Pretreatment with Liposome-Encapsulated Shrimp Shell Extract Attenuated Neuronal Damage and Death in Aß1-42-Induced Memory Deficits in Rats.

The accumulation of amyloid-beta (Aß) peptides is a crucial factor in the neuronal degeneration of Alzheimer's disease (AD). The current study investigated the underlying neuroprotective mechanisms of shrimp shell extract (SSE) and liposome-encapsulated SSE (SSE/L) against Aß1-42-induced neuronal damage and death in rats. Intracerebroventricular infusion of Aß1-42 effectively induced memory decline, as observed in a reduction of the rat's discriminating ability in the novel object recognition and novel object location tasks. Oral pretreatment with 100 mg/kg of SSE demonstrated no preventive effect on the memory decline induced by Aß1-42 infusion. However, treatment with SSE/L 100 mg/kg BW effectively attenuated memory deficits in both behavioral assessments following two and four weeks after Aß1-42 infusion. Moreover, SSE/L exerted neuroprotective effects by reducing lipid peroxidation and increasing Nrf2/HO-1 expression. There was a significant decrease in Iba1 and GFAP (biomarkers of microglia and astrocyte activity, respectively), as well as a decrease in the levels of NF-κB expression and the inflammatory cytokines TNF-α and IL-6 in the cortical and hippocampal tissues. Treatment with SSE/L also reduced the pro-apoptotic proteins Bax and cleaved caspase-3 while raising the anti-apoptotic protein Bcl2. In addition, the beneficial effects of SSE/L were along with the effects of a positive control commercial astaxanthin (AST). The findings of this study indicated that SSE/L provided neuroprotective effects on Aß1-42-induced AD rats by ameliorating oxidative stress, neuroinflammation and apoptotic cell death. Therefore, SSE/L might be employed to prevent and mitigate Aß accumulation-induced neurotoxicity in AD.

Oral Administration of Ethanolic Extract of Shrimp Shells-Loaded Liposome Protects against Aß-Induced Memory Impairment in Rats.

Alzheimer's disease is characterized by a progressive loss of memory and cognition. Accumulation of amyloid-beta (Aß) in the brain is a well-known pathological hallmark of the disease. In this study, the ethanolic extract of white shrimp (Litopenaous vannamei) shells and the ethanolic extract-loaded liposome were tested for the neuroprotective effects on Aß1-42-induced memory impairment in rats. The commercial astaxanthin was used as a control. Treatment with the ethanolic extract of shrimp shells (EESS) at the dose of 100 mg/kg BW showed no protective effect in Aß-treated rats. However, treatment with an EESS-loaded liposome at the dose of 100 mg/kg BW significantly improved memory ability in Morris water maze and object recognition tests. The beneficial effect of the EESS-loaded liposome was ensured by the increase of the memory-related proteins including BDNF/TrkB and pre- and post-synaptic protein markers GAP-43 and PSD-95 as well as pErk1/2/Erk1/2 in the cortex and hippocampus. These findings indicated the neuroprotective effects of the EESS-loaded liposome on Aß-induced memory impairment in rats. It produced beneficial effects on learning behavior probably through the function of BDNF/TrkB/pErk1/2/Erk1/2 signaling pathway and subsequently the upregulation of synaptic proteins. The present study provided evidence that the neuroprotective property of the ESSE-loaded liposome could be a promising strategy for AD protection.

Effects of Astaxanthin from Litopenaeus Vannamei on Carrageenan-Induced Edema and Pain Behavior in Mice.

Carrageenan produces both inflammation and pain when injected in mouse paws via enhancement of reactive oxygen species formation. We have investigated an effect of astaxanthin extracted from Litopenaeus vannamei in carrageenan-induced mice paw edema and pain. The current study demonstrates interesting effects from astaxanthin treatment in mice: an inhibition of paw edema induced in hind paw, an increase in mechanical paw withdrawal threshold and thermal paw withdrawal latency, and a reduction in the amount of myeloperoxidase enzyme and lipid peroxidation products in the paw. Furthermore the effect was comparable to indomethacin, a standard treatment for inflammation symptoms. Due to adverse effects of indomethacin on cardiovascular and gastrointestinal systems, our study suggests promising prospect of astaxanthin extract as an anti-inflammatory alternative against carrageenan-induced paw edema and pain behavior.