Maltol inhibits the progression of osteoarthritis via the nuclear factor-erythroid 2–related factor-2/heme oxygenase-1 signal pathway in vitro and in vivo

Author(s): Ding-Chao Zhu ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , Yi-Han Wang ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , Jia-Hao Lin ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , Zhi-Min Miao ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , Jia-Jing Xu ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵ , Yao-Sen Wu ¹ ^, ² ^, ³ ^, ⁴ ^, ⁵

Publication date (Electronic): 2021

Journal: Food & Function

Publisher: Royal Society of Chemistry (RSC)

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Abstract

Osteoarthritis (OA) is a common degenerative joint disease characterized by articular cartilage degeneration and inflammation.

Abstract

Osteoarthritis (OA) is a common degenerative joint disease characterized by articular cartilage degeneration and inflammation. Currently, there is hardly any effective treatment for OA due to its complicated pathology and the severe side effects of the treatment drugs used. It has been reported that maltol, a Maillard reaction product derived from ginseng, inhibits inflammation and oxidative stress in several animal models. However, the potential anti-inflammatory effects of maltol in OA treatment are unknown. This study aimed to evaluate the anti-inflammatory effects of maltol on interleukin (IL)-1β-induced mouse chondrocytes and protective effects of maltol on these chondrocytes in medial meniscus destabilization (DMM) OA mouse models. Mice, randomly divided into maltol ( n = 15), vehicle ( n = 15) and control ( n = 15) groups were treated with the same dose of maltol or saline, respectively. The cartilage tissues were extracted for histological analysis 8 weeks postoperative. For the in vitro studies, chondrocytes were treated with 10 ng mL ⁻¹ IL-1β combined with maltol at different concentrations. In vitro assays showed that the maltol pre-treatment significantly inhibited the expressions of multiple inflammatory factors induced by IL-1β, such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), nitric oxide (NO), interleukin-6 (IL-6) and tumor necrosis factor (TNF-α). In addition, maltol alleviated the degradation of the extracellular matrix (ECM) by inhibiting the expressions of matrix metalloproteinase-13 (MMP13) and thrombospondin motif 5 (ADAMTS5), as well as reversing the degradation of aggrecan and collagen II. Moreover, maltol suppressed nuclear factor kappa B (NF-κB) signaling by activating the nuclear factor-erythroid 2-related factor-2 (Nrf2) in in vitro and in vivo studies. These findings indicate that maltol reduces the inflammation induced by IL-1β in chondrocytes. Therefore, the results of this study indicated that maltol may be a potential drug for the effective treatment of OA.

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Osteoarthritis.

S. Glyn-Jones, A. J. R. Palmer, R Agricola … (2015)

Osteoarthritis is a major source of pain, disability, and socioeconomic cost worldwide. The epidemiology of the disorder is complex and multifactorial, with genetic, biological, and biomechanical components. Aetiological factors are also joint specific. Joint replacement is an effective treatment for symptomatic end-stage disease, although functional outcomes can be poor and the lifespan of prostheses is limited. Consequently, the focus is shifting to disease prevention and the treatment of early osteoarthritis. This task is challenging since conventional imaging techniques can detect only quite advanced disease and the relation between pain and structural degeneration is not close. Nevertheless, advances in both imaging and biochemical markers offer potential for diagnosis and as outcome measures for new treatments. Joint-preserving interventions under development include lifestyle modification and pharmaceutical and surgical modalities. Some show potential, but at present few have proven ability to arrest or delay disease progression.

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Nrf2 signaling pathway: Pivotal roles in inflammation.

Syed Minhaj Uddin Ahmed, Lin Luo, Akhileshwar Namani … (2017)

Inflammation is the most common feature of many chronic diseases and complications, while playing critical roles in carcinogenesis. Several studies have demonstrated that Nrf2 contributes to the anti-inflammatory process by orchestrating the recruitment of inflammatory cells and regulating gene expression through the antioxidant response element (ARE). The Keap1 (Kelch-like ECH-associated protein)/Nrf2 (NF-E2 p45-related factor 2)/ARE signaling pathway mainly regulates anti-inflammatory gene expression and inhibits the progression of inflammation. Therefore, the identification of new Nrf2-dependent anti-inflammatory phytochemicals has become a key point in drug discovery. In this review, we discuss the members of the Keap1/Nrf2/ARE signal pathway and its downstream genes, the effects of this pathway on animal models of inflammatory diseases, and crosstalk with the NF-κB pathway. In addition we also discuss about the regulation of NLRP3 inflammasome by Nrf2. Besides this, we summarize the current scenario of the development of anti-inflammatory phytochemicals and others that mediate the Nrf2/ARE signaling pathway.