Resveratrol restores the level of key inflammatory cytokines and RANKL/OPG ratio in the femur of rat osteoporosis model

Khera, Alka; Kanta, Poonam; Kalra, Jaswinder; Dumir, Dheeraj; Thungapathra, M.

doi:10.1080/08952841.2018.1522126

Cited by 20 publications

(18 citation statements)

References 33 publications

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“…Resveratrol shows an anti-inflammatory effects in some cells in vitro [28,29]. In disc cells, resveratrol also exhibits protective effects against certain pathological factors, such as inhibiting disc cell apoptosis, promoting disc matrix synthesis and inhibiting disc catabolism [23,30–32].…”

Section: Discussionmentioning

confidence: 99%

Resveratrol attenuates inflammation environment-induced nucleus pulposus cell senescence in vitro

Lin

et al. 2019

Bioscience Reports

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Intervertebral disc degeneration is a disease identified as an inflammation response-participated pathological process. As a classical cellular feature, disc cell senescence is reported to be closely related with disc cell senescence. Resveratrol has a protective role against inflammation in some cells. However, its biological effects on disc cells remain largely unclear. The present study was aimed to study the effects of resveratrol on disc nucleus pulposus (NP) cell senescence in an inflammation environment. Isolated NP cells were cultured in cultured medium with (control group) or without (inflammation group) inflammatory cytokine TNF-α and IL-1β for 14 days. Resveratrol was added along with the NP cells treated with inflammatory cytokines to investigate its effects. NP cell senescence was analyzed by senescence-associated β-Galactosidase (SA-β-Gal) staining, cell proliferation, G0/1 cell cycle arrest, telomerase activity, gene/protein expression of senescence markers (p16 and p53) and NP matrix biosynthesis. In addition, the intracellular reactive oxygen species (ROS) was also analyzed. Compared with the control group, inflammation group significantly increased SA-β-Gal activity and ROS content, decreased cell proliferation and telomerase activity, promoted G0/1 cell cycle arrest, up-regulated gene/protein expression of senescence markers (p16 and p53) and matrix catabolism enzymes (MMP-3, MMP-13 and ADAMTS-4), and down-regulated gene/protein expression of NP matrix macromolecules (aggrecan and collagen II). However, resveratrol partly reversed the effects of inflammatory cytokine on these cell senescence-associated parameters. Together, resveratrol was effective to suppress cell senescence in an inflammatory environment. The present study shows new knowledge on how to retard inflammation response-initiated disc degeneration.

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Section: Discussionmentioning

confidence: 99%

Resveratrol attenuates inflammation environment-induced nucleus pulposus cell senescence in vitro

Lin

et al. 2019

Bioscience Reports

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“…Adding IL-23 to bone marrow stromal cells led to an increased differentiation towards the osteoblast lineage [31]. In the femur of a rat osteoporosis model, IL-23 is reduced after adequate estrogen therapy for improvement of bone mineral density [32]. IL-27 may suppress the expression of RANKL in Th17 cells and CD4+ T cells [33].…”

Section: The Cytokines From Macrophages Contribute To the Process mentioning

confidence: 99%

The Role of Macrophage in the Pathogenesis of Osteoporosis

Yang

2019

IJMS

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Osteoporosis is a systemic disease with progressive bone loss. The bone loss is associated with an imbalance between bone resorption via osteoclasts and bone formation via osteoblasts. Other cells including T cells, B cells, macrophages, and osteocytes are also involved in the pathogenesis of osteoporosis. Different cytokines from activated macrophages can regulate or stimulate the development of osteoclastogenesis-associated bone loss. The fusion of macrophages can form multinucleated osteoclasts and, thus, cause bone resorption via the expression of IL-4 and IL-13. Different cytokines, endocrines, and chemokines are also expressed that may affect the presentation of macrophages in osteoporosis. Macrophages have an effect on bone formation during fracture-associated bone repair. However, activated macrophages may secrete proinflammatory cytokines that induce bone loss by osteoclastogenesis, and are associated with the activation of bone resorption. Targeting activated macrophages at an appropriate stage may help inhibit or slow the progression of bone loss in patients with osteoporosis.

