RANKL and TNF-α-induced JNK/SAPK Osteoclastogenic Signaling Pathway was Inhibited by Caffeic Acid in RAW-D Cells

Sandra, Ferry; Briskila, Junita; Ketherin, Ketherin

doi:10.14499/indonesianjcanchemoprev9iss2pp63-67

Cited by 6 publications

(10 citation statements)

References 17 publications

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“…Some herbal extracts have shown their potencies in inhibiting osteoclastogenesis through different pathways. (3)(4)(5)(6)(7)13) Amongst the herbal extracts, caffeic acid, often found in berries and Japanese sweet potato has been studied for its potential to protect human cells from several diseases including cancer and bone resorption. (3,(5)(6)(7)14) Caffeic acid activated the Caspases, further inducing osteosarcoma cells into apoptosis.…”

Section: Rankl and Tnfα-induced Phosphorylation Of Akt At Ser473 And Thr308 Was Not Inhibited By Caffeic Acidmentioning

confidence: 99%

“…(3)(4)(5)(6)(7)13) Amongst the herbal extracts, caffeic acid, often found in berries and Japanese sweet potato has been studied for its potential to protect human cells from several diseases including cancer and bone resorption. (3,(5)(6)(7)14) Caffeic acid activated the Caspases, further inducing osteosarcoma cells into apoptosis. (15,16) Meanwhile, in bone resorption, caffeic acid has a potential in inhibiting RANKL-TNFainduced osteoclastogenesis through TRAF6, p38 MAPK, JNK/SAPK, Nuclear Factor of Activated T-cells cytoplasmic 1 (NFATc1), and NFkB.…”

Section: Rankl and Tnfα-induced Phosphorylation Of Akt At Ser473 And Thr308 Was Not Inhibited By Caffeic Acidmentioning

confidence: 99%

“…Osteoclast is a major bone resorbing factor derived from hematopoietic stem cells, induced by various cytokines such as Receptor Activator Nuclear Factor kB Ligand (RANKL), Tumor Necrosis Factor (TNF)-a, Macrophage Colony Stimulating Factor (M-CSF), Interleukin (IL)-1a and IL-6. (1,2) The bindings of RANKL to RANK and TNF to TNF receptor further induces intracellular signaling pathways, including Tumor Necrosis Factor Receptor (TNFR)-associated Factor 6 (TRAF6) (3), Mitogen Activated Protein Kinase (MAPK) family (4)(5)(6) and Nuclear Factor kB (NFkB) (7). Activated MAPK family consists of p44/42 MAPK (4), p38 MAPK (4,5), and c-Jun N-Terminal Kinase (JNK) or Stress Activated Protein Kinase (SAPK) (6).…”

Section: Introductionmentioning

confidence: 99%

“…(1,2) The bindings of RANKL to RANK and TNF to TNF receptor further induces intracellular signaling pathways, including Tumor Necrosis Factor Receptor (TNFR)-associated Factor 6 (TRAF6) (3), Mitogen Activated Protein Kinase (MAPK) family (4)(5)(6) and Nuclear Factor kB (NFkB) (7). Activated MAPK family consists of p44/42 MAPK (4), p38 MAPK (4,5), and c-Jun N-Terminal Kinase (JNK) or Stress Activated Protein Kinase (SAPK) (6).…”

Section: Introductionmentioning

confidence: 99%

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Caffeic Acid Inhibits RANKL and TNFa-induced Osteoclastogenesis by Targeting TAK1-p44/42 MAPK

et al. 2021

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BACKGROUND: The potential of the caffeic acid in other important Receptor Activator Nuclear Factor kB Ligand (RANKL)-Tumor Necrosis Factor (TNF)a-induced osteoclastogenic signaling pathways has not been known. Therefore, the current study was conducted to explore as well as to understand the inhibition potential of caffeic acid.METHODS: RAW264.7 cells were cultured, treated with caffeic acid, RANKL and TNFa. Tartrate Resistant Acid Phosphatase (TRAP) staining was performed to detect TRAP+ osteoclast-like polynuclear cells. To detect the activity of p44/42 Mitogen Activated Protein Kinase (MAPK), Akt, and Transforming Growth Factor-β-activated Kinase (TAK)1, the phosphorylated forms of the proteins were investigated with the immunoblotting assay.RESULTS: Pre-treatment of caffeic acid inhibited the RANKL and TNFa-induced differentiation of RAW264.7 cells into TRAP+ osteoclast-like polynuclear cells. RANKL and TNFa induced phosphorylation of p44/42 MAPK at Thr202/Tyr204, phosphorylation of Akt at both Ser473 and Thr308 and phosphorylation of TAK1 at Ser412. Pre-treatment with caffeic acid prior to the RANKL and TNFa induction, inhibited the phosphorylation of MAPK, and TAK1, but not Akt.CONCLUSION: Caffeic acid might regulate the RANKL-TNFa-induced osteoclastogenic pathway in RAW264.7 by targeting TAK1, which later activation of p44/42 MAPK was abolished.KEYWORDS: caffeic acid, osteoclastogenesis, p44/42, Erk1/2, Akt, TAK1, RAW264.7

