Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00369 (ROS)
 19,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study is to investigate the protective actions of guggulsterone against the cytotoxicity produced by exposure to hydrogen peroxide (H2O2) in PC12 cells. It was evaluated by MTT [3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl-tetrazolium bromide] reduction assay, lactate dehydrogenase (LDH) release assay, and the release of nitric oxide (NO). ROS and Ca2+ in cells were evaluated by DCFH and Fura 2-AM, respectively. Mitochondrial membrane potential (MMP) was assessed by the retention of rhodamine 123 (Rh 123). Apoptosis and morphological alteration in PC12 cells were monitored with flow cytometry and electric microscope. Vitamin E, a potent antioxidant, was employed as a comparative agent. The results showed that preincubation of PC12 cells with guggulsterone (0.1 - 10 micromol x L(-1)) prevented cytotoxicity induced by H2O2. Extracellular accumulation of LDH, NO and intracellular accumulation of ROS, Ca2+ resulting from H2O2 were significantly reduced by guggulsterone. Incubation of cells with H2O2 caused a marked decrease in MMP, which was significantly inhibited by guggulsterone. The percentage of H2O2-induced apoptosis in PC12 cells was 24.3%, and decreased in the presence of guggulsterone (0.1 - 10 micromol x L(-1)) by 18.4%, 15.9%, 11.8%, respectively. Guggulsterone exhibited comparable potency against oxidative stress induced by H2O2 in PC12 cells as that of vitamin E. The present findings showed that guggulsterone attenuated H2O2-induced cytotoxicity, extracellular accumulation of LDH and NO, intracellular accumulation of ROS and Ca2+, loss of MMP, and apoptosis, which may represent the cellular mechanisms for its neuroprotective action.
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PMID:Protection against hydrogen peroxide-induced cytotoxicity in PC12 cells by guggulsterone. 1924 48

Fucoxanthin is a carotenoid isolated from Sargassum siliquastrum and is considered to be one of major active compound of marine algae. In this study, we investigated and confirmed the protective effect of fucoxanthin on UV-B induced cell injury in human fibroblast via 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA), 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT), and comet assays. Intracellular ROS generated by exposure to UV-B radiation, which was significantly decreased by addition with various concentrations of fucoxanthin. Cell survival rate was increased with fucoxanthin pre-treated cells, which was reached around 81.47% at 100 microM, and the inhibitory effect of cell damage exhibited dose-dependent manner. Moreover, fucoxanthin having protective properties was demonstrated via Hoechst 33342/PI staining. Hence, on the basis of the above-mentioned studies, fucoxanthin has the ability to protect against oxidative stress induced by UV-B radiation and which might be applied to antioxidant and cosmeceutical industries.
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PMID:Protective effect of fucoxanthin isolated from Sargassum siliquastrum on UV-B induced cell damage. 1926 1

Current therapies for breast cancer are often limited by short-term efficacy due to the emergence of drug resistance. In view of this, there is much interest in the identification of new agents for the treatment of breast cancer. Rose Bengal (RB) has been used as a photosensitiser in photodynamic treatment. In the present study, we investigated the direct cytotoxic and proapoptotic effects of RB, not as a photosensitiser, in MCF-7 cells. Cell viability was quantitated by MTT assay. Apoptotic cells were determined using PI staining of DNA fragmentation by flow cytometry. Bax protein expression was studied by western blotting. ROS was measured using DCF-DA by flow cytometry analysis. The result showed RB decreased cell viability in MCF-7 cells in a concentration- and time-dependent manner. RB induced a sub-G1 peak in flow cytometry histogram of treated cells indicating apoptosis is involved in this toxicity. In Western blot analysis, Bax expression significantly increased in RB-treated cells. RB could also increase ROS production in MCF-7 cells but antioxidant GSH could not decrease the toxicity indicating this toxicity was independent of ROS production. Thus RB exerts proapoptotic effects in a MCF-7 cells and could be considered as a potential chemotherapeutic agent in breast cancer.
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PMID:Direct toxicity of Rose Bengal in MCF-7 cell line: role of apoptosis. 1927 Dec 85

