共查询到20条相似文献,搜索用时 31 毫秒
1.
Sahar A. El-Shatoury Nahla S. El-Shenawy Ibrahim M. Abd El-Salam 《World journal of microbiology & biotechnology》2009,25(9):1547-1555
Sixty-three actinomycete strains isolated from the marine shellfish Donax trunculus anatinus were phenotypically identified as ten genera, in addition to two unidentified strains. Their metabolic extracts exhibited
wide antimicrobial activities towards 11 reference and clinical cultures; and 17.5% showed antitumor activities with solid
tumor selectivity of four Nocardioides, Kitasatosporia and Streptomyces strains. Streptomyces 23-2B was particularly noted for its high antitumor activity against Ehrlich’s ascites carcinoma with plateau inhibitory
effect at 500, 250 and 50 μg/ml concentrations, promising solid tumor selectivity and high cytotoxicity to human carcinoma
of liver (HEPG2), cervix (HELA) and breast (MCF7) (IC50: 3.89, 9.4 and 10 μg/ml, respectively). In vivo cytotoxicity of S.23-2B metabolites showed common sign of unimpaired kidney
and liver functions, as indicated from non-significant elevation in serum enzymatic activities, urea, creatinine, total protein
and albumin levels in response to 0.5 and 5 μg/g doses after alternate-day injection for 2 weeks. Microorganisms associated
with the marine shellfish are suggested to be potential source of bioactive metabolites. 相似文献
2.
Gezginci-Oktayoglu S Tunali S Yanardag R Bolkent S 《Molecular and cellular biochemistry》2008,309(1-2):9-20
Background The aim of this investigation was to demonstrate that benzyloxicarbonyl-l-phenylalanyl-alanine-fluoromethylketone (Z-FA.FMK), which is a pharmacological inhibitor of cathepsin B, has protective role
on the kidney injury that occurs together with liver injury. Methods BALB/c male mice used in this study were divided into four groups. The first group was given physiologic saline only, the
second group was administered Z-FA.FMK alone, the third group received d-galactosamine and tumor necrosis factor-alpha (d-GalN/TNF-α), and the fourth group was given both d-GalN/TNF-α and Z-FA.FMK. One hour after administration of 8 mg/kg Z-FA.FMK by intravenous injection, d-GalN (700 mg/kg) and TNF-α (15 μg/kg) were given by intraperitoneal injection. Results In the group given d-GalN/TNF-α, the following results were found: severe degenerative morphological changes in the kidney tissue, a significant
increase in the number of activated caspase-3-positive tubular epithelial cell, an insignificant increase in the number of
proliferating cell nuclear antigen (PCNA)-positive tubular epithelial cell, a decrease in the kidney glutathione (GSH) levels,
catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, an increase in the kidney lipid peroxidation
(LPO) levels, lactate dehydrogenase (LDH) activity, serum aspartate aminotransferase (AST), and alanine aminotransferase (ALT)
activities, uric acid and urea levels. In contrast, in the group given d-GalN/TNF-α and Z-FA.FMK, a significant decrease in the d-GalN/TNF-α-induced degenerative changes, a decrease in the number of activated caspase-3-positive tubular epithelial cell,
a insignificant decrease in the number of PCNA-positive tubular epithelial cell, an increase in the kidney GSH levels, CAT,
SOD and GPx activities, a decrease in the kidney LPO levels, LDH activity, serum AST and ALT activities, uric acid and urea
levels were determined. Conclusion These results suggest that pretreatment with Z-FA.FMK markedly lessens the degree of impairment seen in d-GalN/TNF-α-induced kidney injury, which occurred together with liver injury in mice. 相似文献
3.
In our study, the short-term effects of caffeine on L- arginine metabolism in the brains of rats were investigated. Caffeine
was given orally at two different doses: 30 mg/kg and 100 mg/kg (a high non-toxic dose). Brain tissue arginase activity in
rats from the caffeine-treated groups decreased significantly compared with the control group. Malondialdehyde (MDA) levels
in the brain tissue and serum of animals in the caffeine groups also decreased significantly. Brain tissue and serum nitric
oxide (NO) levels increased significantly after caffeine administration. Tumor necrosis factor-α (TNF-α) levels were also
investigated in rat serum, but there was no statistically significant difference between the TNF-α levels of the caffeine-treated
rats groups and the control rats. Our study indicates that brain arginase activity decreases after caffeine administration
at doses of 30 mg/kg and 100 mg/kg. As a result, we can say that arginine induces production of NO in the organism. 相似文献
4.
