Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

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

Yongping Zhang^1,2 , Ouping Huang³, Wei Zhang², Luxin Liu², Caiwei Xu²

¹Medical Graduate School of Nanchang University; ²Department of Gynecology, Jiangxi Provincial People's Hospital; ³Jiangxi Provincial Maternal and Children Health Hospital, Nanchang 330006, China.

For correspondence:- Yongping Zhang Email: Zhangyongpingzyp09@163.com Tel:+8679186897371

Accepted: 23 February 2019 Published: 31 March 2019

Citation: Zhang Y, Huang O, Zhang W, Liu L, Xu C. Astragaloside IV exerts anti-inflammatory role in endometriosis by downregulating TLR4/NF-κB pathway. Trop J Pharm Res 2019; 18(3):539-545 doi: 10.4314/tjpr.v18i3.14

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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.

Keywords: Murine model, Astragaloside IV, Endometriosis, Inflammation, TLR4/NF-κB