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Fermented Astragalus Membranaceus by Bacillus subtilis Ameliorates Hyperuricemia in Mice by Suppressing Inflammation via Reducing p38 MAPK and NF-κB Phosphorylation

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Abstract Objectives: Hyperuricemia has become a public health problem that needs to be solved urgently. As traditional Chinese medicine, Astragalus membranaceus has high research value. In recent years, how to improve the bioavailability of Astragalus has been the subject of growing interest in the academic. Microbial fermentation has brought hope and dawn to address the above problem. Methods: Eighty mice were randomly divided into 8 groups (n=10): the normal control group, the hyperuricemia group, the benzbromarone group, the Bacillus subtilis-fermenting Astragalus group (0.25, 0.5 and 1 g/kg Astragalus), the unfermented Astragalus group, and the Bacillus subtilis group. To explore the underlying mechanism, levels of XOD, inflammatory factors, p38 mitogen-activated protein kinase (p38 MAPK), and nuclear factor-κB (NF-κB) were investigated. Results: Fermented Astragalus inhibited liver uric acid synthesis and protected the function of the kidney via anti-inflammation inhibiting the p38 MAPK/NF-κB pathways. It was speculated that increased total flavonoids, formononetin, and astragaloside IV of fermented Astragalus would result in a better therapeutic effect than unfermented Astragalus. Conclusion: The work undertaken sheds light on the development of Astragalus and the prevention and treatment of hyperuricemia.
Title: Fermented Astragalus Membranaceus by Bacillus subtilis Ameliorates Hyperuricemia in Mice by Suppressing Inflammation via Reducing p38 MAPK and NF-κB Phosphorylation
Description:
Abstract Objectives: Hyperuricemia has become a public health problem that needs to be solved urgently.
As traditional Chinese medicine, Astragalus membranaceus has high research value.
In recent years, how to improve the bioavailability of Astragalus has been the subject of growing interest in the academic.
Microbial fermentation has brought hope and dawn to address the above problem.
Methods: Eighty mice were randomly divided into 8 groups (n=10): the normal control group, the hyperuricemia group, the benzbromarone group, the Bacillus subtilis-fermenting Astragalus group (0.
25, 0.
5 and 1 g/kg Astragalus), the unfermented Astragalus group, and the Bacillus subtilis group.
To explore the underlying mechanism, levels of XOD, inflammatory factors, p38 mitogen-activated protein kinase (p38 MAPK), and nuclear factor-κB (NF-κB) were investigated.
Results: Fermented Astragalus inhibited liver uric acid synthesis and protected the function of the kidney via anti-inflammation inhibiting the p38 MAPK/NF-κB pathways.
It was speculated that increased total flavonoids, formononetin, and astragaloside IV of fermented Astragalus would result in a better therapeutic effect than unfermented Astragalus.
Conclusion: The work undertaken sheds light on the development of Astragalus and the prevention and treatment of hyperuricemia.

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