Loganin inhibits the ROS-NLRP3-IL-1β axis by activating the NRF2/HO-1 pathway against osteoarthritis
10.1016/S1875-5364(24)60555-8
- Author:
Miao LI
1
,
2
;
Jiacong XIAO
;
Baihao CHEN
;
Zhaofeng PAN
;
Fanchen WANG
;
Weijian CHEN
;
Qi HE
;
Jianliang LI
;
Shaocong LI
;
Ting WANG
;
Gangyu ZHANG
;
Haibin WANG
;
Jianfa CHEN
Author Information
1. 1st School of Medicine,Guangzhou University of Chinese Medicine,Guangzhou 510405,China
2. The Laboratory of Orthopaedics and Traumatology of Lingnan Medical Research Center,Guangzhou University of Chinese Medicine,Guangzhou 510405,China
- Keywords:
Loganin;
NRF2/HO-1 signaling;
ROS-NLRP3-IL-1β axis;
Osteoarthritis
- From:
Chinese Journal of Natural Medicines (English Ed.)
2024;22(11):977-990
- CountryChina
- Language:Chinese
-
Abstract:
Loganin(LOG),a bioactive compound derived from Cornus officinalis Siebold & Zucc,has been understudied in the context of osteoarthritis(OA)treatment.In this study,we induced an inflammatory response in chondrocytes using lipopolysaccharide(LPS)and subsequently treated these cells with LOG.We employed fluorescence analysis to quantify reactive oxygen species(ROS)levels and measured the expression of NLRP3 and nuclear factor erythropoietin-2-related factor 2(NRF2)using real-time quantitative polymerase chain reaction(qRT-PCR),Western blotting,and immunofluorescence(IF)techniques.Additionally,we developed an OA mouse model by performing medial meniscus destabilization(DMM)surgery and monitored disease progression through micro-com-puted tomography(micro-CT),hematoxylin and eosin(H&E)staining,safranin O and fast green(S&F)staining,and immunohisto-chemical(IHC)analysis.Our results indicate that LOG significantly reduced LPS-induced ROS levels in chondrocytes,inhibited the activation of the NLRP3 inflammasome,and enhanced NRF2/heme oxygenase 1(HO-1)signaling.In vivo,LOG treatment mitigated cartilage degradation and osteophyte formation triggered by DMM surgery,decreased NLRP3 expression,and increased NRF2 expres-sion.These findings suggest that LOG has a protective effect against OA,potentially delaying disease progression by inhibiting the ROS-NLRP3-IL-1β axis and activating the NRF2/HO-1 pathway.
