Shrimp oil (SO) rich in n-3 fatty acids and astaxanthin, mixed with antioxidant-rich tea seed oil (TSO), was microencapsulated using mung bean protein isolate and sodium alginate and fortified into whole wheat crackers. SO and TSO mixed in equal proportions were emulsified in a solution containing mung bean protein isolate (MBPI) and sodium alginate (SA) at varied ratios. The emulsions were spray-dried to entrap SO-TSO in MBPI-SA microcapsules. MBPI-SA microcapsules loaded with SO-TSO showed low to moderately high encapsulation efficiencies (EE) of 32.26–72.09% and had a fair flowability index. Two selected microcapsules with high EE possessed the particle sizes of 1.592 and 1.796 µm with moderate PDI of 0.372 and 0.403, respectively. Zeta potential values were −54.81 mV and −53.41 mV. Scanning electron microscopic (SEM) images indicated that microcapsules were spherical in shape with some shrinkage on the surface and aggregation took place to some extent. Fourier transform infrared (FTIR) and differential scanning calorimetry (DSC) analyses of samples empirically validated the presence of SO-TSO in the microcapsules. Encapsulated SO-TSO showed superior oxidative stability and retention of polyunsaturated fatty acids (PUFAs) to unencapsulated counterparts during storage of 6 weeks. When SO-TSO microcapsules were fortified in whole wheat crackers at varying levels (0–10%), the crackers showed sensorial acceptability with no perceivable fishy odor. Thus, microencapsulation of SO-TSO using MBPI-SA as wall materials could be used as an alternative carrier system, in which microcapsules loaded with PUFAs could be fortified in a wide range of foods.

Beta cyclodextrin (β-CD) used for cholesterol removal from shrimp lipid was reused after the cholesterol bound with β-CD was removed. Efficenicy of recycled β-CD was similar to pure β-CD.

Alzheimer’s disease is characterized by a progressive loss of memory and cognition. Accumulation of amyloid-beta (Aβ) 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 Aβ_1–42-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 Aβ-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 Aβ-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.