Wistin Exerts an Anti-Inflammatory Effect via Nuclear Factor-κB and p38 Signaling Pathways in Lipopolysaccharide-Stimulated RAW264.7 Cells

Abstract

Inflammation is an immune response to cellular damage caused by various stimuli (internal or external) and is essential to human health. However, excessive inflammatory responses may be detrimental to the host. Considering that the existing drugs for the treatment of inflammatory diseases have various side effects, such as allergic reactions, stomach ulcers, and cardiovascular problems, there is a need for research on new anti-inflammatory agents with low toxicity and fewer side effects. As 4′,6-dimethoxyisoflavone-7-O-β-d-glucopyranoside (wistin) is a phytochemical that belongs to an isoflavonoid family, we investigated whether wistin could potentially serve as a novel anti-inflammatory agent. In this study, we found that wistin significantly reduced the production of nitric oxide and intracellular reactive oxygen species in lipopolysaccharide-stimulated RAW 264.7 cells. Moreover, wistin reduced the mRNA levels of pro-inflammatory enzymes (inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2)) and cytokines (interleukin (IL)-1β and IL-6) and significantly reduced the protein expression of pro-inflammatory enzymes (iNOS and COX-2). Furthermore, wistin reduced the activation of the nuclear factor-κB and p38 signaling pathways. Together, these results suggest that wistin is a prospective candidate for the development of anti-inflammatory drugs.

Arteannuin-B and (3-chlorophenyl)-2-spiroisoxazoline derivative exhibit anti-inflammatory effect in LPS-activated RAW 264.7 macrophages and Balb/c mice induced pro-inflammatory responses via down-regulation of NF-κB/P38 MAPK Signalling.

“…When IκB-α and NF-κB are separated, free dimer-activated subunits of NF-κB (p50/p65) can be translocated from the cytosol to the nucleus. LPS alone increased the quantity of NF-κB in the nucleus, whereas 1 and JR-9 reduced LPS-induced nuclear translocation of NF-κB in a dose-dependent manner [31] (Figure 6B). We determined the effect of 1 and JR-9 on LPS-stimulated phosphorylation of P-p38 MAPK and T-p38 MAPK in macrophages to determine whether the inhibition of NF-κB activation is mediated through MAPK pathways.…”

Nrf2 protein in melanoma progression, as a new means of treatment

“…Melanoma is a type of cancer that does not respond well to standard chemotherapy, which results in a 5‐year survival rate of approximately 15% (Davis et al, 2019). The traditional method of treating melanoma has been revolutionized in recent years thanks to the development of cutting‐edge targeted therapies and immunotherapy (An et al, 2022). In recent years, a novel strategy for combating melanoma's resistance to chemotherapy has emerged: identifying the signaling pathways that are involved in the control and execution of apoptosis, and then modifying those pathways to improve melanoma cell sensitivity (Xu et al, 2021).…”