Trihydroxybenzoic acid dimmer is an anti-tumor compound which is separated from water-caltrop. This study is aimed to investigate its anti-proliferation effect on HL-60 cells and the possible mechanism of inducing apoptosis. MTT assay was used to test HL-60 cells proliferation. The apoptosis, ROS levels and the mitochondrial membrane potential were detected by flow cytometry. Cytochrome c released from mitochondria to cytosol fraction was detected by Western blotting. The activity of Caspase-9 and Caspase-3 were measured by colorimetric method. It was found to inhibit HL-60 cells proliferation in a dose and time-dependent manner. Compared with control group, it caused the increase of ROS levels and a concomitant dissipation of the mitochondrial membrane potential and induced cytosolic accumulation of cytochrome c and activities Caspase-9 and Caspase-3. Therefore it can be concluded that mitochondrial-dependent pathways was involved in its induction of apoptosis of HL-60 cells.
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PMID:[Effect of trihydroxybenzoic acid dimmer on induction of apoptosis of HL-60 cells]. 1935 Aug 20

In a previous study, we demonstrated that baicalein induces hydroxyl radical formation in human platelets but the mechanisms are unclear. Herein, we show, using an electron spin resonance technique, that baicalein also induces hydroxyl radical formation in B16F10 melanoma cells in a dose-dependent manner. Baicalein produced superoxide anions in the presence of an iron chelator and superoxide dismutase (SOD) inhibitor. We suggest that superoxide anions produced by baicalein were promptly converted to hydroxyl radicals through SOD and the Fenton reaction in B16F10 melanoma cells. According to Western blotting results, the 12-LOX protein was expressed in B16F10 melanoma cells, but baicalein had no effect on 12-LOX expression. Decreases in 12-LOX protein expression and hydroxyl radical signals occurred in a 12-LOX small interfering RNA knockdown protein group compared with the baicalein control. In the MTT assay, we also found that baicalein caused a reduction in cellular viability, which was reversed by the addition of ROS scavengers. On the basis of these data, we conclude that ROS formation catalyzed by 12-LOX is one possible mechanism of growth inhibition by baicalein in B16F10 melanoma cells.
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PMID:Baicalein induces proliferation inhibition in B16F10 melanoma cells by generating reactive oxygen species via 12-lipoxygenase. 1943 16

The aim of this study was to investigate the anti-tumor effects and mechanism of the selenium heteropoly compound (C(2)H(10)N(2))(5)(NH(4))(4)H(2)[Se(2)W(10)V(8)O(62)].9H(2)O (SeWV) in K562 cells. The results showed that 0.32-10.15 x 10(-3) mmol/l SeWV could significantly inhibit the proliferation of K562 cells in vitro, as determined by the MTT assay, with IC(50) values of 3.07 and 2.69 x 10(-3) mmol/l after 48 and 72 h of treatment with SeWV, respectively. Studies of the cell cycle indicated that SeWV could induce K562 cells gathered in the G(2)/M phase upon treatment for 24 and 48 h, and a significant sub-G1 peak was evident at 0.32 and 2.54 x 10(-3) mmol/l after treatment for 24 h. Morphological observations revealed typical apoptotic features. SeWV caused the accumulation of Ca(2+), Mg(2+) and ROS, and the reduction of pH and mitochondrial membrane potential (MMP) in K562 cells as evidenced by confocal laser scanning microscopy. Experiments also showed that the expression of Bcl-2 was significantly inhibited, but Bax was increased by SeWVat 5.07 x 10(-3) mmol/l. Additionally, the content of cytochrome-C was increased after treatment for 24 h. The experiment implied that SeWV had anti-tumor activity and that its mechanism was partially attributable to the induction of cell cycle distribution and apoptosis that was induced by a change in intracellular ion homeostasis.
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PMID:Antitumor effects of a selenium heteropoly complex in K562 cells. 1944 41

After operative restoration, some monomers released from dentin bonding agents or composite resin may induce tissue inflammation and affect the vitality of dental pulp. Whether BisGMA, a major monomer of composite resin, may induce prostaglandin release and cytotoxicity to pulp cells and their mechanisms awaits investigation. We found that BisGMA induced cytotoxicity to human dental pulp cells at concentrations higher than 0.075 mm as analyzed by 3-(4,5-dimethyldiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. BisGMA (0.1 mm) also stimulated ERK phosphorylation, PGE(2) production, COX-2 mRNA and protein expression as well as ROS production (as indicated by an increase in cellular DCF fluorescence) in dental pulp cells. Catalase (500 and 1000 U/ml) and U0126 (10 and 20 microm, a MEK inhibitor) effectively prevented the BisGMA-induced ERK activation, PGE(2) production and COX-2 expression. Moreover, catalase can protect the pulp cells from BisGMA cytotoxicity, whereas aspirin and U0126 lacked of this protective activity. These results suggest that BisGMA released from composite resin may potentially affect the vitality of dental pulp and induce pulpal inflammation via stimulation of ROS production, MEK/ERK1/2 activation and subsequent COX-2 gene expression and PGE(2) production. Cytotoxicity of BisGMA to dental pulp cells is related to ROS production, but not directly mediated by MEK activation and PGE(2) production.
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PMID:The effect of BisGMA on cyclooxygenase-2 expression, PGE2 production and cytotoxicity via reactive oxygen species- and MEK/ERK-dependent and -independent pathways. 1946 1

