Immuno-regulatory Effects of CKBM on the Activities of Mitogen-Activated Protein Kinases and the Release of Cytokines in THP-1 Monocytic Cells

Chan, Anthony; Yip, E. C. H.; Yung, Lisa Y.; Pang, Haihong; Luk, Sharon; Pang, S.F.; Wong, Yung Hou

doi:10.1248/bpb.28.1645

Cited by 17 publications

(19 citation statements)

References 35 publications

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“…However, recent studies have shown that many naturally occurring compounds in medicinal herbs stimulate intracellular signal transduction pathways for the manifestation of their biological effects (Yu et al, 2004;Chan et al, 2005a,). This is especially true for their regulatory actions on the MAPK cascades.…”

Section: Resultsmentioning

confidence: 99%

Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism

et al. 2006

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Section: Resultsmentioning

confidence: 99%

Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism

et al. 2006

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“…BLCa is a heterogeneous disease with a propensity to become invasive; thus it is essential that any treatment regime targets Table 1 and verified in Table 2. effector molecules, functional systems or metabolic pathways that are active in disease progression. MINA-05 contains a combination of botanical extracts that have been shown individually to induce cell cycle arrest, inhibit tumour growth, have antiviral activity or boost the immune responses in patients with various gastrological and urological conditions [7][8][9][10][11]23]. Additionally, MINA-05 has been shown to inhibit cellular proliferation of human androgen-sensitive and hormone refractory prostate cancer cell lines [13].…”

Section: Discussionmentioning

confidence: 99%

Alterations to the protein profile of bladder carcinoma cell lines induced by plant extract MINA‐05 in vitro

Nguyen-Khuong¹,

White²,

Hung

et al. 2009

Proteomics

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Bladder cancer (BLCa) is a severe urological cancer of both men and women that commonly recurs and once invasive, is difficult to treat. MINA-05 (CK Life Sciences Int'l, Hong Kong) is a derivative of complex botanical extracts, shown to reduce cellular proliferation of bladder and prostate carcinomas. We tested the effects of MINA-05 against human BLCa cell sublines, B8, B8-RSP-GCK, B8-RSP-LN and C3, from a transitional cell carcinoma, grade IV, to determine the molecular targets of treatment by observing the cellular protein profile. Cells were acclimatised for 48 h then treated for 72 h with concentrations of MINA-05 reflecting 1/2 IC(50), IC(50) and 2 x IC(50) (n = 3) or with vehicle, (0.5% DMSO). Dose-dependant changes in protein abundance were detected and characterised using 2-dimensional electrophoresis and MS. We identified 10 proteins that underwent changes in abundance, pI and/or molecular mass in response to treatment. MINA-05 was shown to influence proteins across numerous functional classes including cytoskeletal proteins, energy metabolism proteins, protein degradation proteins and tumour suppressors, suggesting a global impact on these cell lines. This study implies that the ability of MINA-05 to retard cellular proliferation is attributed to its ability to alter cell cycling, metabolism, protein degradation and the cancer cell environment.

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“…23) Briefly, serum-starved THP-1 cells were maintained at a density of 6.25ϫ10 5 cells/ ml in the absence or presence of rotenone for various time intervals. The drug treatment was terminated by centrifugation (1000 rpm, 3 min) at 4°C, followed by aspiration of drug-containing medium and addition of 250 ml icecold lysis buffer (50 mM Tris-HCl, pH 7.4, 150 mM sodium chloride, 1 mM edetic acid, 0.25% Na-deoxycholate, 1% NP-40, 1 mM sodium fluoride, 1 mM sodium orthovanadate, 1 mM PMSF, 5 mg/ml leupeptin, 10 mg/ml aprotinin and 5 mg/ml pepstatin).…”

Section: Methodsmentioning

confidence: 99%

Monocyte-Mediated Rotenone Neurotoxicity towards Human Neuroblastoma SH-SY5Y: Role of Mitogen-Activated Protein Kinases

Zhao

Zhu

2006

Biological & Pharmaceutical Bulletin

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Rotenone, a naturally occurring, lipophilic compound from the roots of certain plants (Derris species) is used as the main component of many insecticides. Increasing evidence has suggested an important role for rotenone in the pathogenesis of Parkinson's disease (PD). Mechanistically, rotenoneinduced dopaminergic neurodegeneration has been associated with both its inhibition of neuronal mitochondrial complex I and the enhancement of activated microglia. [1][2][3][4][5] The activation of glia, particularly microglia is the hallmark of brain inflammation. Recently, increasing evidences from human and animal studies have suggested that neuroinflammation is an important contributor to the neuronal loss in PD. 3,[6][7][8][9] In addition, inhibition of the inflammatory reaction could attenuate degeneration of nigrostriatal dopaminecontaining neurons in several models of PD.10) Previous studies have demonstrated that microglia-enhanced rotenone neurotoxicity can be attributed to the release of NADPH oxidase-derived superoxide from activated microglia and in turn the oxidation of dopamine (DA) to the o-quinone dopaminochrome (DACHR) extracellularly. 4,11) In these cultures, superoxide was considered a dominant degenerative factor for the dopaminergic neurons. However, given that SOD and catalase afforded only a partial neuroprotection and microglia also have the ability to release pro-inflammatory and neurotoxic factors, 3,12,13) exact mechanisms underlying the role of inflammatory response involved in rotenone-induced PD remain to be identified. Though several approaches have been used to examine direct neuron-glia interactions under controlled in vitro conditions, 3,14) in these primary coculture systems it is nearly impossible to study the intracellular events in pure microglia and dopaminergic neuron and the sequence of microglia-activation and DA neurotoxicity can not be clarified specifically. As a result, the potential implications of these two cells can not be validated precisely.Recent evidence indicates that cellular redox state promi- In the present study, we adopted two consequential linking cell systems to study the mechanisms underlying the microglia-enhanced rotenone neurotoxicity. The supernatant from rotenone-stimulated human monocytic THP-1 line was then used as the culture medium for SH-SY5Y neuroblastoma which was used as target neuronal cells. Human postmortem microglia behaved similarly to THP-1 cells. 18,19) We further investigated whether rotenone can regulate the intracellular signaling of monocytic THP-1 cells. MATERIALS AND METHODS MaterialsDulbecco's modified Eagle's medium (DMEM-F12) was purchased from GibcoBRL (Gaithersburg, MD, U.S.A.). Fetal calf serum was obtained from Hyclone (Logan, UT, U.S.A). Rotenone, propidium iodide (PI), 3-(4,5-dimethylthiazal-z-yl)-2,5-diphenylterazolium (MTT), chromatin dye bisbenzimide (Hoechst 33258), RNase were purchased from Sigma (St. Louis, MO, U.S.A). Antibodies for phospho-ERK (Thr202/Tyr204), phospho-JNK (Thr183/ Tyr185), phospho-p38 (Thr180/Tyr182) we...

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Immuno-regulatory Effects of CKBM on the Activities of Mitogen-Activated Protein Kinases and the Release of Cytokines in THP-1 Monocytic Cells

Cited by 17 publications

References 35 publications

Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism

Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism

Alterations to the protein profile of bladder carcinoma cell lines induced by plant extract MINA‐05 in vitro

Monocyte-Mediated Rotenone Neurotoxicity towards Human Neuroblastoma SH-SY5Y: Role of Mitogen-Activated Protein Kinases

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