Long-Term Alternating Fasting Increases Interleukin–13 in the Gerbil Hippocampus, But Does Not Protect BBB and Pyramidal Neurons From Ischemia-Reperfusion Injury
by Ronald
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Questionable whether intermittent fasting (IF) protects against ischemic brain injury. This study examines whether the IF increases anti-inflammatory cytokines and protected neurons from ischemia-reperfusion injury in the gerbil hippocampus. Gerbil was subjected to a 1-day fasting alternating as the IF for 1, 2, or 3 months and assigned to sham or 5 minutes of transient ischemia.
We examined changes in anti-inflammatory cytokines (IL-4 and IL-13), neurons and IgG by immunohistochemistry or immunofluorescence staining horn that ammonis 1 (CA1) hippocampal region before and after ischemia. IF increased IL-13 immunoreactivity in the CA1 region before ischemia, but did not affect IL-4 immunoreactivity. After ischemia, IL-13 and 4 immunoreactivities in the CA1 region was significantly lower in the IF-IF gerbils than in non gerbil.
In gerbils IF, the CA1 pyramidal neurons are not protected from ischemic injury; in this gerbil, strong IgG immunoreactivity seen in CA1 parenchyma, showing the BBB leakage. In short, IF increased IL-13 in the CA1 region, but these neurons are not protected from transient ischemic injury evidenced by IgG immunoreactivity in CA1 parenchyma. This study shows that the IF increased by several anti-inflammatory cytokines but could not afford neuroprotection against ischemic insults through the BBB disruption.
Long-Term Alternating Fasting Increases Interleukin–13 in the Gerbil Hippocampus, But Does Not Protect BBB and Pyramidal Neurons From Ischemia-Reperfusion Injury
interleukin 13 (IL- 13 ) alter genes related to hypoxia and regulate CD73
Background: Interleukin 13 (IL-13) is a pleiotropic cytokine that has been shown to be important in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) and type 2 inflammation-related diseases other. Increased expression of IL-13 may cause some pro-inflammatory effects, including eosinophilia, and pathologies such as increased secretion of mucus. Polypogenesis in chronic rhinosinusitis (CRS) can be caused by hypoxia, which can also cause airway epithelial hyperpermeability and translation of epithelial-to-mesenchymal via upregulation of hypoxia-related genes, such as HIF1. Is the T-helper 2 (Th2) inflammatory cytokines, such as IL-13, also can induce hypoxia-related genes sinonasal epithelial currently unknown.
Methods: Human air-liquid interface (ALI) sinonasal epithelial cell cultures were treated with recombinant IL-13 was analyzed by real-time polymerase chain reaction (PCR) and flow cytometry to determine the effect on epithelial cells.
Result: The entire network of subjects showed increased gene expression CRSwNP HIF1A. Treatment ALI fully differentiated human culture with IL-13 resulted in increased simultaneously in HIF1A and Arnt messenger RNA (mRNA) expression. However, the expression level was significantly reduced EPAS1. IL-13 also has a dose-dependent response at the gene expression of HIF and expression peak time of the study showed HIF1A and Arnt at 5 to 7 days poststimulation. Remarkably, CD73 surface expression also peaked on day 5 poststimulation.
Description: Recombinant IL-13 is a disulfide-linked monomer protein consisting of 115 amino acid residues,and migrates as an approximately 13 kDa protein under non-reducing and reducing conditions in SDS-PAGE. Optimized DNA sequence encoding human Interleukin-13 mature chain was expressed in E. coli.
Description: Recombinant IL-13 is a disulfide-linked monomer protein consisting of 115 amino acid residues,and migrates as an approximately 13 kDa protein under non-reducing and reducing conditions in SDS-PAGE. Optimized DNA sequence encoding human Interleukin-13 mature chain was expressed in E. coli.
Conclusions: Our data suggest that IL-13 can induce hypoxia gene signaling pathway that leads to surface expression of CD73, which have anti-inflammatory effects.Interleukin-4 (IL4) and interleukin 13 (IL13) is involved in the initial response of T helper lymphocytes via the activation of alpha 2 receptors IL4 (IL4RA), which is the common receptor chain for these cytokines. In humans, several single nucleotide polymorphisms (SNPs) were identified in IL4R and interleukin genes coFding associated with atopic disorders. However, the relationship between polymorphisms IL4R dog and atopic disorders have not been studied yet. This study aims to determine the relationship between the four non-synonymous SNPs and canine atopic dermatitis (CAD) in shiba inu and miniature dachshund population.