Cadmium (Cd) exposure has been recognized to result in a wide variety of cellular responses, including oxidative stress and
body weight loss. The aim of the present study was to examine the effect of lycopene supplementation on the antioxidant defense
system, lipid peroxidation (LPO) level, nitric oxide (NO), tumor necrosis factor alpha (TNF-α) production, and body weight
in Cd-exposed rats. Animals were divided into four groups (n = 7): control, Cd-treated, Cd plus lycopene-treated, and lycopene-treated. Cadmium (as CdCl2) was administrated orally for 20 days (6.6 mg kg−1 day−1), and lycopene (10 mg kg−1 day−1) was similarly administered. Lycopene administration significantly suppressed Cd-induced LPO in plasma and kidney homogenates.
Lycopene also reversed Cd-decreased body weight compared to the control. Cadmium treatment had diverse effects on the antioxidant
enzyme activities. Although antioxidant superoxide dismutase activity was unchanged, glutathione peroxidase activity was decreased,
and catalase activity was elevated in kidney homogenates of Cd-administrated group. However, lycopene treatment reversed Cd-changed
enzyme activities to the control level. Xanthine oxidase activity and TNF-α concentration were not altered by Cd administration,
indicating that superoxide anion production and inflammation were not stimulated. Cadmium did not change NO levels in kidney
homogenates but decreased those in plasma, and this effect was not prevented by lycopene supplementation. The result suggests
that consumption of adequate levels of lycopene may be useful to prevent heavy-metal-induced LPO and body weight loss. 相似文献
5.
Miki Watanabe Sulaiman Sheriff Theresa A. Ramelot Nijiati Kadeer Junho Cho Kenneth B. Lewis Ambikaipakan Balasubramaniam Michael A. Kennedy 《International journal of peptide research and therapeutics》2011,17(4):281-299
After severe burn injury, proinflammatory cytokine levels are elevated in serum and skeletal muscle, which in turn increases
protein breakdown and decreases protein synthesis. In this study, C2C12 mouse skeletal muscle cell line myotubes were exposed
to proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) as an in vitro cell-line model of catabolic
response to burn injury and then treated with des-acyl ghrelin (DAG), a 28 amino acid polypeptide hormone thought to inhibit
protein breakdown and increase protein synthesis, to assess its therapeutic potential. Nuclear magnetic resonance-based metabonomics
was used to monitor metabolic activity of C2C12 myotubes under four treatment conditions: (1) control, (2) TNF-α/IFN-γ (TI),
(3) DAG (DA), and (4) TNF-α/IFN-γ followed by DAG (TIDA) to assess the effect of DAG treatment on cellular metabolic response
during basal or catabolic conditions. Twelve metabolites showed significant changes in concentrations following treatments
in the hydrophilic cell extracts. Lactate (P < 10−4) and citrulline (P < 10−9) increased with TNF-α/IFN-γ treatment, indicating increased protein degradation, and returned to control levels in the TIDA
group. Adenosine nucleotide levels had decreased trends in TI myotubes that returned to baseline levels after DAG treatment
(P < 10−4). Guanidinoacetate and pantothenate, metabolites involved in protein synthesis and cell proliferation, had increased concentration
trends following DAG treatment in both the DA and TIDA groups. Our metabonomics analysis provides further evidence that DAG
counteracts the catabolic response caused by elevated muscle TNF-α/IFN-γ cytokine levels following severe burns and can play
a potential therapeutic role in treatment of burn injury. 相似文献
6.
