Antidepressant‐like Effects of Degraded Porphyran Isolated fromPorphyra haitanensis

Abstract

Introduction Degraded porphyran is a bioactive polysaccharide extracted from Porphyra haitanensis (P. haitanensis). According to the previous studies, it produced anti‐inflammatory activity, but little is known about its effects on depression. Methods and Results As inflammation is one of the critical factors involved in the development of depression, this study aims to elucidate the potential antidepressant‐like effects of degraded porphyran. The results show that acute porphyran treatment decreased the immobility time in despair tests. In addition, subchronic porphyran administration reverses depressive‐like behaviors in lipopolysaccharide (LPS)‐treated mice. Meanwhile, porphyran inhibits NF‐κB/NLRP3 signaling, proinflammatory cytokine release, and microglial activation in the hippocampus. Moreover, chronic porphyran treatment activates hippocampal brain derived neurotrophic factor (BDNF)/TrkB/ERK/CREB signaling pathway in chronic unpredictable mild stress (CUMS) in mice. As a result, neurogenesis and spinogenesis are maintained. Conclusions The findings of the present study indicate that degraded porphyran intake provides a potential strategy for depression treatment, which is mediated by the inhibition of neuroinflammation and the enhancement of neurogenesis and spinogenesis in the central nervous systems.

Study onLactiplantibacillus plantarumR6-3 from Sayram Ketteki to prevent chronic unpredictable mild stress-induced depression in mice through the microbiota–gut–brain axis

“…30 Immobility time in FST and TST reflects a state of desperation, which is similar to the symptom of depressed patients, and the two behavioral tests are widely used to initial screening of an antidepressant. 31 In this study, we measured the body weight of mice and conducted three classic behavioral tests, SPT, FST, and TST, to explore the effect of L. plantarum R6-3 on CUMS-induced depressive mice. In this study, the body weights of the mice showed an increasing trend during eight weeks and there was no significant difference between each group in the first two weeks ( p > 0.05) (Fig.…”

“…It is well known that the enhanced activity of the BDNF/TrkB/ERK/CREB signaling pathway is critical for neuronal survival, neural protrusion growth and branching. 31 A systematic review of clinical studies has shown that BDNF is directly involved in the pathophysiology of depression and the recovery of BDNF function may be the basis for antidepressant drug treatment. 40 BDNF plays a role through its high-affinity receptor tyrosine protein kinase B (TrkB), and BDNF and its receptor TrkB are widely and abundantly expressed in the central nervous system, activating various intracellular signaling pathways related to neuroprotection.…”

“…The results showed that, compared with the control group, the levels of 5-HT, DA, NE and BDNF in the brain tissue of CUMS-induced depressive mice were signifi- It is well known that the enhanced activity of the BDNF/TrkB/ ERK/CREB signaling pathway is critical for neuronal survival, neural protrusion growth and branching. 31 A systematic review of clinical studies has shown that BDNF is directly involved in the pathophysiology of depression and the recovery of BDNF function may be the basis for antidepressant drug treatment. 40 BDNF plays a role through its high-affinity receptor tyrosine protein kinase B (TrkB), and BDNF and its receptor TrkB are…”

“…13 BDNF binds to receptor TrkB, resulting in autophosphorylation of TrkB tyrosine residues, which activates downstream ERK/CREB signaling and triggers transcription of synaptic proteins. 14,31 Extracellular signalregulated kinase (ERK) is a widely reported downstream signal transduction protein of BDNF, which is involved in the survival and differentiation of neurons. Phosphorylated ERK is its activation form and the activated ERK enters the nucleus activating the activity of CREB through phosphorylation to exert cellular regulatory effects.…”

Active Flavonoids From Lagotis brachystachya Attenuate Monosodium Urate-Induced Gouty Arthritis via Inhibiting TLR4/MyD88/NF-κB Pathway and NLRP3 Expression

“…Briefly, the maturation of IL-1β needs to go through the following two stages (Ismael et al, 2021): The first stage is that the MSU crystal acts on cell surface TLRs to activate NF-κB, which causes IL-1β and NLRP3 gene transcription and subsequently generates inactive IL-1β precursors. In the second stage, NLRP3 inflammasome, which is activated by the MSU crystal via different pathways, will activate caspase-1 and, thus, cleave IL-1β precursors into mature IL-1β (Kelley et al, 2019;Yi et al, 2021). If there is only the activated TLRs signaling pathway but not the activation of NLRP3, the precursor IL-1β cannot exert any biological activity.…”