Esculetin induces apoptosis in human colon cancer cells by inducing endoplasmic reticulum stress.

Colorectal cancer has become more common in many regions of the world. Recently, we showed that esculetin, a natural coumarin, induces apoptosis in HT-29 colon cancer cells via the reactive oxygen species-mediated mitochondrial pathway. The present study examined whether esculetin induces apoptosis in HT-29 colon cancer cells by inducing endoplasmic reticulum (ER) stress.

Involvement of glutathione and glutathione metabolizing enzymes in human colorectal cancer cell lines and tissues.

Reduced glutathione (GSH) is an abundant tripeptide present in the majority of cell types. GSH is highly reactive and is often conjugated to other molecules, via its sulfhydryl moiety. GSH is synthesized from glutamic acid, cysteine, and glycine via two sequential ATP‑consuming steps, which are catalyzed by glutamate cysteine ligase (GCL) and GSH synthetase (GSS).

Esculetin induces death of human colon cancer cells via the reactive oxygen species-mediated mitochondrial apoptosis pathway.

The present study investigated the apoptotic effects of esculetin, a coumarin derivative, on the human colon cancer cell line HT-29. Esculetin had cytotoxic effects on HT-29 cells in a dose- and time-dependent manner; treatment with 55 μg/mL esculetin reduced cell viability by 50%. Esculetin induced apoptosis, as evidenced by apoptotic body formation, an increased percentage of cells in sub-G1 phase, and DNA fragmentation.

Cytoprotective effect of eckol against oxidative stress-induced mitochondrial dysfunction: involvement of the FoxO3a/AMPK pathway.

This study investigated the cytoprotective effect of Ecklonia cava-derived eckol against H2O2-induced mitochondrial dysfunction in Chang liver cells. While H2O2 augmented levels of mitochondrial reactive oxygen species (ROS), eckol decreased it. Eckol also attenuated high intracellular Ca(2+) levels stimulated by H2O2 and recovered H2O2-diminished ATP levels and succinate dehydrogenase activity.

Cytotoxic effect of clerosterol isolated from Codium fragile on A2058 human melanoma cells.

The cytotoxic effects and mechanism of action of clerosterol, isolated from the marine alga Codium fragile, were investigated in A2058 human melanoma cells. Clerosterol inhibited the growth of A2058 cells with an IC(50) of 150 µM and induced apoptotic cell death, as evidenced by DNA fragmentation, an increase in the number of sub-G(1) hypodiploid cells and the presence of apoptotic bodies. Clerosterol treatment caused the loss of mitochondrial membrane potential.

The green algae Ulva fasciata Delile extract induces apoptotic cell death in human colon cancer cells.

This study investigated the mechanisms underlying the cytotoxicity of the green algae Ulva fasciata Delile. U. fasciata extract (UFE) inhibited the growth of HCT 116 human colon cancer cells by 50% at a concentration of 200 μg/ml.

Increased glutathione synthesis following Nrf2 activation by vanadyl sulfate in human chang liver cells.

Jeju ground water, containing vanadium compounds, was shown to increase glutathione (GSH) levels as determined by a colorimetric assay and confocal microscopy. To investigate whether the effects of Jeju ground water on GSH were specifically mediated by vanadium compounds, human Chang liver cells were incubated for 10 passages in media containing deionized distilled water (DDW), Jeju ground water (S1 and S3), and vanadyl sulfate (VOSO(4)). Vanadyl sulfate scavenged superoxide anion, hydroxyl radical and intracellular reactive oxygen species.

Jeju ground water containing vanadium enhances antioxidant systems in human liver cells.

Vanadium compounds have shown promise in the treatment of diabetes and in cancer prevention. The aim of this study is to investigate the effects of Jeju ground water, containing the vanadium compounds S1 (8.0 ± 0.

Molecular docking studies of a phlorotannin, dieckol isolated from Ecklonia cava with tyrosinase inhibitory activity.

In this study, the phlorotannin dieckol, which was isolated from the brown alga Ecklonia cava, was examined for its inhibitory effects on melanin synthesis. Tyrosinase inhibitors are important agents for cosmetic products. We therefore examined the inhibitory effects of dieckol on mushroom tyrosinase and melanin synthesis, and analyzed its binding modes using the crystal structure of Bacillus megaterium tyrosinase (PDB ID: 3NM8).

Endoplasmic reticulum stress signaling is involved in silver nanoparticles-induced apoptosis.

Although silver nanoparticles (AgNPs) have been reported to exert strong acute toxic effects on various cultured cells by inducing oxidative stress, the molecular mechanisms by which AgNPs-damaged cells are unknown. Because the endoplasmic reticulum (ER) may play an important role in the response to oxidative stress-induced damage and is quite sensitive to oxidative damage, we hypothesized that AgNPs may exert cytotoxic effects on cells by modulating ER stress. In our study, AgNPs resulted in cytotoxicity and apoptotic cell death when analyzing cell viability, DNA fragmentation and the apoptotic sub-G(1) population.

Ginseng saponin metabolite induces apoptosis in MCF-7 breast cancer cells through the modulation of AMP-activated protein kinase.

Previous studies have shown that the ginseng saponin metabolite, Compound K (20-O-d-glucopyranosyl-20(S)-protopanaxadiol, IH901), suppresses proliferation of various cancers and induces apoptosis. AMP-activated protein kinase (AMPK) is a sensor of cellular energy states and is involved in apoptosis of cancer cells. We hypothesized that Compound K may exert cytotoxicity in MCF-7 human breast cancer cells through modulation of AMPK, followed by a decrease in cyclooxygenase-2 (COX-2) expression.

Butin (7,3',4'-trihydroxydihydroflavone) reduces oxidative stress-induced cell death via inhibition of the mitochondria-dependent apoptotic pathway.

Recently, we demonstrated that butin (7,3',4'-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H(2)O(2))-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H(2)O(2)-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3.

Phenylpropanoids from the leaves of Acanthopanax koreanum and their antioxidant activity.

By various chromatographic methods, one new phenylpropanoid, acanthopanic acid (1), and three known compounds, 1,2-O-dicaffeoylcyclopenta-3-ol (2), (4S)-α-terpineol 8-O-β-D-glucopyranoside (3), and rutin (4), were isolated from the methanol extract of the Acanthopanax koreanum leaves. Their structures were elucidated on the basis of spectroscopic analyses, and their antioxidant activities were evaluated by the intracellular reactive oxygen species (ROS) radical scavenging 2',7'-dichlorofluorescein diacetate assay. Among them, compounds 1, 2, and 4 showed significant scavenging capacity with IC(50) values of 3.

Cytoprotective effect of the fruits of Lycium chinense Miller against oxidative stress-induced hepatotoxicity.

Aim Of The Study: Fruits of Lycium chinense Miller (Solanaceae), distributed in northeast Asia, have gained attraction for their hepatoprotective role in traditional oriental medicine. The excessive production of reactive oxygen species (ROS) is hazardous for living organisms and damage major cellular constituents such as DNA, lipid, and protein. The cytoprotective effect of Lycium chinense fruits (Lycium extract) was assessed against H(2)O(2)-induced Chang liver cell damage.