In the present study, three kinds of phlorotannins, marine algal polyphenol, were isolated from a brown alga Ecklonia cava, and their inhibitory effect on melanogenesis as well as the protective effect against photo-oxidative stress induced by UV-B radiation was investigated. The effect on melanogenesis was evaluated via the inhibitory effects of tyrosinase and melanin synthesis. Among the phlorotannins, dieckol showed higher effect than that of the other phlorotannins in the both assays; especially the value of dieckol in the tyrosinase inhibition assay was relatively higher than that of a commercial tyrosinase inhibitor (kojic acid). The UV-B protection effect was evaluated via DCFH-DA, MTT, comet assays, and morphological changes in fibroblast. Intracellular ROS induced by UV-B radiation was reduced by the addition of phlorotannins and cell viability was dose-dependently increased. Moreover, dieckol demonstrated strong protective properties against UV-B radiation-induced DNA damage via damaged tail intensity and morphological changes in fibroblast. Hence, these results indicated that dieckol isolated from E. cava has potential whitening effects and prominent protective effects on UV-B radiation-induced cell damages, which might be used in pharmaceutical and cosmeceutical industries.
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PMID:Effect of phlorotannins isolated from Ecklonia cava on melanogenesis and their protective effect against photo-oxidative stress induced by UV-B radiation. 1949 Sep 39

The energy reduction-induced death of retinal ganglion cells is associated with many ophthalmic diseases. The present study was designed to investigate the apoptosis pathway of retinal ganglion cells (RGC-5) following acute ATP reduction by using glucose deprivation (GD). RGC-5 cells were cultured in glucose-free or normal DMEM for 3 days. The changes in intracellular ATP and cell viability were monitored by ATP assay and MTT assay. APOPercentage and in situ TUNEL assays were used to determine the cell death pattern. The involvement of oxidative stress was assessed by measuring intracellular ROS generation, the HO-1 expression, the effect of antioxidants, and the ratio of GSSG to total GSH. The activation of p53 and apoptosis markers was evaluated by Western blotting. We found that glucose deprivation caused an acute decline of intracellular ATP level, concomitantly decreasing cell viability. The cell death exhibited typical features indicative of apoptosis, including cell shrinkage, phosphatidylserine externalization and DNA fragmentation. Oxidative stress was involved in the cell death process; an antioxidant significantly protected the cells against glucose deprivation. p53 and apoptosis markers, caspase-3 and PARP-1 were activated after RGC-5 cells were cultured in glucose-free media for 32 h. Z-VAD-fmk, a pan-caspase inhibitor, was sufficient to prevent apoptosis. These results suggest that acute energy reduction induced by glucose deprivation triggers caspase-dependent apoptosis and activates p53. Blocking the critical steps in this cell death pathway may have therapeutic effects, rescuing the retinal ganglion cells from damages associated with acute energy reduction.
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PMID:Acute energy reduction induces caspase-dependent apoptosis and activates p53 in retinal ganglion cells (RGC-5). 1952 68

We investigate the correlation between the glycosylation modified prion proteins and apoptosis. The wild-type PRNP gene and four PRNP gene glycosylated mutants were transiently expressed in HeLa cells. The effect of apoptosis induced by PrP mutants was confirmed by MTT assay, Hochest staining, Annexin-V staining and PI staining. ROS test detected ROS generation within the cells. The mitochondrial membrane potential was analyzed by the flow cytometry. The expression levels of Bcl-xL, Bax, cleaved Caspase-9 proteins were analyzed by Western Blot. The results indicated that the expressed non-glycosylated PrP in HeLa cells obviously induced apoptosis, inhibited the growth of cells and reduced the mitochondrial membrane potential, and more ROS generation and low levels of the apoptosis-related proteins Bcl-xL, the activated the cleaved Caspase-9 proteins were found. The apoptosis induced by non-glycosylated PrP demonstrates that its underlying mechanism correlates with the mitochondria-mediated signal transduction pathway.
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PMID:Glycosylation modification of human prion protein provokes apoptosis in HeLa cells in vitro. 1955 90


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