Effect of curcumin on the proliferation and apoptosis of hepatic stellate cells

Shu, Jian-chang; He, Yi; Lv, Xin; Zhao, J-R; Shen, Yan; Ye, GR; Wang, Lexin

doi:10.1590/s0100-879x2009005000041

Cited by 15 publications

(10 citation statements)

References 14 publications

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“…At 46–49 µM curcuminoid concentrations, cell death is largely due to apoptosis via the activation of caspase 3/7 by both extrinsic (caspase 8) and intrinsic pathways (caspase 9). In this respect, these results are consistent with those reported for other cell lines at 20–100 µM curcumin concentrations [36], [57], [58], [59], [60] and for mouse embryos at 6–24 µM concentrations [55]. However, in NT2/D1 cells there is also a generalized activation of caspases in response to higher levels of curcuminoids (Fig.…”

Section: Discussionsupporting

confidence: 92%

Curcuminoid Binding to Embryonal Carcinoma Cells: Reductive Metabolism, Induction of Apoptosis, Senescence, and Inhibition of Cell Proliferation

Quitschke

2012

PLoS ONE

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Curcumin preparations typically contain a mixture of polyphenols, collectively referred to as curcuminoids. In addition to the primary component curcumin, they also contain smaller amounts of the co-extracted derivatives demethoxycurcumin and bisdemethoxycurcumin. Curcuminoids can be differentially solubilized in serum, which allows for the systematic analysis of concentration-dependent cellular binding, biological effects, and metabolism. Technical grade curcumin was solubilized in fetal calf serum by two alternative methods yielding saturated preparations containing either predominantly curcumin (60%) or bisdemethoxycurcumin (55%). Continual exposure of NT2/D1 cells for 4–6 days to either preparation in cell culture media reduced cell division (1–5 µM), induced senescence (6–7 µM) or comprehensive cell death (8–10 µM) in a concentration-dependent manner. Some of these effects could also be elicited in cells transiently exposed to higher concentrations of curcuminoids (47 µM) for 0.5–4 h. Curcuminoids induced apoptosis by generalized activation of caspases but without nucleosomal fragmentation. The equilibrium binding of serum-solubilized curcuminoids to NT2/D1 cells incubated with increasing amounts of curcuminoid-saturated serum occurred with apparent overall dissociation constants in the 6–10 µM range. However, the presence of excess free serum decreased cellular binding in a hyperbolic manner. Cellular binding was overwhelmingly associated with membrane fractions and bound curcuminoids were metabolized in NT2/D1 cells via a previously unidentified reduction pathway. Both the binding affinities for curcuminoids and their reductive metabolic pathways varied in other cell lines. These results suggest that curcuminoids interact with cellular binding sites, thereby activating signal transduction pathways that initiate a variety of biological responses. The dose-dependent effects of these responses further imply that distinct cellular pathways are sequentially activated and that this activation is dependent on the affinity of curcuminoids for the respective binding sites. Defined serum-solubilized curcuminoids used in cell culture media are thus suitable for further investigating the differential activation of signal transduction pathways.

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Section: Discussionsupporting

confidence: 92%

Curcuminoid Binding to Embryonal Carcinoma Cells: Reductive Metabolism, Induction of Apoptosis, Senescence, and Inhibition of Cell Proliferation

Quitschke

2012

PLoS ONE

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“…But our data revealed that S phase in untreated individuals have gradually decrease from zero to 2 nd , 4 th and 6 th day (M±SD= 6.56±2.41, 4.92±8.01, 2.64±3.82 and 2.83±3.71, respectively), was in lower frequency of PBMCs when compared with the treated group, S phase values have marked decrease from zero to 2 nd , 4 th and 6 th days (M±SD= 12.03±10.28, 1.24±2.64, 1.16±2.31 and 2.82±4.75, respectively), these results didn't agree with (36) . But these decrements are in agreement with (37) that have studied the effect of curcumin on the proliferation and apoptosis of hepatic stellate cells (HSC) and indicated that Curcumin inhibits HSC proliferation in the S phase and induces apoptosis, this related to the activation of peroxisome proliferator (38) .…”

Section: Discussionsupporting

confidence: 90%

In Vivo and in Vitro Expressions of Ccr1 and Ccr5 in Patients With Active Schistosomiasis and Chronic Liver Disease

El‐Masry¹,

Gouida²,

El-azab³

et al. 2010

Biochemistry Letters

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The CCL3 receptors, CCR1 and CCR5, are expressed in a series of cell types. The aim of the present study was to demonstrate, in vitro and in vivo, expressions of CCR1 and CCR5 on peripheral blood mononuclear cells (PBMCs) from healthy individuals and Schistosoma mansoni (S. mansoni) infected patients with chronic liver diseases (CLD). PBMCs were isolated from the blood of 55 individuals divided into four groups; Group I: thirty one patients with CLD; group II: six patients with active S. mansoni infection, diagnosed by parasitological examination; group III: eight healthy individuals, non-infected with both schistosomiasis or viral infections, followed by treatment with soluble S. mansoni eggs antigens (SEA) after short term cells culture, for in vitro studies and group IV: ten healthy individuals, non-infected with both schistosomiasis or viral infections and served as a negative control group. All PBMCs from the studied groups were stained with monoclonal antibodies against CD4, CD8, CCR1 and CCR5, then detected by a flow cytometry technique. In-vitro study revealed that CCR1 and CCR5 expressions in SEA treated short term culture of PBMCs were not significantly lower than healthy controls (P=0.56 and 0.298, respectively). Also, In-vivo study, in active schistosomiasis patients, the decrement were not significant (P=0.313 and 0.093, respectively) compared with a healthy control group. While in CLD patients there was an increment in expression of CCR1 with significant value (p=0.014), as well as in CCR5 but the increment were not significant (P=0.099). Patients with active schistosomiasis showed lower CD4 and higher CD8 T-cells count compared with healthy controls. The expressions of CD4 and CD8 T-cells were not significant (P= 0.368, 0.875, respectively). CCR1 and CCR5 expressions may play a role in recruitment of lymphocytes to the CLD patients. CD4 was down regulated and CD8 T cells were up regulated in PBMCs of active schistosomiasis patients.

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“…Dietary administration of curcumin was shown to improve both acute and subacute liver injuries (63) as well as liver fibrosis induced by CCl 4 (64). The possible drug action mechanisms included inhibition of HSC proliferation (65–70) and activation (71), and apoptosis induction (68, 72). Curcumin could also inhibit ECM secretion by HSCs (66) by modulating the expressions and activities of MMPs (73).…”

Section: Liver Fibrosis – Aetiology Pathogenesis and Herbal Medicinamentioning

confidence: 99%

Traditional Chinese herbal medicines for treatment of liver fibrosis and cancer: from laboratory discovery to clinical evaluation

Luk

Wang

Liu

et al. 2007

Liver International

115

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Effect of curcumin on the proliferation and apoptosis of hepatic stellate cells

Cited by 15 publications

References 14 publications

Curcuminoid Binding to Embryonal Carcinoma Cells: Reductive Metabolism, Induction of Apoptosis, Senescence, and Inhibition of Cell Proliferation

Curcuminoid Binding to Embryonal Carcinoma Cells: Reductive Metabolism, Induction of Apoptosis, Senescence, and Inhibition of Cell Proliferation

In Vivo and in Vitro Expressions of Ccr1 and Ccr5 in Patients With Active Schistosomiasis and Chronic Liver Disease

Traditional Chinese herbal medicines for treatment of liver fibrosis and cancer: from laboratory discovery to clinical evaluation

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