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

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          Abstract

          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 β-amyloid proteins (Aβ) 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 (PGE2) and PGD2, PGE2 induced neurogenesis by enhancing the expression of SOD2 and 14-3-3ζ, 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.

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          Author and article information

          Journal
          Biomaterials
          Biomaterials
          Elsevier BV
          1878-5905
          0142-9612
          Nov 2017
          : 145
          Affiliations
          [1 ] College of Life and Health Sciences, Northeastern University, Shenyang, 110819, PR China.
          [2 ] Department of Pharmaceutics, School of Pharmacy, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang, Liaoning Province, 110016, PR China.
          [3 ] College of Life and Health Sciences, Northeastern University, Shenyang, 110819, PR China. Electronic address: wangzy@mail.neu.edu.cn.
          [4 ] College of Life and Health Sciences, Northeastern University, Shenyang, 110819, PR China. Electronic address: wangpu@mail.neu.edu.cn.
          Article
          S0142-9612(17)30473-8
          10.1016/j.biomaterials.2017.07.023
          28865290

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