Antarctic krill peptides improve scopolamine-induced memory impairment in mice

The study aims to investigate the repair effects of Ser-Ser-Asp-Ala-Phe-Phe-Pro-Phe-Arg (SSDAFFPFR) and Ser-Asn-Val-Phe-Asp-Met-Phe (SNVFDMF) peptides on scopolamine-caused memory impairment in mice. Behavioral experiments have revealed that Antarctic krill peptides can ameliorate scopolamine caused memory impairment by changing the behavior of mice. In comparison with the scopolamine group, the two peptides at a dose of 40 mg/kg could improve memory impairment. The serum SOD activity (82.82 +/- 0.19 vs 79.47 +/- 2.42 U/ mg prot) and hippocampal ACh level (101.46 +/- 3.23 vs 99.85 +/- 7.13 mu g/mg prot) of SSDAFFPFR were higher than those of SNVFDMF. Hippocampal AChE activity (0.20 +/- 0.03 vs 0.53 +/- 0.02 U/mg prot), hippocampal MDA level (1.56 & PLUSMN; 0.01 vs 1.63 & PLUSMN; 0.05 nmol/mg prot) and the serum MDA level (3.38 +/- 0.24 vs 3.88 +/- 0.21 nmol/mg prot) was lower than that of SNVFDMF. The state of mouse hippocampal cells was further observed by a microscopic imaging system. In addition, western blot analysis showed that SSDAFFPFR could significantly inhibit the expression of Bax, caspase-3, and p53, and promote the expression of BCL-XL, CREB, and BDNF, thus protecting hippocampal neurons in mice. In conclusion, the Antarctic krill peptide can repair scopolamine-induced memory impairment in mice.

Automated summary

The study shows that Antarctic krill peptides can repair scopolamine-induced memory impairment by enhancing SOD activity and ACh level while reducing AChE and MDA levels in hippocampal neurons.