Cocaine potentiates an inflammatory response in C6 astroglia-like cells.

Cocaine is a highly addictive drug that mediates its effect through altering dopamine metabolism in the central nervous system (CNS), resulting in a feeling of euphoria. Owing to its high lipophilicity, cocaine easily crosses the blood brain barrier of the CNS and reaches various domains of the brain, where it can trigger cellular damage. Cocaine-induced CNS damage may arise due to increased levels of free radicals and nitric oxide (NO) in immunecompetent astroglial cells.

Identification of cytotoxic markers in methamphetamine treated rat C6 astroglia-like cells.

Methamphetamine (METH) is a powerfully addictive psychostimulant that has a pronounced effect on the central nervous system (CNS). The present study aimed to assess METH toxicity in differentiated C6 astroglia-like cells through biochemical and toxicity markers with acute (1 h) and chronic (48 h) treatments. In the absence of external stimulants, cellular differentiation of neuronal morphology was achieved through reduced serum (2.

Cellular and molecular responses to acute cocaine treatment in neuronal-like N2a cells: potential mechanism for its resistance in cell death.

Cocaine is a highly abused drug that causes psychiatric and neurological problems. Its entry into neurons could alter cell-biochemistry and contribute in the manifestation of early pathological symptoms. We have previously shown the acute cocaine effects in rat C6 astroglia-like cells and found that these cells were highly sensitive to cocaine in terms of manifesting certain pathologies known to underlie psychological disorders.

Identification of biochemical and cytotoxic markers in cocaine treated PC12 cells.

Cocaine is one of the powerful addictive drugs, widely abused in most Western countries. Because of high lipophilic nature, cocaine easily reaches various domains of the central nervous system (CNS) and triggers different levels of cellular toxicity. The aim of this investigation was to reproduce cocaine toxicity in differentiated PC12 cells through quantitative knowledge on biochemical and cytotoxicity markers.

Substituted Tetrahydroisoquinolines as Microtubule-destabilizing Agents in Triple Negative Human Breast Cancer Cells.

Triple-negative breast cancer (TNBC) occurs at greater frequency amongst African-Americans, being characterized by the absence of estrogen receptor (ER), progesterone receptor (PR) and human epidermal receptor 2 (HER2). TNBC is often invasive and typically treated with cytostatic agents such as taxanes in combination with anthracyclines or platinum-based drugs. In this study, we synthesized a number of tetrahydroisoquinoline moieties by N-amination of substituted isoquinolines by O-mesytelene sulfonylhydroxylamine followed by ylide formation and reduction, which yielded the desired, substituted tetrahydroisoquinolines (THIQs) in moderate to good yield.

Anti-inflammatory effects of thymoquinone in activated BV-2 microglial cells.

Thymoquinone (TQ), the main pharmacological active ingredient within the black cumin seed (Nigella sativa) is believed to be responsible for the therapeutic effects on chronic inflammatory conditions such as arthritis, asthma and neurodegeneration. In this study, we evaluated the potential anti-inflammatory role of TQ in lipopolysaccharide (LPS)-stimulated BV-2 murine microglia cells. The results obtained indicate that TQ was effective in reducing NO2(-) with an IC50 of 5.

Characterization of 2-amino-1-methyl-6-phenylimidazo[4,5b]pyridine at androgen receptor: mechanistic support for its role in prostate cancer.

2-amino-1-methyl-6-phenylimidazo[4,5b]pyridine (PhIP) is a dietary mutagenic carcinogen that has been shown not only to induce the formation of DNA adducts, but is capable of inducing tumors in the colon, mammary, and prostate glands. The normal development and maturation of the prostate gland, as well as early progression of prostate cancer, is dependent on androgens acting on the androgen receptor (AR). The actual mechanism by which PhIP interacts with our biological system and its potential interaction at the AR has yet to be fully defined.

N-acetyl cysteine mitigates the acute effects of cocaine-induced toxicity in astroglia-like cells.

Cocaine has a short half-life of only about an hour but its effects, predominantly on the central nervous system (CNS), are fairly long-lasting. Of all cells within the CNS, astrocytes may be the first to display cocaine toxicity owing to their relative abundance in the brain. Cocaine entry could trigger several early response changes that adversely affect their survival, and inhibiting these changes could conversely increase their rate of survival.

Milk thistle seed extract protects rat C6 astroglial cells from acute cocaine toxicity.

Cocaine is a powerful addictive drug, widely abused in most Western countries. It easily reaches various domains within and outside of the central nervous system (CNS), and triggers varying levels of cellular toxicity. No pharmacological treatment is available to alleviate cocaine-induced toxicity in the cells without side-effects.

Comparative proteomic analysis reveals growth inhibition by 3-N-alkyloxyestradiol derivative (SERM) in prostate cancer cells.

Background/aim: In this study we evaluated the proteomic profile of PC-3 cells treated with novel, 3-N-alkyloxyestradiol derivative, 3-[2-diisopropylamino]-ethoxy-D1,3,5 (10)-estrien-17-one (DI) (USPTO #7,687,486).

Materials And Methods: The growth inhibitory potential of DI was determined by the National Cancer Institute (NCI) Developmental Therapeutics Program. 2-D gel electrophoresis and mass spectrometry were employed to identify differentially expressed proteins after treatment with DI.

Attenuating effect of N-acetyl-L-cysteine against acute cocaine toxicity in rat C6 astroglial cells.

Astroglial cells are one of the most abundant cell types in the mammalian brain functioning in neuronal survival and in maintenance of fundamental patterns of circuitry. To date, no study has been conducted regarding the short-term impact of cocaine on these cells in cultures. The present study aimed to investigate acute cocaine (1 h) treatment on cell viability in rat C6 astroglial cells.

