scholarly journals Herbal Composition LI73014F2 Alleviates Articular Cartilage Damage and Inflammatory Response in Monosodium Iodoacetate-Induced Osteoarthritis in Rats

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5467
Author(s):  
Hae Lim Kim ◽  
Hae Jin Lee ◽  
Dong-Ryung Lee ◽  
Bong-Keun Choi ◽  
Seung Hwan Yang
Keyword(s):  
Articular Cartilage ◽  
Synovial Fluid ◽  
Inflammatory Mediators ◽  
Curcuma Longa ◽  
Weight Bearing ◽  
Cartilage Damage ◽  
Terminalia Chebula ◽  
Boswellia Serrata ◽  
Monosodium Iodoacetate ◽  
And Cartilage

The aim of this study was to determine the anti-osteoarthritic effects of LI73014F2, which consists of Terminalia chebula fruit, Curcuma longa rhizome, and Boswellia serrata gum resin in a 2:1:2 ratio, in the monosodium iodoacetate (MIA)-induced osteoarthritis (OA) rat model. LI73014F2 was orally administered once per day for three weeks. Weight-bearing distribution and arthritis index (AI) were measured once per week to confirm the OA symptoms. Synovial membrane, proteoglycan layer, and cartilage damage were investigated by histological examination, while synovial fluid interleukin-1β level was analyzed using a commercial kit. Levels of pro-inflammatory mediators/cytokines and matrix metalloproteinases (MMPs) in the cartilage tissues were investigated to confirm the anti-osteoarthritic effects of LI73014F2. LI73014F2 significantly inhibited the MIA-induced increase in OA symptoms, synovial fluid cytokine, cartilage damage, and expression levels of pro-inflammatory mediators/cytokines and MMPs in the articular cartilage. These results suggest that LI73014F2 exerts anti-osteoarthritic effects by regulating inflammatory cytokines and MMPs in MIA-induced OA rats.

scholarly journals CTRP9 protects against MIA-induced inflammation and knee cartilage damage by deactivating the MAPK/NF-κB pathway in rats with osteoarthritis

2020 ◽  
Vol 15 (1) ◽  
pp. 971-980
Author(s):  
Shicheng Zheng ◽  
Jing Ren ◽  
Sihai Gong ◽  
Feng Qiao ◽  
Jinlong He
Keyword(s):  
Synovial Fluid ◽  
Nuclear Factor Kappa B ◽  
Cartilage Damage ◽  
Cartilage Tissue ◽  
Enzyme Linked Immunosorbent Assay ◽  
Nuclear Factor ◽  
Knee Cartilage ◽  
Monosodium Iodoacetate ◽  
Dose Dependent ◽  
Different Doses

AbstractC1q/TNF-related protein 9 (CTRP9), the closest paralog of adiponectin, has been reported to protect against inflammation-related diseases. However, its role in regulating osteoarthritis (OA) has not been fully elucidated. First, a rat model of OA was generated. Furthermore, rats with OA were injected with different doses of recombinant CTRP9 protein (rCTRP9), and the knee cartilage damage was evaluated. Finally, the phosphorylation of p38 and the secretion of matrix metalloproteinases (MMPs) were detected by Western blotting and enzyme-linked immunosorbent assay. Results revealed that CTRP9 was highly expressed in adipose tissue, followed by skeletal muscle and cartilage tissue, and less expressed in liver, kidney and lung. Moreover, the expression of CTRP9 significantly decreased in the monosodium iodoacetate (MIA) group in the knee cartilage and knee synovial fluid, and the contents of interleukin-1β (IL-1β) and IL-6 significantly increased in knee synovial fluid. In addition, rCTRP9 alleviated MIA-induced inflammation, oxidative stress and knee cartilage damage in a dose-dependent way. In addition, rCTRP9 could attenuate the expression of p38MAPK and p-p38 and suppress the expression of nuclear factor-kappa B (NF-κB), p65 and MMPs. Collectively, the results of the present study suggested that CTRP9 alleviates the inflammation of MIA-induced OA through deactivating p38MAPK and NF-κB signaling pathways in rats.

scholarly journals The Effect of a Lower Body Positive Pressure Supported Treadmill Exercise Regime on Systemic Biomarkers of Inflammation and Cartilage Degradation in Individuals with Knee Osteoarthritis: A Pilot Study

