Anti-Inflammatory Effects of Lasia spinosa Leaf Extract in Lipopolysaccharide-Induced RAW 264.7 Macrophages.

Thanh Q C Nguyen,Tuan L A Pham,Kaeko Kamei,Kenji Kanaori,Trong Tuan Nguyen,Tran Duy Binh,Yen D H Nguyen,Dai Thi Xuan Trang

doi:10.3390/ijms21103439

Thanh Q C Nguyen, Tuan L A Pham + Show 6 more

Open Access

https://doi.org/10.3390/ijms21103439

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Abstract

Lasia spinosa (L.) Thwaites was used as a traditional medicine to treat many inflammatory diseases for centuries. However, its effects on the inflammatory response are not yet characterized. In this study, we investigated the anti-inflammatory activities of L. spinosa leaf extract in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. We found that ethanol extracts of L. spinosa leaves showed anti-oxidant activity due to the presence of high levels of polyphenolic compounds. Treatment with the leaf extract significantly repressed the production of inflammatory mediators such as nitric oxide and reactive oxygen species and the expression of pro-inflammatory cytokines in the LPS-stimulated RAW 264.7 cells. Moreover, L. spinosa leaf extract treatment prevented activation of the nuclear factor-kappa B pathway by inhibiting nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) degradation. Furthermore, the mitogen-activated kinase and phosphoinositide-3-kinase/protein kinase B (PI3K/Akt) pathways were suppressed upon treatment with the leaf extract. In addition to suppressing inflammatory factors, the extract also activated the nuclear factor erythroid 2-related factor 2/heme-oxygenase-1 pathway. We propose that L. spinosa leaf extract has the potential as an effective therapeutic agent for alleviating oxidative stress and excessive inflammation.

Highlights

Inflammation is a mechanism used to defend against various infections and injuries; it is a well-appreciated aspect of complex biological responses that maintain homeostasis in the human body [1]
We propose that L. spinosa leaf extract has the potential as an effective therapeutic agent for alleviating oxidative stress and excessive inflammation
Lipopolysaccharide (LPS), a bacterial endotoxin, can induce inflammation signaling pathways via Toll-like receptor 4 (TLR-4), which stimulates the recruitment of cytoplasmic MyD88 and Toll like receptor-domain-containing adapter-inducing interferon-β (TRIF) adaptor proteins to increase the secretion of pro-inflammatory mediators and cytokines [4,5]

Summary

Introduction

Inflammation is a mechanism used to defend against various infections and injuries; it is a well-appreciated aspect of complex biological responses that maintain homeostasis in the human body [1]. Lipopolysaccharide (LPS), a bacterial endotoxin, can induce inflammation signaling pathways via Toll-like receptor 4 (TLR-4), which stimulates the recruitment of cytoplasmic MyD88 and Toll like receptor-domain-containing adapter-inducing interferon-β (TRIF) adaptor proteins to increase the secretion of pro-inflammatory mediators and cytokines [4,5]. Inflammation is related to oxidative stress, which elevates the levels of intracellular reactive oxygen species (ROS) and regulates the production of antioxidant enzymes [7]. The induction of phase II detoxifying enzymes, including heme oxygenase-1 (HO-1), is controlled by translocation of the nuclear factor-erythroid-2-related factor (Nrf2) in the Nrf2/HO-1 signaling pathway, which is a master cellular sensor that protects cells against inflammation and oxidative stress [8]

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