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. 2022 Oct 21;11(2):743-751.
doi: 10.1002/fsn3.3110. eCollection 2023 Feb.

Inhibition of H1N1 by Picochlorum sp. 122 via AKT and p53 signaling pathways

Affiliations

Inhibition of H1N1 by Picochlorum sp. 122 via AKT and p53 signaling pathways

Danyang Chen et al. Food Sci Nutr. .

Abstract

Influenza viruses cause a severe threat to global health, which can lead to annual epidemics and cause pandemics occasionally. However, the number of anti-influenza therapeutic agents is very limited. Polysaccharides, extracted from Picochlorum sp. (PPE), seaweed Polysaccharides, have exhibited antiviral activity and were expected to be used for influenza treatment. In our research, the capability of PPE to inhibit H1N1 infection was proved in MDCK cells. PPE could make MDCK cells avoid being infected with H1N1 and inhibited nuclear fragmentation and condensation of chromatin. PPE evidently inhibited the generation of reactive oxygen species in MDCK cells. Mechanism study revealed that PPE prevented MDCK cells from H1N1 infection through induction of apoptosis by stimulating AKT signaling pathway and suppressing p-p53 signaling pathway. In conclusion, PPE turns out to act as a prospective antiviral drug for H1N1 influenza.

Keywords: Polysaccharides; apoptosis; influenza virus; signaling pathway.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

FIGURE 1
FIGURE 1
(A) The cytotoxicity of PPE against MDCK cells. (B and C) Effects of PPE on the growth of H1N1‐infected MDCK cells.
FIGURE 2
FIGURE 2
(A) Effects of PPE on ROS production of H1N1‐infected MDCK cells. (B) Effects of PPE on the mitochondria depolarization of H1N1‐infected MDCK cells.
FIGURE 3
FIGURE 3
Effects of PPE on DNA fragmentation induced by H1N1 in MDCK cells.
FIGURE 4
FIGURE 4
Effects of PPE on the early and late apoptosis of H1N1‐infected MDCK cells.
FIGURE 5
FIGURE 5
Intracellular apoptotic signaling pathways by PPE in H1N1 infection of MDCK cells.
FIGURE 6
FIGURE 6
Effects of PPE on inflammatory response of H1N1‐infected MDCK cells.

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