Tectorigenin Alleviates Inflammation, Apoptosis, and Ossification in Rat Tendon-Derived Stem Cells via Modulating NF-Kappa B and MAPK Pathways.

Safwat Adel Abdo Moqbel,Zhonggai Chen,Chiyuan Ma,Langhai Xu,Yan Xiong,Kai Xu,Jisheng Ran,Lidong Wu,Yuezhe He,Zhipeng Wu

doi:10.3389/fcell.2020.568894

Abstract

Tendinopathy is a common musculoskeletal disorder that mainly affects athletes and people of older age. Tumor necrosis factor-α (TNF-α) plays an important role in initiating tendinopathy. Tectorigenin, an extract component of Belam-canda Chinesis, possesses anti-inflammatory and anti-apoptosis activity. The present study was established to investigate the role of tectorigenin against the pathogenetic effects of TNF-α on tendon-derived stem cells (TDSCs) in vivo and in vitro. The findings indicated that TNF-α is able to induce TDSC inflammation, apoptosis, and ossification, as well as activate nuclear factor-kappa B and mitogen-activated protein kinase (MAPK). Furthermore, the results confirmed that tectorigenin is able to inhibit the TNF-α-induced inflammation, apoptosis, and ossification. Tectorigenin treatment decreases activation of NF-kappa B and MAPK signaling in TDSCs. Tectorigenin ameliorates tendinopathy in the in vivo rat model. Thus, these data reveal that tectorigenin can serve as a potential treatment for tendinopathy.

Highlights

Tendinopathy is a chronic disorder characterized by swelling, pain, ossification, and dysfunction of the tendon
Tumor necrosis factor-α (TNF-α) is a cytokine associated with tendon inflammation, degeneration, and apoptosis, and it contributes to the suppression of proliferation of Tendon-derived stem cells (TDSCs) (Hosaka et al, 2005; Han et al, 2017)
We examined the role of tectorigenin on the inflammation, apoptosis, and ossification of TDSCs through the targeting of mitogen-activated protein kinase (MAPK) and NF-κB in vitro, in addition to its effect in tendinopathy in the rat model

Summary

Introduction

Tendinopathy is a chronic disorder characterized by swelling, pain, ossification, and dysfunction of the tendon. Tendon-derived stem cells (TDSCs), which are extracted from tendon tissues, possess self-renewal and tendon-like tissue regeneration capabilities (Bi et al, 2007). TDSCs play a central role in tendon regeneration and healing as well as controlling tendon homeostasis (Ni et al, 2012). A change in their microenvironment leads to the dysfunction of TDSCs, resulting in degradation of tendon matrix and tendinopathy (Shi et al, 2019). TNF-α is a cytokine associated with tendon inflammation, degeneration, and apoptosis, and it contributes to the suppression of proliferation of TDSCs (Hosaka et al, 2005; Han et al, 2017). TNF-α is able to induce the production of matrix degradation enzymes (Machner et al, 2003), which are associated with the inhibition of ECM synthesis (John et al, 2010).

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Conclusion