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

机译:Picochlorum sp. 122 通过 AKT 和 p53 信号通路抑制 H1N1

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摘要

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.
机译:流感病毒对全球健康构成严重威胁,这可能导致每年的流行病,偶尔也会导致大流行。然而,抗流感治疗药物的数量非常有限。从 Picochlorum sp. (PPE) 中提取的多糖,海藻多糖,已显示出抗病毒活性,有望用于流感治疗。在我们的研究中,PPE 抑制 H1N1 感染的能力在 MDCK 细胞中得到证明。PPE 可以使 MDCK 细胞避免感染 H1N1 并抑制核碎裂和染色质浓缩。PPE 明显抑制了 MDCK 细胞中活性氧的产生。机制研究显示,PPE 通过刺激 AKT 信号通路和抑制 p-p53 信号通路诱导细胞凋亡,从而阻止 MDCK 细胞感染 H1N1。总之,PPE 被证明是 H1N1 流感的前瞻性抗病毒药物。

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