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.
Highlights
Endometriosis (EMs) is a common and highlyrecurrent disorder [1] which causes about 10 to 15 % of cases of gynecological diseases such as dysmenorrhea, infertility, and chronic pelvic pain in women of childbearing age [2]
It is speculated when various stimulating factors act on normal endometrial cells, they can up-regulate nuclear factor-κB (NF-κB) expression, initiate an inflammatory response, and promote various inflammations involved in Astragaloside IV (AIV) is a high-purity drug extracted from Astragalus membranaceus, which is called “super Astragalus polysaccharide.”
IL-1β, IL-6, chemotactic protein-2 (Ccl-2), and tumor necrosis factor-α (TNF-α) mRNA expressions increased in endometriosis lesions of EMs mice compared with control mice (Figure 1 B; p < 0.01)
Summary
Endometriosis (EMs) is a common and highlyrecurrent disorder [1] which causes about 10 to 15 % of cases of gynecological diseases such as dysmenorrhea, infertility, and chronic pelvic pain in women of childbearing age [2]. Many factors leading to the inflammatory environment associated with endometriosis are upregulated by NF-κB [3,4]. It is speculated when various stimulating factors act on normal endometrial cells, they can up-regulate NF-κB expression, initiate an inflammatory response, and promote various inflammations involved in Astragaloside IV (AIV) is a high-purity drug extracted from Astragalus membranaceus, which is called “super Astragalus polysaccharide.”. The anti-inflammatory effect of AIV is mediated through its ability in inhibiting the activation of NF-κB signaling [9,10]. In present study, the effect of AIV on inflammation and the TLR4/NFκB pathway was studied using an EMs mouse model as well as in vitro experiments
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