Regulation of mammalian MOR-1 gene expression after chronic treatment with morphine.

Morphine is an effective analgesic that acts by binding to the µ-opioid receptor (MOR) coded in the human by the OPRM1 gene. In the present study, we investigated the regulation of µ-opioid receptor (MOR-1) mRNA levels in all-trans-retinoic acid-differentiated SH-SY5Y human neuroblastoma cells under in vitro conditions with 10 µM morphine treatment for 24 h. In addition, we measured the MOR-1 levels in recombinant Chinese hamster ovary (CHO) cells, transfected with human µ-opioid receptor gene (hMOR) with 10 µM morphine treatment for 24 h.

Effects of chronic cocaine in rat C6 astroglial cells.

Investigations with astroglial cells carry equal importance as those with neurons in drug abuse studies. The present study was aimed to investigate the effect of chronic cocaine administration on cell viability, nitric oxide (NO) production, general respiratory status of mitochondria and total protein levels in rat astroglioma cells after 24 h of treatment. In addition, the effect of cocaine was assessed for 24 h on brine shrimp larvae in order to study their sensitivity to the drug.

Autoxidation of gallic acid induces ROS-dependent death in human prostate cancer LNCaP cells.

Background: Prostate cancer is the second most common cause of mortality. Gallic acid (GA) is a natural polyphenol, and we tested its in-vitro cytotoxicity after 24 h in prostate cancer LNCaP cells.

Materials And Methods: GA autoxidation was measured fluorimetrically for H(2)O(2), and O(2)(•-) radicals by chemiluminescence.

Differential cytotoxicity of triphala and its phenolic constituent gallic acid on human prostate cancer LNCap and normal cells.

Background: Prostate cancer is one of the most commonly diagnosed solid malignancies among US men. We identified gallic acid (GA) as a major bioactive cytotoxic constituent of a polyherbal Ayurvedic formulation - triphala (TPL). Both TPL and GA were evaluated on (AR)(+) LNCaP prostate cancer and normal epithelial cells.

Cocaine induces alterations in mitochondrial membrane potential and dual cell cycle arrest in rat c6 astroglioma cells.

Investigations with astroglial cells carry more prominence in drug abuse studies. However, due to earlier perception that astroglial cells were only passive bystanders in neural signal transmission, not many investigations were conducted on the toxicity of various abused drugs, like cocaine. The present study was aimed to discern the effect of cocaine on rat astroglioma cells and analyzed qualitatively for morphological features as well as vacuolation by phase contrast microscope, quantitatively for cytotoxicity, mitochondrial membrane potential by rhodamine- 123 fluorometric assay, and cell cycle analysis by flow cytometry.

Selective cytotoxic activities of two novel synthetic drugs on human breast carcinoma MCF-7 cells.

Background: Breast cancer is the second leading cause of cancer deaths in US women. We evaluated two novel compounds, piperidinyl-diethylstilbestrol (DES) and pyrrolidinyl-diethylstilbestrol (DES) for cytotoxicity against brine shrimp larvae, MCF-7 and rat normal liver cells.

Materials And Methods: In vivo cytotoxicity was evaluated against shrimp larvae for 24 h, while in vitro cell toxicity was evaluated by dye binding crystal-violet method after 48 h.

Hydrogen peroxide induces lysosomal protease alterations in PC12 cells.

Alterations in lysosomal proteases have been implicated in many neurodegenerative diseases. The current study demonstrates a concentration-dependent decrease in PC12 cell viability and transient changes in cystatin C (CYSC), cathepsin B (CATB), cathepsin D (CATD) and caspase-3 following exposure to H2O2. Furthermore, activation of CATD occurred following exposure to H2O2 and cysteine protease suppression, while inhibition of CATD with pepstatin A significantly improved cell viability.

Anaerobic glycolysis protection against 1-methy-4-phenylpyridinium (MPP+) toxicity in C6 glioma cells.

The neurotoxin 1-methy-4-phenylpyridinium (MPP(+)) is used for its' capacity to induce Parkinsonism through its inhibitory effects on mitochondrial complex I. This inhibition disrupts cellular energy formation and aerobic glycolysis. The objective of this study was to demonstrate that the toxic effect of mitochondrial aerobic pathway inhibition with MPP(+ )can be reduced by stimulating anaerobic glycolysis using glucose supplementation.

Effects of NMDA receptor inhibition by phencyclidine on the neuronal differentiation of PC12 cells.

Phencyclidine (PCP) is a non-competitive N-methyl-d-aspartate (NMDA) receptor antagonist and exposing the developing brain to PCP has been shown to cause deficits in neurobehavioral functions. In the present study we tested the effects of PCP, as an NMDA receptor inhibitor, on the neuronal differentiation and biogenic amines levels including norepinephrine (NE), epinephrine, dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-HT), and 5-hydroxyindole-3-acetic acid (5-HIAA) in the rat pheochromocytoma (PC12) cells. After PC12 cells were differentiated with nerve growth factor (NGF) in the presence of PCP, NMDA binding kinetics, biogenic amines analysis and NMDA receptor protein expression assay were conducted.

Enhanced cystatin C and lysosomal protease expression following 6-hydroxydopamine exposure.

6-Hydroxydopamine (6-OHDA) is a selective neurotoxin used to induce apoptosis in catecholamine-containing neurons. Although biochemical products and reactive oxygen species (ROS) of 6-OHDA have been well documented, the activation of cellular pathways following exposure are not well understood. Apoptosis in PC12 (Pheochromocytoma) cells was induced by 6-OHDA in a dose (10-150 microM) and time-dependent (24-72 h) manner compared to experimental controls (no treatment).