2021 ◽  
Vol 9 (3) ◽  
pp. 18
Author(s):  
Stephen Cornish ◽  
Jason Peeler
Keyword(s):  
Articular Cartilage ◽  
Knee Pain ◽  
Weight Bearing ◽  
Cartilage Degradation ◽  
Treadmill Walking ◽  
Positive Pressure ◽  
Control Group ◽  
Knee Oa ◽  
And Cartilage

Background: Knee osteoarthritis (OA) has been linked to a chronic low-grade inflammatory response and altered metabolic activity of articular cartilage. Objective: The purpose of this investigation was to evaluate the effectiveness of a 12-week (3 times/week) lower body positive pressure (LBPP) treadmill walking regime on knee pain and systemic biomarkers of inflammation and cartilage degradation. Methods: Sixteen overweight (BMI > 25 kg/m2) knee OA patients were randomized to a LBPP treadmill walking exercise group (N = 7) or non-exercise control group (N = 9). Baseline and 12-week follow-up assessments evaluated the following dependent variables: acute knee pain during full weight bearing treadmill walking; inflammatory biomarkers (C-reactive protein, interleukin-1β, interleukin-6, s100A8/A9, and tumor necrosis factor-α), and catabolic metabolism of articular cartilage (sCOMP). Results: Knee pain at baseline and follow-up remained unchanged for the non-exercise control group (P > 0.05). However, knee pain for the LBPP exercise group was significantly decreased at follow-up (P ≤ 0.05). No differences in the biomarkers of inflammation and cartilage degradation were observed for between and within group comparisons (all P > 0.05). Conclusions: Data suggested that the LBPP supported walking regime could be effectively used to promote regular weight bearing exercise without exacerbation of knee joint pain and did not increase levels of systemic inflammation or catabolic activity of articular cartilage in overweight knee OA patients. This pilot investigation offers important insight regarding the potential role that the LBPP technology could play in facilitating investigations examining the disease modifying effect of exercise on knee OA pathogenesis.

scholarly journals Effect of Moxibustion on the Intestinal Flora of Rats with Knee Osteoarthritis Induced by Monosodium Iodoacetate

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Yu Chen ◽  
Jiuheng Lv ◽  
Yejuan Jia ◽  
Ruiqing Wang ◽  
Zidi Zhang ◽  
...  
Keyword(s):  
Treatment Group ◽  
Knee Osteoarthritis ◽  
High Throughput Sequencing ◽  
Cartilage Damage ◽  
Intestinal Flora ◽  
Inflammatory Factors ◽  
Knee Cartilage ◽  
Model Group ◽  
Monosodium Iodoacetate ◽  
And Cartilage

In this study, a knee osteoarthritis (KOA) rat model induced by monosodium iodoacetate (MIA) was used to study the effect of moxibustion on improving knee cartilage damage and its effect on the intestinal flora. The experimental rats were divided into the normal group (N), model group (M), moxibustion treatment group (MS), and diclofenac sodium treatment group (DS). After 4 weeks, cartilage pathological damage in the knee joint was evaluated using hematoxylin-eosin and safranin O-fast green staining analysis. ELISAs and Western blots were used to detect the expression levels of IL-1β and TNF-α in the serum and cartilage, respectively. The total DNA of the fecal samples was extracted and subjected to high-throughput sequencing of the V3-V4 region of the 16S rRNA gene to analyze the changes in the intestinal flora. In the model group, the cartilage was obviously damaged, the expression levels of IL-1β and TNF-α in the serum and cartilage were increased, and the abundance and diversity of the intestinal flora were decreased. Moxibustion treatment significantly improved the cartilage damage and reduced the concentration of inflammatory factors in the serum and cartilage. The high-throughput sequencing results showed that compared to the model group, the moxibustion treatment regulated some specific species in the intestinal microorganisms rather than the α diversity. In conclusion, our findings suggest that moxibustion treatment may work through two aspects in rats. On one hand, it directly acts on knee cartilage to promote repair, and on the other hand, it regulates the composition of the intestinal flora and reduces the production of inflammatory factors.

scholarly journals Andrographis paniculata Extract Relieves Pain and Inflammation in Monosodium Iodoacetate-Induced Osteoarthritis and Acetic Acid-Induced Writhing in Animal Models

Processes ◽  
2020 ◽  
Vol 8 (7) ◽  
pp. 873
Author(s):  
Donghun Lee ◽  
Chae Yun Baek ◽  
Ji Hong Hwang ◽  
Mi-Yeon Kim
Keyword(s):  
Acetic Acid ◽  
Weight Bearing ◽  
Cartilage Damage ◽  
Degenerative Joint Disease ◽  
Andrographis Paniculata ◽  
Joint Disease ◽  
Tnf Α ◽  
Monosodium Iodoacetate ◽  
History Of

