5W, 9W in each group in a random sample of3, application of chloral hydrate intraperitoneal injection anesthesia death, cardiac lavage after removing the damaged spinal cord tissue, immunohistochemical determination of GAP-43. Results: The first, to model after 1D,1W,2W,3W,5W,9W. BBB score, molding 1D after each score is 0points,1W groups of rat hindlimb has recovered, but the score is low, the group had no difference (P>0.05);2W B group, C group, D group was higher than that of A group were significantly different (P<0.05);3W,5W,9W score in group D was higher than that in group B, group C had significant difference (P<0.05). The second ,in the 1W,2W,3W,5W growth to protein GAP-43 immunohistochemical assay,1W group content were increased but no significant difference;2W,3W,5W B group, C group, D group was higher than that of A group were significantly different (P < 0.05), D group higher than that of B group, C group had significant difference (P < 0.01).The third in B group, C group, D group than in A group light complications. Conclusions: The BBB scoreandGAP-43detection, inference of electroacupuncture combined with OECs transplantation in treatment of spinal cord injury in rats at the axon growth there is a synergy, spinal nerve function is greatly improved.
released in the culture supernatant, caspase 3/7-luciferase reporter assay and TUNEL staining. The level of IL-1b and IL-6 was determined by TaqMan assays. The level of reactive oxygen species (ROS) was determined by DHR123 staining followed by flow cytometry and MitoSOX Red staining followed by confocal microscopy. The loss of mitochondrial membrane potential was determined by JC-1 dye staining and ATP levels were determined using a kit. The accumulation of dysfunctional mitochondria was determined by staining with MitoTracker Deep Red followed by flow cytometry. The signaling pathway activation was investigated by immunoblot analysis of NFkB and MAPK pathways and its involvement was confirmed by using small molecule inhibitors of the induced pathway. The role of ROS in CQ and Baf induced expression of IL-1b and IL-6 was determined by using anti-oxidants, MitoTempo and Trolox. Results: The expression of LAMP1 was highly downregulated in OA cartilage compared to normal cartilage. CQ and Baf significantly induced apoptosis of primary human OA chondrocytes as determined by LDH activity assay, caspase3/7 luciferase reporter assay and TUNEL staining. Similar results were obtained with mouse chondrocytes. Human OA cartilage explants as well as mouse femoral head cartilage explant culture treated with CQ or Baf showed significant increase in LDH release and TUNEL staining. The CQ and Baf induced inhibition of lysosomal function resulted in the loss of mitochondrial membrane potential, excessive levels of ROS, lower levels of ATP and the accumulation of dysfunctional mitochondria in the treated chondrocytes. Treatment of primary human OA chondrocytes with CQ or Baf significantly increased the gene and protein expression of IL-1b and IL-6. Investigation of the signaling pathways showed no role of NFkB signaling in the CQ and Baf induced upregulation of IL-1b and IL-6 expression. However, the JNK-MAPK, but not ERK-or p38-MAPK pathway, was activated in response to Baf treatment. Inhibition of JNK activation by using a specific inhibitor abrogated the upregulation of IL-1b and IL-6 expression in Baf treated human chondrocytes. The use of anti-oxidants, MitoTempo and Trolox also suppressed the CQ and Baf induced expression of IL-1b and IL-6. JNK inhibition and treatment with MitoTempo or Trolox failed to suppress apoptosis suggesting that this was independent of ROS levels and JNK pathway in chondrocytes with inhibited lysosomal function. Conclusions:We demonstrate here that inhibition of lysosomal function promotes inflammation, oxidative stress and chondrocyte apoptosis through JNK activation. Our data suggest that protecting lysosomal function may be a therapeutic target for OA management.Purpose: Osteoarthritis (OA) is a chronic disease characterized by an irreversible loss of articular cartilage. Articular chondrocytes in OA undergo phenotypic and gene expression changes that recapitulate the terminal differentiation in the growth plate during endochondral ossification. Signal transducers and activators of transcription...
Sost mRNA suggesting that Sclerostin might be regulated by Wnt. We further observed an enhanced expression of Sclerostin in osteoarthritic cartilage compared to cartilage of control mice. Conclusions: We here show that Wnt3a increases the catabolic activity and inhibits the anabolic activity in murine chondrocytes. Sclerostin alleviates the expression of catabolic genes induced by Wnt and rescued proteoglycan production. Moreover, Sclerostin promotes the cartilage maintenance through the inhibition of chondrocyte hypertrophy. Finally, the expression of Sclerostin expression in osteoarthritic mice suggests that Sclerostin might be involved in the pathophysiology in cartilage damage and might constitute a target for the prevention of osteoarthritis.
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