Carnosine Prevents Type 2 Diabetes-Induced Osteoarthritis Through the ROS/NF-κB Pathway

Yang, Yue; Wang, Yang; Kong, Yawei; Zhang, Xiaoning; He, Zhao; Ye, Gang; Bai, Lan

doi:10.3389/fphar.2018.00598

Cited by 32 publications

(21 citation statements)

References 47 publications

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“…Especially, PLM200 showed a significant increase. The pain of cartilage leads to decrease of HWBD, which has been proved by several studies [ 49 , 50 ]. These results demonstrate a balance and relief of cartilage discomfort in the PLM-treated group.…”

Section: Discussionmentioning

confidence: 87%

Protective Effects of Phellinus linteus Mycelium on the Development of Osteoarthritis after Monosodium Iodoacetate Injection

Shin

Lee

Kim

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Objective. The aim of this study was to identify the protective effects of Phellinus linteus mycelium (PLM) and its possible mechanisms in a model of monosodium iodoacetate- (MIA-) induced osteoarthritis (OA). Methods. Intra-articular injection of MIA was injected to 50 μL with 80 mg/mL using a 0.3 mL insulin syringe into the right knee joint. Changes in hindpaw weight-bearing distribution between the right (osteoarthritic) and left (contralateral control) legs were used as an index of joint discomfort. PLM (50, 100, and 200 mg/kg body weight) was orally administered once daily for 14 days from day 7 after MIA treatment. And then, various factors associated with inflammatory response and cartilage degeneration in cartilage tissues detected by western blotting. Results. PLM treatment showed a concentration-dependent elevation in change in hindpaw weight-bearing distribution (HWBD). PLM200 demonstrated the capacity to significantly increase HWBD, indicating that the change in weight-bearing distribution means the reduction of spontaneous pain. Our results indicate that PLM suppressed the inflammatory factors via NF-κB signaling pathway induced by p38 phosporlyation. Moreover, PLM200 exhibited a significant reduction of ROS produced by the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. PLM100 and PLM200 inhibited the levels of matrix metalloproteinase (MMP)-1, one of proteinase that degrades extracellular matrix (ECM). Conclusions. Taken together, our results indicated that PLM has a strong chondroprotective effect through the suppression both ROS production and inflammation.

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Section: Discussionmentioning

confidence: 87%

Protective Effects of Phellinus linteus Mycelium on the Development of Osteoarthritis after Monosodium Iodoacetate Injection

Shin

Lee

Kim

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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“…However, the anti-inflammatory potential of CARN in OA is still poorly studied. In a recent report, the potential protective effect of an oral CARN supplement was assessed to improve type 2 diabetes-induced OA [46].…”

Section: Discussionmentioning

confidence: 99%

The Protective Effect of New Carnosine-Hyaluronic Acid Conjugate on the Inflammation and Cartilage Degradation in the Experimental Model of Osteoarthritis

et al. 2020

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Osteoarthritis (OA) is a disease that currently has no cure. There are numerous studies showing that carnosine and hyaluronic acid (HA) have a positive pharmacological action during joint inflammation. For this reason, the goal of this research was to discover the protective effect of a new carnosine conjugate with hyaluronic acid (FidHycarn) on the inflammatory response and on the cartilage degradation in an in vivo experimental model of OA. This model was induced by a single intra-articular (i.ar.) injection of 25 µL of normal saline with 1 mg of monosodium iodoacetate solution (MIA) in the knee joint of rats. MIA injection caused histological alterations and degradation of the cartilage, as well as behavioral changes. Oral treatment with FidHycarn ameliorated the macroscopic signs, improved thermal hyperalgesia and the weight distribution of the hind paw, and decreased histological and radiographic alterations. The oxidative damage was analyzed by evaluating the levels of nitrotyrosine and inducible nitric oxide synthase (iNOS) that were significantly reduced in FidHycarn rats. Moreover, the levels of pro-inflammatory cytokines and chemokines were also significantly reduced by FidHycarn. Therefore, for the first time, the effectiveness of oral administration of FidHycarn has been demonstrated in an osteoarthritis model. In conclusion, the new FidHycarn could represent an interesting therapeutic strategy to combat osteoarthritis. affects the joints that support most of the weight (such as the knees and feet) and the joints we use the most (e.g., hand joints). In a healthy joint, the cartilage shelters the surface of the bones and supports the bones to move liberally against each other. When a joint develops OA, part of the cartilage tapers and the surface becomes coarser. This means the articulation does not move as easily as it should. When the cartilage becomes worn out or damaged, all the tissues within the articulation become more active than usual as the body attempts to repair the damage. However, the reparation processes do not always operate well, and thus, modifications to the joint structure can occasionally cause or contribute to symptoms such as swelling, pain, and ultimately, disability.One of the leading characteristics of OA is collagen deterioration, as suggested by augmented tissue swelling and the loss of proteoglycans [1]. Both collagen destruction and the loss of proteoglycans unfavorably affect the mechanical properties of cartilage. Chondrocytes respond to tissue injury by increasing collagen and proteoglycan synthesis in an attempt to repair the tissue [2]. If repair fails, the damage will progress to articular cartilage degeneration. It is still not clear exactly what causes osteoarthritis. We do know that it is not simply 'wear and tear' and that the danger of developing OA depends on a number of factors.Furthermore, these degradation processes are thought to be largely elicited through excess production of pro-inflammatory and catabolic mediators. Among them, interleukin-1β (IL-1β) has...