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“… 9 RES could competitively bind to estrogen receptors in vitro and exert estrogen-like effects; as such, RES is considered a phytoestrogen. 9 RES also exhibits several important bioactivities, such as estrogen-like regulatory lipid function, anti-platelet aggregation, anti-oxidation, and anti-tumor. 9 – 12 RES could effectively prevent bone loss, as indicated by the in vitro experiments in rats, which lost bone mass due to lack of physical activity and estrogen deficiency.…”

Section: Introductionmentioning

confidence: 99%

“… 9 RES also exhibits several important bioactivities, such as estrogen-like regulatory lipid function, anti-platelet aggregation, anti-oxidation, and anti-tumor. 9 – 12 RES could effectively prevent bone loss, as indicated by the in vitro experiments in rats, which lost bone mass due to lack of physical activity and estrogen deficiency. 13 RES inhibits the synthesis of reactive oxygen species, resulting in an increase in the alkaline phosphatase levels and proline hydroxylase activity in MC3 T3-E1 cells and prevention of the differentiation of RAW264.7 cells into osteoclasts.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of resveratrol on estrogen deficiency-induced osteoporosis though attenuating NADPH oxidase 4/nuclear factor kappa B pathway by increasing miR-92b-3p expression

Zhang

Liu

et al. 2020

Int J Immunopathol Pharmacol

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Introduction: Resveratrol (RES) exhibits estrogen-like effects and has potential applications to treatment of osteoporosis caused by estrogen deficiency; however, the specific mechanism of action of RES remains unclear. Here, we examined the therapeutic effects of RES on ovariectomized (OVX) rats with osteoporosis and determined the underlying mechanism. Methods: We established an OVX rat model to study osteoporosis caused by estrogen deficiency. The treatment groups were given orally with RES (50, 100, and 200 mg/day), the estrogen group received 0.8 mg/kg E2 daily via oral route, and the sham-operated and control groups received an equivalent dose of sodium carboxymethylcellulose orally. After 12 weeks of treatment, we used real-time quantitative polymerase chain reaction (PCR) and Western blot analysis to measure the gene and protein expression of miR-92b-3p, Nox4, NF-κBp65, IκB, BMP2, Smad7, and RUNX-2 in bone tissues. Right femur structural parameters were evaluated by micro-CT. Dual-energy X-ray 4500 W was used to determine systemic bone mineral density (BMD). Enzyme-linked immunosorbent assay (ELISA) kits were used to determine the serum levels of bone alkaline phosphatase (BALP), osteoprotegerin (OPG), anti-tartrate acid phosphatase-5b (PTRA5b), and carboxylated terminal peptide (CTX-I). The rat femoral bone specimens were stained using hematoxylin and eosin for pathological examination Results: We observed increased levels of serum estrogen in both ovaries, elevated miR-92b-3p levels in bone tissues, reduced levels of Nox4, NF-κBp65, p-IκB-a, and cathepsin K, and elevated gene and protein expression of BMP2, Smad7, and RUNX-2 in the OVX rat model of osteoporosis after treatment with RES. Elevated levels of BALP, OPG, ALP, and BMD along with reduced levels of TRAP-5b and CTX-I were also observed. The structural model index (SMI) and the trabecular space (Tb. Sp) decreased, while the trabecular thickness (Tb. Th), bone volume fraction (BV/TV), trabecular number (Tb.N), and tissue bone density (Conn.D) increased, thereby improving osteoporosis induced by estrogen deficiency in both ovaries. Conclusion: Cathepsin K expression and Nox4/NF-κB signaling pathway were suppressed by the elevated expression of miR-92b-3p. This inhibition was pivotal in the protective effect of RES against osteoporosis induced by estrogen deficiency in both ovaries. Thus, RES efficiently alleviated osteoporosis induced by estrogen deficiency in rats.

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Resveratrol restores the level of key inflammatory cytokines and RANKL/OPG ratio in the femur of rat osteoporosis model

Cited by 20 publications

References 33 publications

Resveratrol attenuates inflammation environment-induced nucleus pulposus cell senescence in vitro

Resveratrol attenuates inflammation environment-induced nucleus pulposus cell senescence in vitro

The Role of Macrophage in the Pathogenesis of Osteoporosis

Protective effect of resveratrol on estrogen deficiency-induced osteoporosis though attenuating NADPH oxidase 4/nuclear factor kappa B pathway by increasing miR-92b-3p expression

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