Abstract
Natural plant extracts and compounds (NPECs), which originate from herbs or plants, have been used in the clinical treatment of rheumatoid arthritis (RA) for many years. Over the years, many scientists have carried out a series of studies on the treatment of RA by NPEC. They found a high quantity of active NPECs with broad application prospects. In view of various complex functions of these NPECs, exploring their potential as medicines for RA treatment will be beneficial for RA patients. Thus, to help advance the development of high-quality NPECs for RA, we herein aimed to review the research progress of NPECs in the treatment of RA in recent years. Our findings showed that, from the pharmacological perspective, natural plant extracts or mixed herbal compounds effectively regulate the immune system to alleviate RA by inhibiting pro-inflammatory cytokines. Further, individualized medication can be applied according to each patient’s physical condition. However, the pathogenesis of RA and its immune mechanism has not been fully understood and requires further studies.
Highlights
Rheumatoid arthritis (RA) is a chronic systemic inflammatory autoimmune disease of the joint [1]
Recent studies have shown that antigen-activated CD4+ T cells, monocytes, macroph2aogf 1e1s, and synovial fibroblasts can produce many inflammatory factors, including TNF-α, IL-1, and IL-6, leading to the secretion of metalloproteinases by chondrocytes, fibroblasts, and aonsdteIoLc-l6a,sltesa[d4i]n. gSutobstheqeusecnrtelyti,otnheofemroestiaolnloopfrbootenienaasneds cbayrctihlaognedcroacuysteesst,hfiebgrorbadlausatsl,daensdtrousc-tetioocnlaasntsd[4fu].nScutibosneaqluleonsstlyo,ftthheeejrooisnitosn[7o]f. bone and cartilage causes the gradual destruction and fuRnActpioantiaelnlotsssaroef trheqeujoirinedtst[o7]c.hange their lifestyle [8]
The results showed that Total flavonoids of astragalus (TFA) significantly decreased TNF-α, IL-1β, IL-6, iNOS, and COX-2 mRNA levels and increased IL-10 mRNA levels in LPS-stimulated RAW 264.7 cells in a dose-dependent manner [81]
Summary
Rheumatoid arthritis (RA) is a chronic systemic inflammatory autoimmune disease of the joint [1]. TNF-α is a pro-inflammatory factor that causes the activation and aggregation of the cell inflammasome. This induces the release of other inflammatory mediators and aggravates the inflammatory response [4]. Recent studies have shown that antigen-activated CD4+ T cells, monocytes, macrophages, and synovial fibroblasts can produce many inflammatory factors, including TNF-α, IL-1, Medicina 2021, 57, 266 response [5]. Recent studies have shown that antigen-activated CD4+ T cells, monocytes, macroph2aogf 1e1s, and synovial fibroblasts can produce many inflammatory factors, including TNF-α, IL-1, and IL-6, leading to the secretion of metalloproteinases by chondrocytes, fibroblasts, and aonsdteIoLc-l6a,sltesa[d4i]n. IninflfalammmmaattoorryyeefffeeccttssaaggaaiinnssttRRAA..TThheetthheerraappeeuuttiicceefffeeccttssooffCCAAwweerreerreevveeaaleleddininininvvitirtoro eexxppeerrimimeenntstsuussininggaacctitvivaateteddmmaaccroropphhaaggeess(R(Raaww224466.7.7cecelllsl)s)aannddininaararattmmooddeel looffaaddjujuvvaanntt aarrtthhrrititisis((AAAA))ininvvivivoo[1[144].].CCAAisisaannαα,β,β-u-unnssaatuturraatteeddaarroommaatitcicaaldldeehhyyddeeththaattccaannbbeeuusseedd aassaaflfalavvoorrininggaaggeenntt(F(Figiguurree11).).ItItisisththeepprirninccipipaal lflfalavvoorrcocommppoonneennttoof fcicninnnaammoonnooili.l.TThhee rreesseeaarrcchheerrssccoonncclluuddeeddtthhaattCCAAisisaappootetenntitaial lththeerraappeeuutitcicccoommppoouunnddththaattccaannininhhibibititRRAA pprrooggreresssisoionnbbyysusupppprersessisninggILIL-1-β1βbbyymmoodduulaltaitninggththe esusucccicninataet/eH/HIFIF-1-1ααaaxxisisaannddininhhibibitiitningg NNLLRRPP33[[1144]]..MMoorreeoovveerr,,CCAAssigignnifiifcicaanntltylyrreedduucceeddssyynnoovviaiallininflfalammmmaattioionnininAAAAraratstsaanndd ininththeeppeerripiphheerraallbbloloooddmmoonnoonnuuccleleaarrcceelllslsooffRRAAppaatiteienntstsbbyyininhhibibitiitninggththeeeexxppreressssioionnooff pprroo-i-ninflfalammmmaattoorryyccyyttookkiinneess((IILL--11ββ,, TTNNFF--αα,, aanndd IILL--66))[[1155,1,166]]. CA inhibited the expression of the succinate receptor GPR91, thereby inhibiting the activation of HIF-1α [14,15]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
