scholarly journals Sanmiao formula inhibits chondrocyte apoptosis and cartilage matrix degradation in a rat model of osteoarthritis

2014 ◽  
Vol 8 (4) ◽  
pp. 1065-1074 ◽  
Author(s):  
YING XU ◽  
GUO-JING DAI ◽  
QIAN LIU ◽  
ZHEN-LI LIU ◽  
ZHI-QIAN SONG ◽  
...  
Keyword(s):  
Rat Model ◽  
Cartilage Matrix ◽  
Chondrocyte Apoptosis ◽  
Matrix Degradation ◽  
And Cartilage

scholarly journals Acupuncture Delays Cartilage Degeneration through Upregulating SIRT1 Expression in Rats with Osteoarthritis

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Hui Liu ◽  
Tingting Zhang ◽  
Min Liu ◽  
Chunhong Wang ◽  
Jinfeng Yan
Keyword(s):  
Cartilage Degeneration ◽  
Cartilage Matrix ◽  
Enzyme Linked Immunosorbent Assay ◽  
Matrix Degradation ◽  
Matrix Synthesis ◽  
Sirt1 Expression ◽  
Tnf Α ◽  
Related Proteins ◽  
And Cartilage

Silent mating type information regulation 2 homolog 1 (SIRT1) has been reported to inhibit osteoarthritic gene expression in chondrocytes. Here, efforts in this study were made to unveil the specific role of SIRT1 in the therapy of acupuncture on cartilage degeneration in osteoarthritis (OA). Specifically, OA was established by the anterior cruciate ligament transection method in the right knee joint of rats, subsequent to which acupuncture was performed on two acupoints. Injection with shSIRT1 sequence–inserted lentiviruses was conducted to investigate the role of SIRT1 in acupuncture-mediated OA. Morphological changes and cell apoptosis in rat OA cartilages were examined by safranin-O staining and terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assay, respectively. The serum levels of tumor necrosis factor (TNF)-α and interleukin (IL)-2 in OA rats were assessed by enzyme-linked immunosorbent assay (ELISA). The expressions of SIRT1, cartilage matrix degradation-related proteins (matrix metalloproteinase (MMP)-9 and ADAMTS5), NF-κB signaling-related markers (p-p65/p65 and p-IκBα/IκBα), and cartilage matrix synthesis-related proteins (collagen II and aggrecan) in the OA cartilage were analyzed by western blot. As a result, acupuncture counteracted OA-associated upregulation of TNF-α, IL-2, cartilage matrix degradation-related proteins, and NF-κB signaling-related markers, morphological damage, apoptosis, SIRT1 downregulation, and loss of cartilage matrix synthesis-related proteins in rat articular cartilages. SIRT1 silencing reversed acupuncture-induced counteractive effects on the aforementioned OA-associated phenomena (except apoptosis, the experiment regarding which under SIRT1 silencing was not performed). Collectively, acupuncture inhibited chondrocyte apoptosis, inflammation, NF-κB signaling activation, and cartilage matrix degradation by upregulating SIRT1 expression to delay OA-associated cartilage degeneration.

miR-211 Reduces the Degradation of Articular Cartilage Matrix by Targeting Matrix Metalloproteninase 9

2019 ◽  
Vol 9 (9) ◽  
pp. 1292-1297
Author(s):  
Yumei Tian ◽  
Jian Wang
Keyword(s):  
Cartilage Damage ◽  
Cartilage Matrix ◽  
Cartilage Tissue ◽  
Control Group ◽  
Matrix Degradation ◽  
Mankin Score ◽  
Joint Cavity ◽  
Mmp9 Expression ◽  
Col2a1 Expression ◽  
And Cartilage

Matrix metalloproteninase 9 (MMP9) promotes osteoarthritis (OA) cartilage matrix degradation. Abnormal miR-211 expression is associated with OA. Bioinformatics analysis showed a targeted relationship between miR-211 and MMP9 mRNA 3′-UTR. Our study intends to evaluate miR-211’s role in the destruction of chondrocyte matrix in OA model rats. The OA model rats were divided into OA group, OA group+agomir-NC group, OA group+agomir-211 group, followed by analysis of the arthritis Mankin score, Hyp and IL-1β content by ELISA, MMP-9 and COL2A1 expression by western blot and miR-211 level by qRT-PCR. The cartilage tissues were divided into control group, IL-1β+ agomir-NC group, IL-1β+ agomir-211 group, and the expression of MMP-9 and COL2A1 in chondrocytes were detected. Compared with Sham group, IL-1β and Hyp levels in the joint cavity fluid of the OA group were significantly increased and miR-211 expression was significantly decreased with increased MMP9 expression and decreased COL2A1 expression. Injection of agomir-211 into the joint cavity of OA rats significantly reduced MMP9 expression in cartilage tissue, decreased Hyp content in the joint cavity fluid, increased COL2A1 expression, and decreased Mankin score and cartilage damage. IL-1β treatment significantly up-regulated MMP9 expression and decreased COL2A1 expression; miR-211 overexpression attenuated IL-1β-induced cartilage matrix degradation and cartilage destruction. miR-211 plays a role in regulating MMP9 expression and promoting OA. miR-211 overexpression inhibits MMP9 expression, reduces the degradation of cartilage matrix and increases collagen synthesis, thus ameliorating OA development.

miR-211-5p contributes to chondrocyte differentiation by suppressing Fibulin-4 expression to play a role in osteoarthritis

2019 ◽  
Vol 166 (6) ◽  
pp. 495-502 ◽  
Author(s):  
Hao Liu ◽  
Jun Luo
Keyword(s):  
Inflammatory Cytokines ◽  
Rat Model ◽  
Cartilage Matrix ◽  
Chondrocyte Differentiation ◽  
Matrix Degradation ◽  
Downstream Target ◽  
Promising Target ◽  
Human Disorders ◽  
Pro Inflammatory Cytokines

Abstract MicroRNAs (miRNAs) serve as key regulators in human disorders. Previous research reported that miR-211-5p is down-regulated in osteoarthritis (OA) and that Fibulin-4 inhibits chondrocyte differentiation. However, the role of miR-211-5p in the development of OA has not been clarified, and its downstream target has not been studied. This study aimed to explore the effect of miR-211-5p on chondrocyte differentiation and its influence on OA pathogenesis, as well as the interaction between miR-211-5p and Fibulin-4. In this study, we found that miR-211-5p is significantly down-regulated in articular cartilage tissues in an OA rat model, whereas it is clearly up-regulated during chondrocyte differentiation of ATDC5 cells. Silencing miR-211-5p in ATDC5 cells had an adverse effect on chondrocyte differentiation. Fibulin-4 was identified as a target of miR-211-5p, and miR-211-5p participated in chondrocyte differentiation by negatively regulating Fibulin-4 expression. In the OA rat model, miR-211-5p overexpression facilitated chondrocyte differentiation, along with the reduced pro-inflammatory cytokines level and the level of proteinases responsible for cartilage matrix degradation. In summary, miR-211-5p promotes chondrocyte differentiation by negatively regulating Fibulin-4 expression, and represses the expression of pro-inflammatory cytokines and proteinases responsible for cartilage matrix degradation in OA. miR-211-5p may serve as a promising target for OA treatment.

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