Osteoarthritis (OA), being the most prominent degenerative joint disease is affecting millions of elderly people worldwide. Although Andrographis paniculata is an ethnic medicine with a long history of being used as analgesic agent, no study using a monosodium iodoacetate (MIA) model has investigated its potential activities against OA. In this study, experimental OA was induced in rats with a knee injection of MIA, which represents the pathological characteristics of OA in humans. A. paniculata extract (APE) substantially reversed the loss of hind limb weight-bearing and the cartilage damage resulted from the OA induction in rats. Additionally, the levels of serum pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α as well as the concentration of matrix metalloproteinases, including MMP-1, MMP-3, MMP-8, and MMP-13 were decreased by APE administration. Acetic acid-induced writhing responses in mice which quantitatively measure pain were significantly reduced by APE. In vitro, APE inhibited the generation of NO and downregulated the expression of IL-1β, IL-6, COX-2, and iNOS in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The above results suggest the potential use APE as a therapeutic agent against OA.

scholarly journals An Anti-Inflammatory Composition of Boswellia serrata Resin Extracts Alleviates Pain and Protects Cartilage in Monoiodoacetate-Induced Osteoarthritis in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Venkata Krishnaraju Alluri ◽  
Sreenath Kundimi ◽  
Krishanu Sengupta ◽  
Trimurtulu Golakoti ◽  
Eswar Kumar Kilari
Keyword(s):  
Articular Cartilage ◽  
Structural Damage ◽  
Weight Bearing ◽  
Prostaglandin E ◽  
Thermal Stimulus ◽  
Sprague Dawley ◽  
Boswellia Serrata ◽  
Anti Inflammatory ◽  
Safranin O ◽  
Unique Composition

The boswellic acids, the active compounds in Boswellia serrata gum resin extract, are potent anti-inflammatory agents and are specific nonredox inhibitors of 5-Lipoxygenase (5-LOX). Here, we present the anti-osteoarthritis (OA) efficacy of LI13019F1 (also known as Serratrin®), a unique composition containing the acidic and nonacidic fractions of B. serrata gum resin. This composition strongly inhibited 5-LOX activity with the half-maximal inhibitory concentration (IC50) of 43.35 ± 4.90 μg/mL. Also, LI13019F1 strongly inhibited the leukotriene B4 (IC50, 7.80 ± 2.40 μg/mL) and prostaglandin E2 (IC50, 6.19 ± 0.52 μg/mL) productions in human blood-derived cells. Besides, LI13019F1 reduced TNF-α production with the IC50 of 12.38 ± 0.423 μg/mL. On average, 1, 2.5, and 5 μg/mL doses of LI13019F1 protected 34.62, 47.66, and 62.29% SW1353 human chondrosarcoma cells from IL-1β induced SOX-9 depletion, respectively. Further, a 28-day preclinical proof-of-concept study evaluated the pain relief efficacy of LI13019F1 in monoiodoacetate- (MIA-) induced Sprague-Dawley rats. At the end of the study, 150 and 300 mg/kg doses of LI13019F1 supplemented rats showed significant improvements (55.17 ± 5.81 g (p<0.05), and 66.22 ± 6.30 g (p<0.05), respectively, vs. MIA: 31.22 ± 7.15 g) in body-weight-bearing capacities. Concurrently, LI13019F1-150 and LI13019F1-300 rats substantially (p<0.05) increased the threshold of pain sensitivity to pressure (26.98 ± 2.36 and 28.06 ± 2.72-gram force, respectively; vs. 18.63 ± 5.82 in MIA) and increased (p<0.05) the latent time to withdraw the paw after a thermal stimulus (23.61 ± 2.73 and 28.18 ± 1.90 sec, respectively; vs. 16.56 ± 1.22 sec. in MIA). Besides, the histological observations on Safranin-O green stained articular cartilage revealed that LI13019F1 also prevented the MIA-induced structural damage of the cartilage and reduced the loss of the extracellular matrix (ECM) components in the experimental rats. In conclusion, the present observations suggest that LI13019F1, a new composition of B. serrata gum resin extracts, reduces pain and protects articular cartilage from the damaging action of MIA in a rodent model.

