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黄芪甲苷通过活性氧/核苷酸结合寡聚结构域样受体热蛋白结构域相关蛋白 3/半胱氨酸天冬氨酸蛋白酶-1 信号通路抑制流感病毒引起的炎症。

Astragaloside IV inhibits inflammation caused by influenza virus via reactive oxygen species/NOD-like receptor thermal protein domain associated protein 3/Caspase-1 signaling pathway.

机构信息

Department of Infectious Diseases, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, China.

Central Laboratory, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, China.

出版信息

Immun Inflamm Dis. 2024 Jun;12(6):e1309. doi: 10.1002/iid3.1309.

Abstract

BACKGROUND

Astragaloside IV (AS-IV) is the most active monomer in the traditional Chinese herbal medicine Radix Astragali, which has a wide range of antiviral, anti-inflammatory, and antifibrosis pharmacological effects, and shows protective effects in acute lung injury.

METHODS

This study utilized the immunofluorescence, flow cytometry, enzyme-linked immunosorbent assay, quantitative reverse transcription-polymerase chain reaction, western blot, and hematoxylin and eosin staining methods to investigate the mechanism of AS-IV in reducing viral pneumonia caused by influenza A virus in A549 cells and BALB/c mice.

RESULTS

The results showed that AS-IV suppressed reactive oxygen species production in influenza virus-infected A549 cells in a dose-dependent manner, and subsequently inhibited the activation of nucleotide-binding oligomerization domain-like receptor thermal protein domain associated protein 3 inflammasome and Caspase-1, decreased interleukin (IL) -1β and IL-18 secretion. In BALB/c mice infected with Poly (I:C), oral administration of AS-IV can significantly reduce Poly (I:C)-induced acute pneumonia and lung pathological injury.

CONCLUSIONS

AS-IV alleviates the inflammatory response induced by influenza virus in vitro and lung flammation and structural damage caused by poly (I:C) in vivo.

摘要

背景

黄芪甲苷(AS-IV)是中药黄芪中最活跃的单体,具有广泛的抗病毒、抗炎和抗纤维化的药理作用,并在急性肺损伤中表现出保护作用。

方法

本研究采用免疫荧光、流式细胞术、酶联免疫吸附试验、定量逆转录聚合酶链反应、western blot 和苏木精和伊红染色方法,研究 AS-IV 降低甲型流感病毒感染 A549 细胞和 BALB/c 小鼠病毒性肺炎的机制。

结果

结果表明,AS-IV 呈剂量依赖性抑制流感病毒感染 A549 细胞中活性氧的产生,随后抑制核苷酸结合寡聚结构域样受体热蛋白结构域相关蛋白 3 炎性体和 Caspase-1 的激活,减少白细胞介素(IL)-1β和 IL-18 的分泌。在 Poly(I:C)感染的 BALB/c 小鼠中,AS-IV 的口服给药可显著减轻 Poly(I:C)诱导的急性肺炎和肺病理损伤。

结论

AS-IV 减轻了体外流感病毒诱导的炎症反应以及体内 Poly(I:C)引起的肺部炎症和结构损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e05a/11165686/68c8caa1045f/IID3-12-e1309-g006.jpg

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