Resveratrol ameliorates inflammatory damage and protects against osteoarthritis in a rat model of osteoarthritis

Wei, Yulong; Jia, Jie; Jin, Xin; Tong, Wei; Tian, Hongtao

doi:10.3892/mmr.2017.8036

Cited by 51 publications

(69 citation statements)

References 28 publications

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“…Besides, RSV alleviated LPS-induced inflammation, as the release of IL-1β, IL-6 and TNF-α was significantly repressed by RSV preconditioning. Consistent with previous studies [14,27,28], these findings suggested the anti-apoptotic and anti-inflammatory functions of RSV on ATDC5 cells and provided evidences that RSV might be a promising therapeutic option for osteoarthritis treatment. It is believed that RSV affects the initiation and progression of many diseases through several mechanisms.…”

Section: Cellular Physiology and Biochemistrysupporting

confidence: 80%

Resveratrol Protects Murine Chondrogenic ATDC5 Cells Against LPS-Induced Inflammatory Injury Through Up-Regulating MiR-146b

Jin

Zhang²,

et al. 2018

Cell Physiol Biochem

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Background/Aims: Resveratrol (RSV) has been reported as a promising oral supplementation for osteoarthritis treatment, while the mechanism of its action is still unclear. The specific aim of this study is to decode one of the mechanisms by which RSV protects chondrocyte. Methods: Mouse chondrogenic cell line ATDC5 was treated with 30 µM RSV for 24 h, and 10 µg/ml LPS for 12 h, after which cell viability, apoptosis, and the release of pro-inflammatory cytokines were assessed. The expression of miR-146b in ATDC5 cells was silenced by the specific inhibitor transfection, and then cell viability, apoptosis and inflammation were re-assessed. Results: The IC50 value of LPS in ATDC5 cells was about 10.27 µg/ml. LPS with a dosage of 10 µg/ml repressed cell viability, induced apoptosis, and increased the release of IL-1β, IL-6 and TNF-α. RSV pre-treatment (30 µM) significantly alleviated LPS-induced apoptosis and inflammation. More importantly, miR-146b was up-regulated by RSV, and the protective functions of RSV on ATDC5 cells were attenuated by miR-146b silence. Further, NF-κB and p38MAPK pathways were activated by LPS, and were deactivated by RSV. Besides, RSV-induced the deactivation of NF-κB and p38MAPK pathways was reversed by miR-146b silence. Conclusions: Our findings suggest that RSV protects ATDC5 cells from LPS-induced inflammatory and apoptotic injury via up-regulation of miR-146b and thereby deactivation of NF-κB and p38MAPK pathways.

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Section: Cellular Physiology and Biochemistrysupporting

confidence: 80%

Resveratrol Protects Murine Chondrogenic ATDC5 Cells Against LPS-Induced Inflammatory Injury Through Up-Regulating MiR-146b

Jin

Zhang²,

et al. 2018

Cell Physiol Biochem

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“…Activation of Nrf2 plays an important role in antioxidation and anti‐inflammation mechanisms, while ROS are produced in the course of endogenous cellular oxidation. Data have shown that Res ameliorates inflammatory damage and protects against osteoarthritis in a rat model of osteoarthritis via NF‐κB and HO‐1/Nrf2 signaling . Res might protect rat vascular smooth muscle cells against redox injury induced by calcification through the involvement of the Nrf2 pathway .…”

Section: Discussionmentioning

confidence: 99%

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

Zhang

Wang

et al. 2019

Annals of the New York Academy of Sciences

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Resveratrol (Res) is a polyphenolic compound that has a variety of biological functions and activities. This study aimed to explore the mechanisms of the antioxidant and proapoptotic effects of Res in H2O2‐treated rheumatoid arthritis fibroblast‐like synoviocytes (RA‐FLSs) by the Nrf2–Keap1 signaling pathway. We found that 5 µM H2O2 promoted cell proliferation and increased intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) content in RA‐FLSs. However, Res could reverse these effects in 5 µMH2O2‐treated RA‐FLSs by (1) promoting expression of nuclear factor erythroid 2–related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1), (2) reducing expression of Kelch‐like ECH–related protein 1 (Keap1), (3) inhibiting production of ROS and MDA, (4) blocking activation of nuclear factor‐κB (NF‐κB) p65, (5) inhibiting cell proliferation and migration, and (6) activating Bcl‐2/Bax to induce apoptosis. After lentiviral silencing of Nrf2 (siNrf2) mRNA expression in RA‐FLSs, Res addition did not increase the expression of Nrf2 or HO‐1 to reduce the production of mitochondrial ROS caused by 5 µM H2O2. Res reduced the Bcl‐2/Bax ratio, but siNrf2 reduced the ability of Res to promote apoptosis. We conclude that Res inhibits ROS production by activating the Nrf2 pathway, thereby inhibiting activation of NF‐κB and proliferation and migration of RA‐FLSs, to induce apoptosis. Targeting the Nrf2–Keap1 pathway may be a relevant aim of using Res in the treatment of RA.

