Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment.
Study Goal
The researchers aimed to determine whether krill oil has anti-inflammatory, antioxidative, and anti-amyloidogenic effects in an Alzheimer's disease mouse model.
Results Summary
Krill oil treatment prevented LPS-induced memory loss, reduced oxidative stress markers (ROS, malondialdehyde), suppressed neuroinflammation (iNOS, COX-2), and inhibited amyloid beta peptide generation by downregulating APP and BACE1 expression. EPA and DHA from krill oil also dose-dependently reduced LPS-induced inflammatory markers in microglial cells.
Population
Alzheimer's disease mouse model (LPS-injected mice) and cultured microglial BV-2 cells.
Effective Dosage
80 mg/kg/day for mice; 50 and 100 µM for EPA and DHA in cell culture.
Duration
One month for mice; seven daily LPS injections.
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
krill oil diet (80 mg/kg/day for one month) | decrease | amyloidogenesis and cognitive impairment induced by intraperitoneal lipopolysaccharide (LPS) (250 µg/kg, seven times daily) injections | AD mice model | - | prevents | #1 |
krill oil treatment | decrease | the LPS-induced memory loss | AD mice model | - | inhibited | #2 |
krill oil treatment | decrease | the LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) | AD mice model | - | inhibited | #3 |
krill oil treatment | decrease | reactive oxygen species (ROS) and malondialdehyde levels | AD mice model | - | decreased | #4 |
Krill oil | decrease | IκB degradation as well as p50 and p65 translocation into the nuclei | LPS-injected mice brain cells | - | suppresses | #5 |
krill oil | decrease | amyloid beta (1-42) peptide generation | in vivo | - | suppressed | #6 |
krill oil | decrease | APP and BACE1 expression | in vivo | - | down-regulating | #7 |
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (50 and 100 µM) | decrease | LPS-induced nitric oxide and ROS generation | cultured microglial BV-2 cells | - | dose-dependently decreased | #8 |
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (50 and 100 µM) | decrease | COX-2 and iNOS expression as well as nuclear factor-κB activity | cultured microglial BV-2 cells | - | decreased | #9 |
Oxidative stress and neuroinflammation are implicated in the development and pathogenesis of Alzheimer's disease (AD). Here, we investigated the anti-inflammatory and antioxidative effects of krill oil. Oil from Euphausia superba (Antarctic krill), an Antarctic marine species, is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). We examined whether krill oil diet (80 mg/kg/day for one month) prevents amyloidogenesis and cognitive impairment induced by intraperitoneal lipopolysaccharide (LPS) (250 µg/kg, seven times daily) injections in AD mice model and found that krill oil treatment inhibited the LPS-induced memory loss. We also found that krill oil treatment inhibited the LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and decreased reactive oxygen species (ROS) and malondialdehyde levels. Krill oil also suppresses IκB degradation as well as p50 and p65 translocation into the nuclei of LPS-injected mice brain cells. In association with the inhibitory effect on neuroinflammation and oxidative stress, krill oil suppressed amyloid beta (1-42) peptide generation by the down-regulating APP and BACE1 expression in vivo. We found that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (50 and 100 µM) dose-dependently decreased LPS-induced nitric oxide and ROS generation, and COX-2 and iNOS expression as well as nuclear factor-κB activity in cultured microglial BV-2 cells. These results suggest that krill oil ameliorated impairment via anti-inflammatory, antioxidative, and anti-amyloidogenic mechanisms.