The articular cartilage preservative effects of genistein in an experimental model of knees osteoarthritis

Author(s):  
Xiangjun Cheng ◽  
Peilian Xu

The study aimed to investigate the preservative effects of genistein on articular cartilage in an experimental model of knee osteoarthritis in rats. Thirty male Wistar rats were assigned to three equal groups: the sham group (SG), osteoarthritis control group (OAG), and genistein-treated osteoarthritis group (GTG). Intra-articular injections of monosodium iodoacetate were used for osteoarthritis induction. After two weeks of rest for the induction of the inflammatory process, genistein (30 mg/kg/day) vs. saline gavage was administered for eight weeks. The expression of matrix metalloproteinase (MMP) 8 and 13, Sox5/Sox6, Indian hedgehog (IHH), and Col2 were evaluated in medial femoral condyle sections by immunohistochemical staining. The number of chondrocytes and cartilage thicknesses were also measured and compared among the groups. No significant change in cartilage thickness was observed in GTG compared with OAG (p=0.188). Chondrocyte count was significantly higher in the articular cartilage of GTG compared with OAG (p=0.006). Induction of OA significantly increased the expression of MMP-8, MMP-13, and IHH, but decreased Col2, Sox5, and Sox6 expression (p<0.001); these were partially prevented in the GTG. Our findings support the effectiveness of genistein treatment in the prevention of articular cartilage damage in the experimental model of knee osteoarthritis. The proposed mechanism of action is through the suppression of the MMP, IHH, Col2 pathways, besides the induction of Sox5 and Sox6 expression. Novelty: -Genistein prevent articular cartilage damage in the experimental model of knee osteoarthritis. -The osteoprotective effect is trough modulation of expression of MMP, Sox, IHH, and Col2 proteins.

2017 ◽  
Vol 62 (3) ◽  
pp. 167 ◽  
Author(s):  
H A Amaratunga ◽  
S B Adikari ◽  
T L Dassanayake ◽  
J Gamage ◽  
H J Suraweera

2021 ◽  
Vol 62 (5) ◽  
Author(s):  
Nguyen Thi Thuy Linh

Objectives: Describing the characteristics of ultrasound and magnetic resonance imaging of knee joints in patients with primary knee osteoarthritis.Subjects and methods: Prospective, descriptive, cross-sectional study on patients diagnosed with primary knee osteoarthritis who were examined as an outpatient or inpatient at 108 Military CentralHospital.Results: Ultrasound features: 100% articular cartilage damage, 87.8% bone spurs, 73.0% effusion, 9.3% popliteal cocoon, 3.4% synovial thickening. Degree of cartilage damage according toSaarakkala: grade 1: 2.1%, grade 2A: 63.7%, grade 2B: 29.1%, grade 3: 5.1%. Magnetic resonance characteristics: 100% articular cartilage damage, 96.3% bone spurs, 90.6% effusion, 84.1% bonemarrow edema, 69.2% bone cocoon, 61.7% meniscus tear, popliteal cocoon 11.3%. osteoarthritis lesions were more common in the medial femoral and tibial joints than in the lateral tibial and patellar joints.Conclusion: Cartilage damage, bone spurs, and effusion were common lessions on ultrasound and magnetic resonance imaging on patients with knee osteoarthritis.


2021 ◽  
Vol 23 (3) ◽  
pp. 239-244
Author(s):  
Maciej Materkowski

Osteoarthritis led to the articular cartilage damage and cause different kind of problems – from social to biological. The analysis of existing research unfortunately subjected questioned the reliability of spontaneous regeneration of damaged cartilage, which makes it necessary to focus on the possibilities of protection of the tissue from further its degradation. Treatment of osteoarthritis require to use many drugs, which would lead to slowdown the this process. The aim of below publication is to analyse the practical, clinical biological possibilities of articular cartilage protection with a usage of SYSADOA – (symptomatic slow acting drugs of OA). Osteoarthritis is most frequent disease of the joints and prescription of the SYSADOA should be main principle of that treatment.


2017 ◽  
Vol 45 (3) ◽  
pp. 203-223 ◽  
Author(s):  
Weilong J. Shi ◽  
Fotios P. Tjoumakaris ◽  
Mayan Lendner ◽  
Kevin B. Freedman

2021 ◽  
Vol 72 (2) ◽  
pp. 11-18
Author(s):  
Nina Gatarić ◽  
Ana Ilić ◽  
Dušan Todorović ◽  
Slavica Mutavdžin ◽  
Jovana Jakovljević-Uzelac ◽  
...  

Introduction: Isoprenaline or isoproterenol (1-(3,4-dihydroxyphenyl)-2-isopropylaminoethanolhydrochloride; ISO), a synthetic b-adrenergic agonist, can be used to establish myocardial ischemia, cardiotoxicity, necrosis and/or an experimental model of infarction in rats. Aim: Determination of the dynamics of myocardial injury biomarkers production of aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK), and high-sensitive troponin T (hsTnT), with changes on electrocardiogram (ECG) parameters during the subcutaneous aplication of ISO in male Wistar rats. Material and methods: All animals (n = 23) were divided into two groups: control group (n = 11) treated with a saline solution, during two consecutive days (0,2 ml/kg b.m. daily, sc); and the ISO group (n = 12) treated with isoprenaline, during two consecutive days (85 mg/kg b.m. daily, sc). Blood was drawn from the rat tail vein in both groups, in order to determine serum activity levels of myocardial injury biomarkers, and an ECG (n = 6) was registered prior to the application, as well as 48h following the first dose of of saline solution or isoprenaline. Results: In comparison to the control group, in which no significant enzyme activities elevation (p > 0.05) nor ECG changes were registered, ISO group presented a significant rise of two clinically significant biomarkers of acute myocardial injury/myocardial infarction (AMI), CK (p = 0.05) and hsTnT (p < 0.01), as well as an ST segment elevation, with a patognomonic ECG change. Conclusion: Obtained results support previous studies, proving that isoprenaline represents an adequate experimental model for myocardial injury/AMI induction, and a "golden standard" for evaluating potential cardioprotective effects of pharmacological and non-pharmacological therapeutic modalities, with the ultimate goal of lowering the degree of lesions and improving post-infarction myocardium function.


2020 ◽  
Author(s):  
Tristan Maerz ◽  
Michael D. Newton ◽  
Mackenzie Fleischer ◽  
Samantha E. Hartner ◽  
Karissa Gawronski ◽  
...  

ABSTRACTObjectiveAssess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR).MethodsTwelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo μCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and articular cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections.ResultsACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (∼15-20%), and a ∼32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, cartilage thickness, and cartilage surface deviation.ConclusionACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate articular cartilage damage at 14 days post-injury.


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