Spirulinadiet to lactating mothers protects the antioxidant system and reduces inflammation in post-natal brain after systemic inflammation

Patil, Jaspal; Matte, Ashok; Mallard, Carina; Sandberg, Mats

doi:10.1080/1028415x.2016.1221496

Cited by 17 publications

(10 citation statements)

References 46 publications

(51 reference statements)

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“…The effect on IL-1β is in agreement with earlier studies using this model [6] and appears to be region specific as the effect of LPS was normalized in cortex after 65 days [19]. The decrease in Nrf2 has to our knowledge not been demonstrated earlier and could be an important mechanism behind the elevated vulnerability in the substantia nigra after neonatal infection [6].…”

Section: Discussionsupporting

confidence: 89%

“…From these results we argue that one mechanism by which increased neuroinflammtion can mediate increased vulnerability is via a decreased Nrf2 function. This prolonged effect on Nrf2 is evident in the substantia nigra but not in cortex [19], which, at least partly, could explain the increased vulnerability to toxins of substantia nigra in animals subjected to neonatal inflammation [9] and could potentially be an important determinant behind sporadic Parkinson’s disease (PD).…”

Section: Discussionmentioning

confidence: 99%

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Sustained Effects of Neonatal Systemic Lipopolysaccharide on IL-1β and Nrf2 in Adult Rat Substantia Nigra Are Partly Normalized by a Spirulina-Enriched Diet

Patil

Matte²,

Nissbrandt³

et al. 2016

Neuroimmunomodulation

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Background/Aim: Neonatal infection can sensitize the adult substantia nigra (SN) to secondary insults, causing a decrease in antioxidant capacity which may lead to Parkinson's disease in adults. We studied the prolonged effect of systemic infection by (i.p.) administration of lipopolysaccharide (LPS) on interleukin (IL)-1β, the antioxidant regulator nuclear factor-erythroid 2-related factor 2 (Nrf2), and the peroxisome proliferator-activated receptor γ coactivator (PGC)-1α in rat SN. Method and Results: Five-day-old rat pups were treated with LPS (i.p. 2 mg/kg). After 65 days, the mRNA level of IL-1β was significantly increased, in parallel with a decrease in that of the rate-limiting enzyme in glutathione synthesis, the γ-glutamylcysteine ligase catalytic subunit (γGCLc), Nrf2, and brain-derived neurotrophic factor (BDNF). Protein levels of γGCLc and Nrf2 were decreased while IL-1β protein was significantly increased. These LPS-induced long-term changes correlated with a decrease in phosphorylated (active) AKT (pAKT) and phosphorylated (inactive) GSK-3β (pGSK-3β). In another set of experiments, a 0.1% Spirulina-containing diet was given to lactating mothers 24 h before the LPS treatment of the pups. The Spirulina-supplemented diet decreased IL-1β protein expression in SN and elevated the mRNA level of γGCLc, Nrf2 protein, PGC-1α protein, and pAKT. Conclusion: Early-life infection can negatively affect Nrf2, pAKT, and pGSK-3β for a long time in SN. A diet enriched with antioxidant and anti-inflammatory phytochemicals can partly restore some, but not all, of the effects on the antioxidant defense, possibly via normalizing effects on pAKT.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Sustained Effects of Neonatal Systemic Lipopolysaccharide on IL-1β and Nrf2 in Adult Rat Substantia Nigra Are Partly Normalized by a Spirulina-Enriched Diet

Patil

Matte²,

Nissbrandt³

et al. 2016

Neuroimmunomodulation

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“…Nrf2 is a major transcription factor that regulates cell antioxidant response. Nrf2 is transported to the nucleus under oxidative stress and binds to the antioxidant response elements (ARE) to regulate the expression of antioxidant enzymes such as HO-1 [37].In the previous study, the expression of the Nrf2-systerm (Nrf2 and HO-1) in rat brain were still increased 3 days after the LPS systemic injection, decreased by 7 days and then gradually normalized after LPS [38]. Our results showed that the contents of Nrf2 and HO-1 were nearly normalized in the hippocampus of rats after 14 days of LPS-induced.…”

Section: Discussionmentioning

confidence: 94%

Dihydrolipoic acid protects against lipopolysaccharide-induced behavioral deficits and neuroinflammation via regulation of Nrf2/HO-1/ NLRP3 signaling in rat

