Regulation of osteoclastogenesis by Simon extracts composed of caffeic acid and related compounds: successful suppression of bone destruction accompanied with adjuvant-induced arthritis in rats

Tang, Qiulin; Kukita, Toshio; Ushijima, Yuki; Kukita, Akiko; Nagata, Kazuhiro; Sandra, Ferry; Watanabe, Toshiyuki; Toh, Kazuko; Okuma, Yutaka; Kawasaki, Sadamichi; Rasubala, Linda; Teramachi, Junpei; Miyamoto, Ichiko; Wu, Zhou; Iijima, Tadahiko

doi:10.1007/s00418-005-0062-4

Cited by 43 publications

(35 citation statements)

References 41 publications

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“…Approach through the mechanism of cancer cell apoptosis and the empowerment of natural materials to be one promising alternative, such as Ayamurasaki and Simon extract. (3,4) Two varieties of sweet potato (Ipomoea batatas L.) are reported to contain caffeic acid compounds that proved to have the ability to inhibit osteoclastogenesis. (4)(5)(6) Caffeic acid significantly reduces the activity of nuclear factor κB (NFκB), a cell signaling pathway involved in osteoclastogenesis (5), in which NFκB inhibition can cause tumor cells to stop proliferating or becoming more sensitive to the actions of anti-tumor agents.…”

Section: Introductionmentioning

confidence: 99%

Caspase Inhibitor Diminishes Caffeic Acid-induced Apoptosis in Osteosarcoma Cells

et al. 2017

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B ACKGROUND:Caffeic acid has been shown to induce apoptosis in MG63 osteosarcoma cells. Along with the apoptotic induction, caffeic acid was shown to activate caspase-8, -9 and -3. However, the role of caspase in mediating caffeic acid-induced apoptosis in MG63 cells are not clear yet. In this study, caspase role was further investigated by inhibiting caspase activity in the caffeic acid-induced apoptosis system in the MG63 cells. METHODS:MG63 cells were cultured, starved, pretreated with/without Z-VAD FMK and treated with/without 10 µg/mL caffeic acid. To quantify the number of apoptotic MG63 cells, Sub-G1 method was performed. The caffeic acid-induced apoptotic morphology was confirmed with 4',6-diamidino-2-phenylindole (DAPI) staining and Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Meanwhile, to detect apoptotic underlying mechanism, immunoblotting was performed to detect caspase-8, -9 and -3. RESULTS:The MG63 cells were significantly induced into apoptosis with the treatment of 10 µg/mL caffeic acid for 48 hours. However, pretreatment of 100 µM Z-VAD-FMK, a pan caspase inhibitor, for 2 hours, the percentage of apoptotic MG63 cells was significantly diminished. The apoptotic phenomenon induced by caffeic acid as well as the inhibition of Z-VAD-FMK were confirmed by DAPI staining and TUNEL assay. Cleaved caspase-8, -9 and -3 were formed markedly upon the treatment of caffeic acid. Pretreatment of 100 µM Z-VAD-FMK could inhibit the cleaved caspase-8, -9 and -3. CONCLUSION:Taken together, caffeic acid has the potential to induce apoptosis in MG63 cells, specifically through the caspase signaling pathway. KEYWORDS

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Section: Introductionmentioning

confidence: 99%

Caspase Inhibitor Diminishes Caffeic Acid-induced Apoptosis in Osteosarcoma Cells

et al. 2017

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“…(16) Inhibition on RANKL and TNF-α-induced osteoclastogenesis by some agents has been reported, including osteoprotegerin (17), Simon extract (13) and its constituent, caffeic acid (10,(12)(13)(14). However, mechanism of caffeic acid in inhibiting osteoclastogenesis remained unclear.…”

Section: Discussionmentioning

confidence: 99%

“…(6,7) Among the MAPK family, p38 MAPK has been reported to play an important role in osteoclastogenesis. (8,9) Caffeic acid attracts much special attention because of its ability to protect the human from several diseases, including cancer (10,11) and bone resorption (12)(13)(14). Caffeic acid induced osteosarcoma cells into apoptosis by activation of Caspases, including Caspase-8, -9 and -3.…”

Section: Introductionmentioning

confidence: 99%

“…(10,11) Meanwhile in order to protect from bone resorption, caffeic acid targets osteoclastogenesis. (12)(13)(14) Caffeic acid did not induce apoptosis in PNCs (12), but it inhibited osteoclastogenesis by inhibiting expression of Cathepsin K and Nuclear Factor of Activated T cells (NFATc)1 (13), as well as inhibiting activity of Nuclear Factor kB (NFkB) (12). However, caffeic acid did not target the expression of TNF Receptor-associated Factor (TRAF)6.…”

Section: Introductionmentioning

confidence: 99%

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Caffeic Acid Inhibits RANKL and TNF-α-induced Phosphorylation of p38 Mitogen-activated Protein Kinase in RAW-D Cells