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“…Serial 5‐μm sagittal sections were cut, then stained with hematoxylin and eosin. Injuries to the articular cartilage in the femur and tibia were assessed by the Osteoarthritis Research Society International (OARSI) score (scale of 0–24 points) (Gerwin, Bendele, Glasson, & Carlson, ; Yang et al, ). The OARSI pathology scoring system is used in clinical OA diagnosis and criteria for endpoint, they are also widely applied in animal model evaluation.…”

Section: Methodsmentioning

confidence: 99%

Protective effects of quercetin against inflammation and oxidative stress in a rabbit model of knee osteoarthritis

Wei

Zhang

Tang

et al. 2019

Drug Development Research

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Hit, Lead & Candidate Discovery This study investigated the effects of a natural phenolic compound quercetin on surgical‐induced osteoarthritis (OA) in rabbits. Forty‐eight New Zealand White rabbits were used to establish OA model by Hulth modified method, and subsequently randomized into untreated OA group (treatment was drinking water), celecoxib treated group (celecoxib 100 mg kg‑1 by gavage), and quercetin treated group (25 mg kg‑1 by gavage). Sixteen nonoperated rabbits served as the normal controls (drinking water was given). The treatment (length: 4 weeks) started on the 5th week postoperation when the OA pathological changes were manifested. Expressions of superoxide dismutase (SOD), matrix metalloproteinase‐13 (MMP‐13) and tissue inhibitor of metalloproteinases‐1 (TIMP‐1) in serum, synovial fluid, and synovial tissue were measured at 8 and 12 weeks postoperation. Pathological analysis was performed with synovial tissue section and Osteoarthritis Research Society International histopathology grading and staging scores were determined. The quercetin treated group showed higher SOD and TIMP‐1 expressions but lower MMP‐13 expression than untreated OA group in the serum, synovial fluid and synovial tissues (p < .05). There was no significant difference in the SOD, MMP‐13 and TIMP‐1 expressions between the quercetin‐treated and celecoxib‐treated groups. The MMP‐13/TIMP‐1 ratio of the quercetin treated group was significantly lower than that of the untreated OA group (p < .05). Quercetin can up‐regulate SOD and TIMP‐1, down‐regulate MMP‐13, and improve the degeneration of OA through weakening the oxidative stress responses and inhibiting the degradation of cartilage extracellular matrix.

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Carnosine Prevents Type 2 Diabetes-Induced Osteoarthritis Through the ROS/NF-κB Pathway

Cited by 32 publications

References 47 publications

Protective Effects of Phellinus linteus Mycelium on the Development of Osteoarthritis after Monosodium Iodoacetate Injection

Protective Effects of Phellinus linteus Mycelium on the Development of Osteoarthritis after Monosodium Iodoacetate Injection

The Protective Effect of New Carnosine-Hyaluronic Acid Conjugate on the Inflammation and Cartilage Degradation in the Experimental Model of Osteoarthritis

Protective effects of quercetin against inflammation and oxidative stress in a rabbit model of knee osteoarthritis

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