scholarly journals Reprogrammed Synovial Fluid-Derived Mesenchymal Stem/Stromal Cells Acquire Enhanced Therapeutic Potential for Articular Cartilage Repair

Cartilage ◽  
2021 ◽  
pp. 194760352110408
Author(s):  
Brian E. Walczak ◽  
Hongli Jiao ◽  
Ming-Song Lee ◽  
Wan-Ju Li
Keyword(s):  
Animal Model ◽  
Articular Cartilage ◽  
Synovial Fluid ◽  
Cartilage Repair ◽  
Stromal Cells ◽  
Cartilage Damage ◽  
Cellular Reprogramming ◽  
Human Mscs ◽  
Articular Cartilage Repair

Objectives Functions of mesenchymal stem/stromal cells (MSCs) are affected by patient-dependent factors such as age and health condition. To tackle this problem, we used the cellular reprogramming technique to epigenetically alter human MSCs derived from the synovial fluid of joints with osteoarthritis (OA) to explore the potential of reprogrammed MSCs for repairing articular cartilage. Materials and Methods MSCs isolated from the synovial fluid of three patients’ OA knees (Pa-MSCs) were reprogrammed through overexpression of pluripotency factors and then induced for differentiation to establish reprogrammed MSC (Re-MSC) lines. We compared the in vitro growth characteristics, chondrogenesis for articular cartilage chondrocytes, and immunomodulatory capacity. We also evaluated the capability of Re-MSCs to repair articular cartilage damage in an animal model with spontaneous OA. Results Our results showed that Re-MSCs increased the in vitro proliferative capacity and improved chondrogenic differentiation toward articular cartilage-like chondrocyte phenotypes with increased THBS4 and SIX1 and decreased ALPL and COL10A1, compared to Pa-MSCs. In addition, Re-MSC-derived chondrocytes expressing elevated COL2A and COL2B were more mature than parental cell-derived ones. The enhancement in chondrogenesis of Re-MSC involves the upregulation of sonic hedgehog signaling. Moreover, Re-MSCs improved the repair of articular cartilage in an animal model of spontaneous OA. Conclusions Epigenetic reprogramming promotes MSCs harvested from OA patients to increase phenotypic characteristics and gain robust functions. In addition, Re-MSCs acquire an enhanced potential for articular cartilage repair. Our study here demonstrates that the reprogramming strategy provides a potential solution to the challenge of variation in MSC quality.

scholarly journals The Natural History of Haemophilic Arthritis

1977 ◽  
Author(s):  
J.E. Handelsman ◽  
A.L. Lurie ◽  
J.J. Rippey ◽  
R.R. Hill ◽  
M.B.E. Sweet ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Biochemical Analysis ◽  
Weight Bearing ◽  
Cartilage Damage ◽  
Joint Destruction ◽  
Knee Joints ◽  
Round Cell Infiltration ◽  
Infiltrating Cells ◽  
Cell Layers ◽  
History Of

Surgical exploration of eight chronically afflicted haemophilic knee joints in patients aged 6 to 31 years, has revealed a pattern of progressive arthropathy.Significant synovial changes occurred very early. Cellular overgrowth produced thickening, convolution and increased vascularity. Haemosiderin was deposited heavily in all cell layers. Fibrosis ultimately contracted the synovium.Chronic inflammation produced epiphyseal overgrowth. Initially, articular cartilage changes resembled chondromalacia, but fissuring soon occurred and ultimately cartilage was totally lost over central weight-bearing areas and in the intercondylar region. Anomalies of matrix, chondrocyte aggregation and death, and subchondral round cell infiltration were features. Haemosiderin staining was sparse, occurring only in some chondrocytes and infiltrating cells.Biochemical analysis of articular cartilage biopsies revealed a severe depletion of glycosaminoglycans. There was no biochemical evidence of a reaction of repair.Articular cartilage damage occurred mainly between the ages of 6 and 10 years. This evidence suggests that early surgical synovectomy may arrest the process that produces progressive joint destruction.

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

2021 ◽  
Author(s):  
Xiangjun Cheng ◽  
Peilian Xu
Keyword(s):  
Articular Cartilage ◽  
Knee Osteoarthritis ◽  
Experimental Model ◽  
Femoral Condyle ◽  
Cartilage Damage ◽  
Control Group ◽  
Articular Cartilage Damage ◽  
Genistein Treatment ◽  
Male Wistar Rats ◽  
Monosodium Iodoacetate

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.

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