Bian

Wang

Huang

et al. 2020

Preprint

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Background: Recently, depression has been identified as prevalent and severe mental disorder. However, the mechanisms underlying the depression risk remain elusive. The neuroinflammation and NLRP3 inflammasome activation are known to be involved in the pathology of depression. Dihydrolipoic acid (DHLA) has been reported as a strong antioxidant and exhibits anti-inflammatory properties in various diseases, albeit the direct relevance between DHLA and depression is yet unknown. The present study aimed to investigate the preventive effect and potential mechanism of DHLA in the Lipopolysaccharide (LPS)-induced sickness behavior in rats. Methods: Adult male Sprague–Dawley rats were utilized. LPS and DHLA were injected intraperitoneally every 2 days and daily, respectively. Fluoxetine (Flu) was injected intraperitoneally daily. PD98059, an inhibitor of ERK, was injected intraperitoneally one hour before DHLA injection daily. Small interfering ribonucleic acid (siRNA) for nuclear factor erythroid 2-like (Nrf2) was injected into the bilateral hippocampus 14 days before the DHLA injection. Depression-like behavior tests were performed. Western blot and immunofluorescence staining detected the ERK/Nrf2/HO-1/ROS/NLRP3 pathway-related proteins.Results: The DHLA and fluoxetine treatment exerted preventive effects in LPS-induced sickness behavior rats. The DHLA treatment increased the expression of ERK, Nrf2, and HO-1 but decreased the ROS generation levels and reduced the expression of NLRP3, caspase-1, and IL-1b in LPS-induced sickness behavior rats. PD98059 abolished the effects of DHLA on preventive effect as well as the levels of Nrf2 and HO-1 proteins. Similarly, Nrf2 siRNA reversed the preventive effect of DHLA administration via the decreased expression of HO-1.Conclusions: These findings suggested that DHLA exerted a preventive effect via ERK/Nrf2/HO-1/ROS/NLRP3 pathway in LPS-induced sickness behavior rats. Thus, DHLA may serve as a potential therapeutic strategy for depression.

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“…Nrf2 is transported to the nucleus under oxidative stress and binds to the antioxidant response elements (ARE) to regulate the expression of antioxidant enzymes such as HO-1 [37].In the previous study, the expression of the Nrf2-systerm (Nrf2 and HO-1) in rat brain were still increased 3 days after the LPS systemic injection, decreased by 7 days and then gradually normalized after LPS [38]. Our results showed that the contents of Nrf2 and HO-1 were nearly normalized in the hippocampus of rats after 14 days of LPS-induced.…”

Section: Discussionmentioning

confidence: 94%

Dihydrolipoic acid protects against lipopolysaccharide-induced behavioral deficits and neuroinflammation via regulation of Nrf2/HO-1/ NLRP3 signaling in rat

Bian

Wang

Huang

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Recently, depression has been identified as prevalent and severe mental disorder. However, the mechanisms underlying the depression risk remain elusive. The neuroinflammation and NLRP3 inflammasome activation are known to be involved in the pathology of depression. Dihydrolipoic acid (DHLA) has been reported as a strong antioxidant and exhibits anti-inflammatory properties in various diseases, albeit the direct relevance between DHLA and depression is yet unknown. The present study aimed to investigate the preventive effect and potential mechanism of DHLA in the Lipopolysaccharide (LPS)-induced sickness behaviors in rats. Methods: Adult male Sprague–Dawley rats were utilized. LPS and DHLA were injected intraperitoneally every 2 days and daily, respectively. Fluoxetine (Flu) was injected intraperitoneally daily. PD98059, an inhibitor of ERK, was injected intraperitoneally one hour before DHLA injection daily. Small interfering ribonucleic acid (siRNA) for nuclear factor erythroid 2-like (Nrf2) was injected into the bilateral hippocampus 14 days before the DHLA injection. Depression-like behavior tests were performed. Western blot and immunofluorescence staining detected the ERK/Nrf2/HO-1/ROS/NLRP3 pathway-related proteins. Results: The DHLA and fluoxetine treatment exerted preventive effects in LPS-induced sickness behaviors rats. The DHLA treatment increased the expression of ERK, Nrf2, and HO-1 but decreased the ROS generation levels and reduced the expression of NLRP3, caspase-1, and IL-1b in LPS-induced sickness behaviors rats. PD98059 abolished the effects of DHLA on preventive effect as well as the levels of Nrf2 and HO-1 proteins. Similarly, Nrf2 siRNA reversed the preventive effect of DHLA administration via the decreased expression of HO-1. Conclusions: These findings suggested that DHLA exerted a preventive effect via ERK/Nrf2/HO-1/ROS/NLRP3 pathway in LPS-induced sickness behaviors rats. Thus, DHLA may serve as a potential therapeutic strategy for depression.

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Spirulinadiet to lactating mothers protects the antioxidant system and reduces inflammation in post-natal brain after systemic inflammation

Abstract: A Spirulina diet given to lactating mothers can protect against neuroinflammation and decreased antioxidant defence in brain of suckling pups subjected to peripheral inflammation, possibly via decreased activation of p38 and high levels of the antioxidant miRNA-146a.

Cited by 17 publications

References 46 publications

Sustained Effects of Neonatal Systemic Lipopolysaccharide on IL-1β and Nrf2 in Adult Rat Substantia Nigra Are Partly Normalized by a <b><i>Spirulina</i></b>-Enriched Diet

Sustained Effects of Neonatal Systemic Lipopolysaccharide on IL-1β and Nrf2 in Adult Rat Substantia Nigra Are Partly Normalized by a <b><i>Spirulina</i></b>-Enriched Diet

Dihydrolipoic acid protects against lipopolysaccharide-induced behavioral deficits and neuroinflammation via regulation of Nrf2/HO-1/ NLRP3 signaling in rat

Dihydrolipoic acid protects against lipopolysaccharide-induced behavioral deficits and neuroinflammation via regulation of Nrf2/HO-1/ NLRP3 signaling in rat

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