Gouty arthritis is a familiar type of inflammatory arthritis caused due to deposition of monosodium urate crystal (MSU) within and around the joints. It is characterized by an acutely red swollen joint with unbearable pain1. Many investigations had confirmed that inflammatory response to MSU is principally mediated by macrophages.
Various inflammatory mediators (TNF-α, IL-1β and IL-6) are released by activated macrophages and inflammatory micro-environment can employ more inflammatory cells to aggravate the edema and joint injury. IL-1β is a critical inflammatory factor in gouty arthritis. Inflammatory responses are alleviated in MSU-induced mice deficient in IL-1β or the IL-1 receptor2.
Monosodium urate crystal (MSU)-induced IL-1β release is mediated by NOD (nucleotide-binding oligomerization domain)-like receptors containing a PYD 3 (NLRP3) inflammasomes3. Inflammation and pain responses are significantly reduced in MSU-treated NLRP3-deficient mice5. Thus, NLRP3 inflamma-some is a potential therapeutic target in MSU-induced arthritis.
Osthole is a natural compound which is an active constituent derived from Cnidium monnieri plant. It exhibits broad pharmacological effects including; anti-oxidative, anti-inflammatory, anti-cancer, vascular protection and immune-modulatory properties. It also inhibits the inflammatory mediators to protect kidney failure and carotid artery injury4-6.
Apart from all these studies the effect of osthole on monosodium urate crystal (MSU) induced arthritis hasn’t been reported yet. So the researchers conducted a new study in which they studied the anti-inflammatory effect of osthole in arthritis on NLRP3 inflammasome in MSU-induced acute gouty arthritis and the possible mechanisms involved7.
It was revealed that Osthole could alleviate MSU-induced arthritis through inhibiting the generation of inflammatory factors and NLRP3 inflammasome activation in vivo. Pre-treatment with osthole significantly suppressed MSU or LPS induced NF-κB signal along with the transcription of inflammatory factors.
In addition, osthole decreased MSU induced oxidative stress and lysosomal damage. Current findings illustrated that osthole significantly suppressed NLRP3 inflammasome in synovial tissue and macrophage cells. The potential mechanism may be based on the attenuation of NF-κB mediated first signal and oxidative stress and lysosome mediated second signal in NLRP3 inflammasome activation.
So it was established that Osthole might be a promising therapeutic agent for alleviating gouty arthritis through inhibiting NLRP3 inflammasome.
Written by: Rabeeia
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25 August, 2019