4.8 Article

Erythrocyte membrane-encapsulated celecoxib improves the cognitive decline of Alzheimer's disease by concurrently inducing neurogenesis and reducing apoptosis in APP/PS1 transgenic mice

Journal

BIOMATERIALS
Volume 145, Issue -, Pages 106-127

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.biomaterials.2017.07.023

Keywords

Celecoxib-encapsulated erythrocyte membrane; beta-amyloid protein; Neurogenesis; Apoptosis; Cyclooxygenase-2

Funding

  1. National Natural Science Foundation of China (CN) [81500934, 31571064, 31300777, 31371091]
  2. Fundamental Research Funds of China [N152004004, N120520001, N120320001, N130120002, N142004002, N141008001/7, L1520001]
  3. National Natural Science Foundation of Liaoning, China (CN) [2015020662]
  4. Liaoning Provincial Talent Support Program [LJQ2013029]

Ask authors/readers for more resources

Alzheimer's disease (AD) is characterized by the loss of neurogenesis and excessive induction of apoptosis. The induction of neurogenesis and inhibition of apoptosis may be a promising therapeutic approach to combating the disease. Celecoxib (CB), a cyclooxygenase-2 specific inhibitor, could offer neuroprotection. Specifically, the CB-encapsulated erythrocyte membranes (CB-RBCMs) sustained the release of CB over a period of 72 h in vitro and exhibited high brain biodistribution efficiency following intranasal administration, which resulted in the clearance of aggregated beta-amyloid proteins (A beta) in neurons. The high accumulation of the CB-RBCMs in neurons resulted in a decrease in the neurotoxicity of CB and an increase in the migratory activity of neurons, and alleviated cognitive decline in APP/PS1 transgenic (Tg) mice. Indeed, COX-2 metabolic products including prostaglandin E2 (PGE(2)) and PGD(2), PGE2 induced neurogenesis by enhancing the expression of SOD2 and 14-3-zeta, and PGD2 stimulated apoptosis by increasing the expression of BIK and decreasing the expression of ARRB1. To this end, the CB-RBCMs achieved better effects on concurrently increasing neurogenesis and decreasing apoptosis than the phospholipid membrane-encapsulated CB liposomes (CB-PSPD-LPs), which are critical for the development and progression of AD. Therefore, CB-RBCMs provide a rational design to treat AD by promoting the self-repairing capacity of the brain. (C) 2017 Elsevier Ltd. All rights reserved.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.8
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available