Sandra

Ketherin

2018

Indones Biomed J

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B ACKGROUND:Caffeic acid inhibits osteoclastogenesis by downregulating expression of Cathepsin K and Nuclear Factor of Activated T cells (NFATc)1, as well as inhibiting activity of Nuclear Factor kB (NFkB). Meanwhile TNF Receptor-associated Factor (TRAF)6 was not influenced by caffeic acid. In order to investigate further caffeic acid's mechanism in inhibiting osteoclastogenesis, regulation of caffeic acid on p38 Mitogen-activated Protein Kinase (MAPK) was investigated.METHODS: RAW-D cells were pretreated with/without caffeic acid and treated with/without 20 ng/mL RANKL and 1 ng/mL TNFα for 0.2, 1, 6, and 12 hour. Tartrate Resistant Acid Phosphatase (TRAP) staining was performed. Then, western blot analysis was performed to detect p38 MAPK and phosphorylated-p38 MAPK. Resulted protein bands were quantified and statistically analyzed. RESULTS:Under induction of 20 ng/mL RANKL and 1 ng/ mL TNF-α, RAW-D cells were successfully differentiated into TRAP + osteoclast-like polynuclear cells. Under treatment of 20 ng/mL of RANKL and 1 ng/mL of TNF-α for 0.2 or 1 hour, significant (p=0,000, T test) increment of phosphorylated p38 MAPK was observed as compared with control. Pretreatment of 10 µg/mL caffeic acid significantly (p=0.000, T test) suppressed the 20 ng/mL of RANKL and 1 ng/mL of TNF-α-induced phosphorylation of p38 MAPK.

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“…Indonesia with its wide biodiversities has plenty of resourceful natural materials those should be explored. Previously our team reported several potential extracts derived from plants including Ipomea batatas (1)(2)(3), Artocarpus altilis (4), Piper crocatum (5), Kleinhovia hospita (6), Artocarpus heterophyllus (7), Catharanthus roseus (8), Piper betle (9), Catharanthus roseus (9), Dendrophtoe petandra (9), Curcuma mangga (9), Curcuma longa (10), Ananas comosus (11), Brucea javanica (12,13), Nephelium lappaceum (14), Cucumis melo (15,16), Caesalpinia sappan (17) and Artocarpus elasticus (18). These extracts shows various activities, including osteoclastogenesis inhibition (1-3), apoptosis induction or proliferation Results inhibition on breast cancer cells (4,5,(7)(8)(9), antioxidant (6,14,16,18), proliferation and differentiation induction on stem cell (10,15), and apoptosis induction on human oral squamous cell carcinoma (12,13,16,17).…”

Section: Introductionmentioning

confidence: 99%

Cytotoxicity of Alpinia galanga Rhizome Crude Extract on NIH-3T3 Cells

et al. 2017

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B ACKGROUND:Alpinia galanga (A. galanga) was reported as a potential medicinal source due to its wide effect. A. galanga rhizome crude extract (ARCE) was reported to have high cytotoxic effect in cancer cells, but low in normal cells. However half maximal inhibitory concentration (IC 50 ) of ARCE is not clearly known yet. Hence, current study was conducted to investigate the IC 50 of ARCE in normal standard fibroblast cell line, NIH-3T3 cells. METHODS:Rhizomes of A. galanga were collected, peeled, dried, milled and weighed. Extraction was performed using maceration method, then filtered and evaporated. ARCE with various concentrations were applied in NIH-3T3 cells for 24 or 48 hours. Cells were documented and counted with 3-(4,5-dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium bromide (MTT) assay. RESULTS:Five hundreds grams of simplicia were macerated with ethanol and evaporated, 1 mg/mL crude extract with total volume of 114 mL was obtained. By addition of ARCE in NIH-3T3 cell culture, number of NIH-3T3 cells were shown less when treated with higher concentration of ARCE. Cell numbers of 0, 3.125, 6.25, 12.5, 25 and 50% ARCE treatment for 24 hours are 11, 531, 11,352, 10,920, 10,365, 9,471, 8,360, respectively, meanwhile for 48 hours are 13,219, 12,686, 12,278, 11,390, 10,279, 8,390, respectively. CONCLUSION: IC 50 of ARCE in 24 hours treatment was 620.5 mg/mL, while in 48 hours treatment was 666.6 mg/ mL. Hence, ARCE is suggested to have low cytotoxic effect in NIH-3T3 cells. KEYWORDS:

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Regulation of osteoclastogenesis by Simon extracts composed of caffeic acid and related compounds: successful suppression of bone destruction accompanied with adjuvant-induced arthritis in rats

Cited by 43 publications

References 41 publications

Caspase Inhibitor Diminishes Caffeic Acid-induced Apoptosis in Osteosarcoma Cells

Caspase Inhibitor Diminishes Caffeic Acid-induced Apoptosis in Osteosarcoma Cells

Caffeic Acid Inhibits RANKL and TNF-α-induced Phosphorylation of p38 Mitogen-activated Protein Kinase in RAW-D Cells

Cytotoxicity of Alpinia galanga Rhizome Crude Extract on NIH-3T3 Cells

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