Astragaloside IV exerts anti-inflammatory role in endometriosis by downregulating TLR4/NF-κB pathway

Yongping Zhang, Ouping Huang, Wei Zhang, Luxin Liu, Caiwei Xu
In: Tropical Journal of Pharmaceutical Research · 2021 · vol. 18(3) , pp. 539–545 · doi:10.4314/tjpr.v18i3.14 · W3162016955
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Astragaloside IV treatment repressed inflammation in endometriosis lesions by downregulating TLR4/NF-κB signaling and reducing pro-inflammatory cytokine expression in mice.

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Abstract

Purpose: To investigate the effect of astragaloside IV administration on the inflammatory response in endometriosis and the underlying mechanism of action. Methods: Mice were divided into two groups: endometriosis (EMs) mice and control mice (n = 12). EMs induction in mice was achieved by transplantation of mouse uterine tissue. The same procedure was performed in control mice except that a separate suture was inserted instead of endometrial tissue. After 5 weeks, EMs mice were treated with or without astragaloside IV (AIV). The tissue lesions in EMs and control mice were stained with hematoxylin and eosin staining. The activation of toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) p65 signaling was evaluated by western blot, while expression of inflammatory cytokines was evaluated by quantitative real-time-polymerase chain reaction (qRT-PCR), and enzyme-linked immunosorbent assay (ELISA). Results: Astragaloside IV repressed the inflammation of murine Ems lesions, and also dampened the activation of TLR4/NF-κB signaling in vivo and vitro (p < 0.01 and p < 0.001, respectively). In addition, the expression levels of inflammatory cytokines (IL-1β, IL-6, Ccl-2, and TNF-α) decreased following AIV treatment in vivo. Conclusion: The results indicate that TLR4/NF-κB signaling pathways are closely related to the inhibition of Ems inflammation by astragaloside IV. Thus, astragaloside IV may be a novel drug for the prevention and treatment of endometrioses.
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Abstract

Purpose: To investigate the effect of astragaloside IV administration on the inflammatory response in endometriosis and the underlying mechanism of action.

Methods

Mice were divided into two groups: endometriosis (EMs) mice and control mice (n = 12). EMs induction in mice was achieved by transplantation of mouse uterine tissue. The same procedure was performed in control mice except that a separate suture was inserted instead of endometrial tissue. After 5 weeks, EMs mice were treated with or without astragaloside IV (AIV). The tissue lesions in EMs and control mice were stained with hematoxylin and eosin staining. The activation of toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) p65 signaling was evaluated by western blot, while expression of inflammatory cytokines was evaluated by quantitative real-time-polymerase chain reaction (qRT-PCR), and enzyme-linked immunosorbent assay (ELISA).

Results

Astragaloside IV repressed the inflammation of murine Ems lesions, and also dampened the activation of TLR4/NF-κB signaling in vivo and vitro (p < 0.01 and p < 0.001, respectively). In addition, the expression levels of inflammatory cytokines (IL-1β, IL-6, Ccl-2, and TNF-α) decreased following AIV treatment in vivo.

Conclusion

The results indicate that TLR4/NF-κB signaling pathways are closely related to the inhibition of Ems inflammation by astragaloside IV. Thus, astragaloside IV may be a novel drug for the prevention and treatment of endometrioses.

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Condition tags

endometriosis

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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