Avdekking av effektene av ginsenosid Rg3-behandling på IL-1β-indusert skade hos NPC-er
Introduksjon
Intervertebral disc degeneration (IDD) is a frequently seen orthopedic disease, which is accompanied with excessive apoptosis of nucleus pulposus cells (NPCs) and degeneration of extracellular matrix (ECM), with main symptoms of pain and numbness in the waist, legs and feet, as well as inflammation on and around the surface of bone tissues. Strikingly, ginsenoside Rg3, the main active ingredient of ginseng, has been attested to exhibit anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs and IDD rats by inactivating the p38 MAPK pathway.The risk factors for IDD
IDD is generally associated with risk factors such as aging, excessive exercise, working environment, and genetics. As one ages, the amount of water in the body and in the intervertebral discs will be reduced accordingly. Intervertebral discs that lack moisture will lose their elastic function and become hard. Once there is any stimulation or pressure, the intervertebral disc may crack, leading to intervertebral disc injury. For instance, the mechanical trauma caused by excessive exercise and work may accelerate the fragility of disc and exacerbate IDD.Anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β-treated human NPCs and IDD rats
Ginsenosid Rg3 plays an anti-apoptotic role in IL-1β-treated human NPCs and IDD rats, as evidenced by the down-regulation of pro-apoptosis protein Bax and up-regulation of anti-apoptosis protein Bcl-2 in IL-1β-stimulated NPCs and IDD model rats. Besides, ginsenoside Rg3 represses ECM degradation in IL-1β-stimulated NPCs and intervertebral disc tissues of IDD rats, as attested by the decreased expression of ECM degradation-related factors MMPs (MMP2 and MMP3) and ADAMTSs (Adamts4, and Adamts5).
Ginsenosid Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs.
Ginsenosid Rg3 reduces apoptosis and catabolism in IDD rats.
Alleviation of ginsenoside Rg3 in IDD via p38 MAPK pathway
Ginsenosid Rg3 can alleviate NPC degeneration, recover the arrangement of annulus fibrous, and preserve more proteoglycan matrix via inactivating p38 MAPK pathway. In vitro, the fluorescence intensity of p38 is enhanced in IL-1β-stimulated NPCs, yet ginsenoside Rg3 offsets this promoting effect. In vivo, det fosforylerte p38-nivået er forhøyet hos NPC-er og mellomvirvelskivevevet hos IDD-rotter, mens ginsenosid Rg3 virker omvendt.
Ginsenosid Rg3 suppresses the IL-1β-stimulated p38 MAPK pathway in human NPCs
Ginsenosid Rg3 inactivates the p38 MAPK pathway in IDD rats.
Konklusjon
The anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration are accomplished by inactivating the MAPK pathway, providing new clues on the treatment of IDD.Referanse
Chen J, Zhang B, Wu L, et al. Ginsenosid Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration by inactivating the MAPK pathway. Cell Mol Biol. 2024;70(1):233-238. doi:10.14715/cmb/2024.70.1.32BONTAC Ginsenosidr
BONTAC har siden 2012 vært dedikert til forskning og utvikling, produksjon og salg av råvarer for koenzymer og naturlige produkter, med egeneide fabrikker, over 170 globale patenter samt et sterkt FoU-team. BONTAC har rik erfaring innen forskning og utvikling og avansert teknologi innen biosyntese av sjeldne ginsenosider Rh2/Rg3, med rene råvarer, høyere konverteringsrate og høyere innhold (opptil 99 %). En alt-i-ett-tjeneste for skreddersydde produktløsninger er tilgjengelig i BONTAC. Med unik Bonzyme enzymatisk synteseteknologi kan både S-type og R-type isomerer syntetiseres nøyaktig her, med sterkere aktivitet og presis målretting. Våre produkter er underlagt streng tredjeparts selvinspeksjon, som er pålitelige.