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“…Possessing a stilbene structure, resveratrol acts as a non-flavonoid polyphenol compound. It has been proven that resveratrol can make plants more resistant to pathogens as well as improve environment deterioration [6] . Wei et al [6] also revealed that resveratrol could improve the inflammatory damage as well as protect against OA in an OA rat model.…”

Section: Discussionmentioning

confidence: 99%

“…We used CCK-8 kit to measure chondrocytes viability following the instruction of manufacturers. In brief, we seeded human OA chondrocytes in 96-well plates (5×10 5 cells/ml) and treated them with or without resveratrol (6,12,24, 48 μM) for 24h. After that, we added 10 uL CCK-8 into the plates.…”

Section: Cell Viabilitymentioning

confidence: 99%

“…Thus, reducing the IL-1β in articular cavity could delay the development of OA [4] .Resveratrol is a common polyphenolic compound in the skin of red grapes [5] . Resveratrol exhibits anti-ageing, anti-inflammatory, and anti-oxidant activities, and has cardio-, neuro-, and chondroprotective effects as proved by many studies [6] . Nuclear factor-kappa B (NF-κB) signaling XFS, YC and QRD conducted experiments; MQZ analyzed data; QRD and XFS wrote manuscript; YC revised manuscript; XFS and YC designed the experiment and edited manuscript.…”

mentioning

confidence: 94%

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Resveratrol inhibit interleukin-1β induced inflammatory response in human osteoarthritis chondrocytes through NF-κB signaling pathway

Shen

Cheng

Dong

et al. 2019

Preprint

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Osteoarthritis (OA) is a common degenerative disease and affect millions of people. Resveratrol is a coumarin compound refined from traditional Chinese medicines with potential anti-inflammatory ability. This study aimed to evaluate protective anti-inflammatory effects of resveratrol in human OA chondrocytes. The chondrocytes were isolated from OA patients. CCK-8 method was used to explore the optimal dose of resveratrol for chondrocyte. Next, we used PCR and Western-blot method to assess the relative mRNA and protein expression in IL-1β group. We further explored relevant mechanism of resveratrol for anti-inflammatory in human OA chondrocytes by immunofluorescence and Western-blot. The results showed that resveratrol blocked IL-1β-stimulated production of NO and PGE2. In addition, resveratrol inhibited the expression of COX-2, iNOs, MMP-1, MMP-3, MMP-13, and increased the levels of aggrecan and collagen-II. Mechanistically, resveratrol suppressed IL-1βinduced IκB-α degradation and NF-κB activation. In conclusion, our results demonstrate that resveratrol inhibits inflammation in OA via the regulation of NF-κB signaling pathway, and suggested that resveratrol may be a potential therapeutic agent for OA. BackgroundOsteoarthritis (OA) acts as a prevalent chronic age-related disease joint disease featuring cartilage degradation, osteophyte formation, and joint stiffness, which seriously affects the health of the elderly people [1] . There is an increase in the incidence rate of OA with the aging of population, thus it is necessary to find an effective strategy for the treatment of OA [2] .During the progression of OA, the increased expression of interleukin-1β (IL-1β) in the articular cartilage and synovium leads to the destruction of cartilage, downregulation of type II collagen [3] .Furthermore, IL-1β has the function of inducing the chondrocyte release of prostaglandin E2 (PGE2) and nitric oxide (NO). Thus, reducing the IL-1β in articular cavity could delay the development of OA [4] .Resveratrol is a common polyphenolic compound in the skin of red grapes [5] . Resveratrol exhibits anti-ageing, anti-inflammatory, and anti-oxidant activities, and has cardio-, neuro-, and chondroprotective effects as proved by many studies [6] . Nuclear factor-kappa B (NF-κB) signaling XFS, YC and QRD conducted experiments; MQZ analyzed data; QRD and XFS wrote manuscript; YC revised manuscript; XFS and YC designed the experiment and edited manuscript.

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Resveratrol ameliorates inflammatory damage and protects against osteoarthritis in a rat model of osteoarthritis

Cited by 51 publications

References 28 publications

Resveratrol Protects Murine Chondrogenic ATDC5 Cells Against LPS-Induced Inflammatory Injury Through Up-Regulating MiR-146b

Resveratrol Protects Murine Chondrogenic ATDC5 Cells Against LPS-Induced Inflammatory Injury Through Up-Regulating MiR-146b

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

Resveratrol inhibit interleukin-1β induced inflammatory response in human osteoarthritis chondrocytes through NF-κB signaling pathway

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