title: [Protective effect of diosgenin on chondrocytes mediated by JAK2/STAT3 signaling pathway in mice with osteoarthritis].
abstract: Objective:To investigate the effect of diosgenin (Dgn) on chondrocytes and its relation to JAK2/STAT3 signaling pathway in mice with osteoarthritis (OA).Methods:Fifteen male C57BL/6 mice were randomly divided into three groups:control group, OA group and OA+Dgn group. After 4 weeks of treatment, the histopathological changes of cartilage tissue were observed by toluidine blue staining under light microscopy and the ultrastructure of chondrocytes was observed under electron microscopy. The primarily cultured chondrocytes of OA mice were randomly divided into 4 groups:(1) OA group, (2) Dgn group, (3) Dgn+AG490 group, (4) AG490 group. The expression of p-JAK2, p-STAT3, Bax, succinate dehydrogenase (SDH) and cytochrome c oxidase (COX) were detected by Western blotting, and superoxide dismutase (SOD) was detected using colorimetric method.Results:The morphological observation showed that the chondrocytes of OA group presented considerable pathological changes, while the chondrocytes in OA+Dgn group maintained intact membrane. Electron microscopy observation found obvious injury in cartilage tissues of OA group, while that in OA+Dgn group remained smooth. Compared with OA group, the expressions of p-JAK2 and p-STAT3 in chondrocytes of Dgn group were increased (allP<0.05), and the expressions of Bax protein, SDH, COX and SOD were decreased (allP<0.05). While compared with Dgn group, the expressions of p-JAK2, p-STAT3, SDH, COX and SOD in chondrocytes of Dgn+AG490 group were decreased (allP<0.05), and the expression of Bax protein was increased (P<0.05).Conclusion:Diosgenin can inhibit apoptosis and increase mitochondrial oxidative stress capacity of chondrocytes in mice with osteoarthritis, which is closely related to the activation of JAK2/STAT3 signaling pathway.
authors.affiliation: Department of Orthopaedics Center, Lanzhou General Hospital of PLA, Lanzhou 730050, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Gerontology, Xijing Hospital, the Fourth Military Medical University, Xi'an 710032, China.
authors.forename: Xiaole
authors.initials: X
authors.lastname: He
authors.affiliation: Department of Orthopaedics Center, Lanzhou General Hospital of PLA, Lanzhou 730050, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Zhen
authors.affiliation: Department of Orthopaedics Center, Lanzhou General Hospital of PLA, Lanzhou 730050, China.
authors.forename: Shenghu
authors.initials: S
authors.lastname: Zhou
authors.affiliation: Department of Orthopaedics Center, Lanzhou General Hospital of PLA, Lanzhou 730050, China. lixush1968@sina.com.
authors.forename: Xusheng
authors.initials: X
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002356:Cartilage / Q000187:drug effects / Q000473:pathology*; D019902:Chondrocytes / Q000737:chemistry / Q000187:drug effects* / Q000473:pathology; D004144:Diosgenin / Q000494:pharmacology*; D003576:Electron Transport Complex IV / Q000378:metabolism; D053614:Janus Kinase 2 / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000187:drug effects / Q000235:genetics; D010003:Osteoarthritis / Q000235:genetics / Q000503:physiopathology*; D018384:Oxidative Stress / Q000187:drug effects; D050796:STAT3 Transcription Factor / Q000187:drug effects*; D015398:Signal Transduction; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D020032:Tyrphostins / Q000494:pharmacology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D050796:STAT3 Transcription Factor; D020032:Tyrphostins; C095512:alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; D051028:bcl-2-Associated X Protein; D013482:Superoxide Dismutase; D013385:Succinate Dehydrogenase; D003576:Electron Transport Complex IV; D053614:Janus Kinase 2; D004144:Diosgenin