROS and superoxide was suppressed by co-treatment with Se-SE. Moreover, Se-SE was able to prevent hIAPP-induced depletion of??m and intracellular ATP, reduction in mitochondrial mass, changes in the expression of Bcl-2 family members, release of mitochondrial apoptogenic factors. Furthermore, hIAPP-mediated AKT inhibition was restored by co-treatment with Se-SE.
Conclusion:
Our results showed that Se-SE protects INS-1E cells from hIAPP-induced cell death through preventing ROS overproduction, mitochondrial dysfunction and modulating PI3K/AKT pathway.
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