<p>Lentinan Inhibits AGE-Induced Inflammation and the Expression of Matrix-Degrading Enzymes in Human Chondrocytes</p>

Abstract

Background: Chondrocyte-mediated inflammation is an important pathological component of osteoarthritis (OA) development. There are currently no therapies that completely reverse the development of OA. Lentinan, a type of polysaccharide derived from Lentinus edodes, has been demonstrated to possess significant anti-viral, anti-cancer, and anti-inflammatory effects, and has been recently used in the treatment of several inflammatory diseases. However, little research has focused on the pharmacological effect of lentinan in human OA. Materials and Methods: We evaluated the anti-inflammatory and anti-ROS effects of lentinan in SW1353 chondrocytes treated with AGEs using real-time polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), and the nitro oxide-specific stain DAF-FM DA. The regulatory effects of lentinan on NF-κB and MAPK p38 signaling were investigated via promoter assay and Western blot analysis. Results: We found that lentinan inhibits the production of pro-inflammatory cytokines, including IL-1β, TNF-α, IL-8 and the secretion of PGE 2 and NO, by reducing the expression of COX-2 and iNOS in AGE-challenged chondrocytes. Lentinan also reduces AGE-induced increased expression of matrix metalloproteinases-1, −3, and −13 (MMP-1, MMP-3, MMP-13). Furthermore, lentinan has a similar effect on a disintegrin and metalloproteinase with thrombospondin motifs-4 and −5 (ADAMTS-4, ADAMTS-5). Mechanistically, lentinan reduces the activation of NF-κB. Conclusion: Our findings indicate that lentinan shows a protective effect against AGEinduced inflammatory response in chondrocytes. These findings suggest that lentinan is a promising agent for the treatment of OA that could be used as a dietary supplement for patients with OA.

Lentinan alleviates arsenic-induced hepatotoxicity in mice via downregulation of OX40/IL-17A and activation of Nrf2 signaling

“…Interestingly, the intervention with LNT showed an effective antagonism against arsenic-induced the elevations of IL-17A and inflammasomes NLRP3 in mice, indicating the downregulation in IL-17A secreted by Th17 cells, contributing to the amelioration of downstream NF-κB inflammatory signaling in hepatocytes and the attenuation of arsenic-induced hepatotoxicity in mice. Similarly, the previous studies showed that LNT reduces the activation of NF-κB and inhibits the production of pro-inflammatory cytokines IL-1β, TNF-α, IL-8 in chondrocytes [ 26 ], LNT intervention improves hepatic cell morphology by the decreased activity of NF-κB signal in rat’s liver with sepsis [ 27 ].…”

Continuous mild stimulation with advanced glycation end products reduce aggrecan and type II collagen production via the RAGE without inducing cell death in human OUMS-27 chondrosarcoma cells

“…It is reported that 24 or 48 h of 100 µg/mL AGE3 stimulation increases the expression levels of MMP1, MMP3, MMP13, ADAMTS4, and ADAMTS5 up to four-fold(Gao and Zhang 2019; Zhang et al 2020). In our experimental setup, 10 µg/mL AGE3 did not alter protease expression for 1-24 h or for one to eight weeks (Fig.…”

Anti-Inflammatory and Antioxidant Chinese Herbal Medicines: Links between Traditional Characters and the Skin Lipoperoxidation “Western” Model

“…Lentinan (Figure 11), extracted from its fruiting body, has clinically significant anticancer, antibacterial, antiviral, and anticoagulant effects. There is a report on its preventive effects on skin oxidative damage by H 2 O 2 , reduction MDA formation, and increased SOD activity in HaCat cells [115] as well as on the inhibition of the production of proinflammatory cytokines, including IL-1β, TNF-α, IL-8 and the secretion of PGE 2 and NO, by reducing the expression of COX-2 and iNOS in AGE-challenged chondrocytes [116].…”