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Section: Rankl and Tnfα-induced Phosphorylation Of Akt At Ser473 And Thr308 Was Not Inhibited By Caffeic Acidmentioning

confidence: 99%

Section: Rankl and Tnfα-induced Phosphorylation Of Akt At Ser473 And Thr308 Was Not Inhibited By Caffeic Acidmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Caffeic Acid Inhibits RANKL and TNFa-induced Osteoclastogenesis by Targeting TAK1-p44/42 MAPK

et al. 2021

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“…25,27 IL-6, which produced by the influence of LPS, IL-1β and TNF-α, also causes bone resorption and enhances the synthesis of PGE2, acute phase proteins, and chemokines. 1,[28][29][30][31][32] IL-6 generates oxidative stress and may lead to a short-term aggregation of H 2 O 2 in mitochondria, resulting in damage of mitochondrial. 33 IL-6 also affects the invasion and metastasis process by promoting MMPs expressions.…”

Section: Stimulation Of Chronic Inflammationmentioning

confidence: 99%

Microbiome in Oral Squamous Cell Carcinoma: Mechanisms and Signaling Pathways

Hayati¹,

Panjaitan²,

Sandra³

2020

Mol Cell Biomed Sci

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Oral squamous cell carcinoma is part of head and neck squamous cell carcinoma which is the ultimate cause of morbidity and mortality in cancer. The alteration of microbial community in the saliva might act as a helpful marker for the prediction, detection and prognosis oral cancer, particularly the transition of cancer precursor lesion. There are three mechanisms of action of oral microbiota in cancer pathogenesis, chronic inflammation of bacterial stimulation, carcinogenesis by cytoskeletal rearrangements, and carcinogenic substances that produced by microorganisms. Changes in the composition of microbiota could therefore have the potential to be used as a significant oral biomarker to predict the pathological transition from oral epithelial precursor lesion to cancer.Keywords: microbiome, oral cancer cellular proliferation, microorganism, oral cancer, oral squamous cell carcinoma

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Caffeic acid mitigates aflatoxinB1‐mediated toxicity in the male rat reproductive system by modulating inflammatory and apoptotic responses, testicular function, and the redox‐regulatory systems

Owumi

Irozuru

Arunsi

et al. 2022

Journal of Food Biochemistry

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Aflatoxin B1 (AFB1) is a toxic metabolite of public health concern. The present study investigates the protective effects of caffeic acid (CA) against AFB1‐induced oxidative stress, inflammation, and apoptosis in the hypothalamus, epididymis, and testis of male rats. Five experimental rat cohorts (n = 6) were treated per os for 28 consecutive days as follows: Control (Corn oil 2 ml/kg body weight), AFB1 alone (50μg/kg), CA alone (40 mg/kg) and the co‐treated rat cohorts (AFB1: 50μg/kg + CA1: 20 or 40 mg/kg). Following sacrifice, the biomarkers of hypothalamic, epididymal, and testicular toxicities, antioxidant enzyme activities, myeloperoxidase (MPO) activity, as well as levels of nitric oxide (NO), reactive oxygen and nitrogen (RONS) species and lipid peroxidation (LPO) were analysed spectrophotometrically. Besides, the concentration of tumour necrosis factor‐alpha (TNF‐α), Bcl‐2 and Bax proteins were assessed using ELISA. Results showed that the AFB1‐induced decrease in biomarkers of testicular, epididymal and hypothalamic toxicity was significantly (p < .05) alleviated in rats coexposed to CA. Moreover, the reduction of antioxidant status and the increase in RONS and LPO were lessened (p < .05) in rats co‐treated with CA. AFB1 mediated increase in TNF‐α, Bax, NO and MPO activity were reduced (p< .05) in the hypothalamus, epididymis, and testis of rats coexposed to CA. In addition, Bcl‐2 levels were reduced in rats treated with CA dose‐dependently. Light microscopic examination showed that histopathological lesions severity induced by AFB1 were alleviated in rats coexposed to CA. Taken together, the amelioration of AFB1‐induced neuronal and reproductive toxicities by CA involves anti‐inflammatory, antioxidant, antiapoptotic mechanisms in rats. Practical applications The beneficial antioxidant effects of caffeic acid (CA) are attributed to CA delocalized aromatic rings and free electrons, easily donated to stabilize reactive oxygen species. We report in vivo findings on CA and AfB1 mediated oxidative stress and reproductive dysfunction in rats. CA conjugated esters including chlorogenic acids are widely distributed in plants, and they act as a dietary source of natural defense against infections. CA can chelate heavy metals and reduce production of damaging free radicals to cellular macromolecules. Along these lines, CA can stabilize aflatoxin B1‐epoxide as well and avert deleterious conjugates from forming with deoxyribonucleic acids. Hence CA, as a dietary phytochemical can protect against the damaging effects of toxins including aflatoxin B1 that contaminate food. CA dose‐dependently abated oxidative, inflammatory, and apoptotic stimuli, improved functional characteristics of spermatozoa and reproductive hormone levels, and prevented histological alterations in experimental rats’ hypothalamus and reproductive organs brought about by AFB1 toxicity.

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RANKL and TNF-α-induced JNK/SAPK Osteoclastogenic Signaling Pathway was Inhibited by Caffeic Acid in RAW-D Cells

Cited by 6 publications

References 17 publications

Caffeic Acid Inhibits RANKL and TNFa-induced Osteoclastogenesis by Targeting TAK1-p44/42 MAPK

Caffeic Acid Inhibits RANKL and TNFa-induced Osteoclastogenesis by Targeting TAK1-p44/42 MAPK

Microbiome in Oral Squamous Cell Carcinoma: Mechanisms and Signaling Pathways

Caffeic acid mitigates aflatoxinB1‐mediated toxicity in the male rat reproductive system by modulating inflammatory and apoptotic responses, testicular function, and the redox‐regulatory systems

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