Rhamnazin inhibits LPS-induced inflammation and ROS/RNS in raw macrophages

Abstract

Purpose: The aim of this work was to investigate the beneficial effects of rhamnazin against inflammation, reactive oxygen species (ROS)/reactive nitrogen species (RNS), and anti-oxidative activity in murine macrophage RAW264.7 cells. Methods: To examine the beneficial properties of rhamnazin on inflammation, ROS/ RNS, and anti-oxidative activity in the murine macrophage RAW264.7 cell model, several key markers, including COX and 5-LO activities, NO • , ONOO-, total reactive species formation, lipid peroxidation, • O 2 levels, and catalase activity were estimated. Results: Results show that rhamnazin was protective against LPS-induced cytotoxicity in macrophage cells. The underlying action of rhamnazin might be through modulation of ROS/RNS and anti-oxidative activity through regulation of total reactive species production, lipid peroxidation, catalase activity, and • O 2 , NO • , and ONOO • levels. In addition, rhamnazin down-regulated the activities of pro-inflammatory COX and 5-LO. Conclusion: The plausible action by which rhamnazin renders its protective effects in macrophage cells is likely due to its capability to regulate LPS-induced inflammation, ROS/ RNS, and anti-oxidative activity.

So Shiho Tang Reduces Inflammation in Lipopolysaccharide-Induced RAW 264.7 Macrophages and Dextran Sodium Sulfate-Induced Colitis Mice

“…LPS, a component of bacterial cell walls, activates the TLR-4 on host cells to initiate oxidative stress and inflammatory responses [51]. Reactive oxygen and nitrogen species contribute to LPS-triggered macrophage activation by regulating nuclear transcription factors, including NRF2 [52]. In this study, LPS treatment increased NO generation and iNOS protein expression, demonstrating that LPS induced oxidative stress and the inflammatory response.…”

Rhamnazin Ameliorates Traumatic Brain Injury in Mice via Reduction in Apoptosis, Oxidative Stress, and Inflammation

“…It leads to the generation of pro-inflammatory cytokines within the brain (TNF-α, IL-1β, and IL-6) and activation of peripheral immune cells [6,7,42]. Encouraged by the previous anti-inflammatory effect of RMZ in acute lung injury [41] and the critical role of inflammation in TBI [43,44], next we thought to examine the effect of RMZ on the serum pro-inflammatory cytokines. It has been found that RMZtreated group showed a significant reduction in the serum level of studied pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 in a dose-dependent manner as compared to the TBI group.…”

Antioxidant Activity and Probiotic Properties of Lactic Acid Bacteria

“…All LAB reduced iNOS/COX-2 gene expression: among them, MG5048 showed the highest inhibitory activity of iNOS/COX-2 (Figure 2). iNOS/COX-2 is expressed in LPS-activated macrophages and is known to be a factor related to NO production [10]. In addition, Choi et al and Wang et al reported that LAB treatment reduced NO production by decreasing the iNOS/COX-2 expression in LPS-activated cells [35,36].…”

“…NO interacts with superoxide anion (•O 2 − ), an anionic radical, to form peroxynitrite (ONOO − ), which is a powerful oxidizing agent and cytotoxic RNS, causing septic shock, brain damage, and local or systemic inflammatory disorders [5][6][7][8]. Additionally, RNS is known to induce iNOS and cyclooxygenase-2 (COX-2) by activating nuclear factor-κB (NF-κB), a pro-inflammatory transcription factor [9,10]. Therefore, it is necessary to maintain homeostasis by regulating oxidative stress through ROS/RNS-related enzymes and transcription factors [2,11].…”