Ting-Chun Weng Chien-Chang Shen Yung-Tsung Chiu Yun-Lian Lin Cheng-Deng Kuo Yi-Tsau Huang 《Journal of biomedical science》2009,16(1):78-13
Activation of hepatic stellate cells (HSCs) plays a crucial role in liver fibrogenesis. armepavine (Arm, C19H23O3N), an active compound from Nelumbo nucifera, has been shown to exert immunosuppressive effects on T lymphocytes and on lupus nephritic mice. The aim of this study was
to investigate whether Arm could exert anti-hepatic fibrogenic effects in vitro and in vivo. A cell line of rat HSCs (HSC-T6) was stimulated with tumor necrosis factor-α (TNF-α) or lipopolysaccharide (LPS) to evaluate
the inhibitory effects of Arm. An in vivo therapeutic study was conducted in bile duct-ligated (BDL) rats. BDL rats were given Arm (3 or 10 mg/kg) by gavage twice
daily for 3 weeks starting from the onset of BDL. Liver sections were taken for fibrosis scoring, immuno-fluorescence staining
and quantitative real-time mRNA measurements. In vitro, Arm (1-10 μM) concentration-dependently attenuated TNF-α- and LPS-stimulated α-SMA protein expression and AP-1 activation
by HSC-T6 cells without adverse cytotoxicity. Arm also suppressed TNF-α-induced collagen collagen deposition, NFκB activation
and MAPK (p38, ERK1/2, and JNK) phosphorylations. In vivo, Arm treatment significantly reduced plasma AST and ALT levels, hepatic α-SMA expression and collagen contents, and fibrosis
scores of BDL rats as compared with vehicle treatment. Moreover, Arm attenuated the mRNA expression levels of col 1α2, TGF-β1, TIMP-1, ICAM-1, iNOS, and IL-6 genes, but up-regulated metallothionein genes. Our study results showed that Arm exerted both in vitro and in vivo antifibrotic effects in rats, possibly through anti-NF-κB activation pathways. 相似文献
7.
8.
Nakaizumi A Horie T Kida T Kurimoto T Sugiyama T Ikeda T Oku H 《Cellular and molecular neurobiology》2012,32(1):95-106
Modulation of enzyme activity through nitrosylation has recently been identified as a new physiological activity of nitric
oxide (NO). We hypothesized that NO enhances the TNF-α-induced death of retinal neurons through a suppression of nuclear factor-κB
(NF-κB) by nitrosylation. In this study, cells from the RGC-5 line were exposed to different concentrations (2.0, 10, and
50 ng/ml) of TNF-α, and the degree of TNF-α-induced cell death was determined by the WST-8 assay and by flow cytometric measurements
of the externalization of phosphatidylserine. The effects of etanercept, a soluble TNFR-Fc fusion protein, and S-nitroso-N-penicillamine (SNAP), an NO donor, on the toxicity were determined. Experiments were also performed to determine whether
nitric oxide synthase (NOS) was associated with the toxicity of TNF-α. The activation of NF-κB was determined by the detection
of the p65 subunit in the nuclear extracts. Our results showed that exposure of RGC-5 cells to different concentrations of
TNF-α significantly decreased the number of living cells in a dose-dependent way. The death was partially due to apoptosis
with an externalization of phosphatidylserine, and the death was suppressed by etanercept. Exposure to TNF-α increased the
activation of NF-κB and the expression of iNOS. Although NF-κB inhibitors suppressed the increase of iNOS, they also potentiated
the TNF-α-induced death. Both L-NAME and aminoguanidine, both NOS inhibitors, rescued the cells from death. In contrast, addition
of SNAP caused nitrosylation of the inhibitory κB kinase, and suppressed the NF-κB activation and potentiated the TNF-α-induced
neurotoxicity. These results indicate that NO potentiates the neurotoxicity of TNF-α by suppressing NF-κB. 相似文献
9.
Changes in the levels of antiapoptotic protein B-cell lymphoma 2 (Bcl-2) protein has been reported in murine and human tuberculosis.
We investigated the role of mitogen-activated protein kinase pathways in the production of Bcl-2 protein in THP-1 human monocytes
infected with Mycobacterium tuberculosis H37Rv and H37Ra. Analysis of phosphorylation profiles of mitogen-activated protein kinase kinase-1, extracellular-signal
regulated kinase 1/2, mitogen-activated protein kinase kinase 3/6, and p38 mitogen-activated protein kinase; B-cell lymphoma
2 kinetics; and tumor necrosis factor-α (TNF-α) secretion levels showed variation between the two strains. Mycobacterium tuberculosis H37Rv induced higher Bcl-2 and lower TNF-α levels, whereas H37Ra the reverse. The strains also differed in their usage of
CD14 and human leukocyte antigen-DR receptors in mediating extracellular-signal regulated kinase 1/2 and p38 mitogen-activated
protein kinase activation. Mycobacterium tuberculosis H37Rv- and H37Ra-induced Bcl-2 production was reduced by specific inhibitors of mitogen-activated protein kinase kinase-1
(PD98059) and p38 (SB203580), but increased by nuclear factor κB (NF-κB) inhibitor (BAY 11-7082). TNF-α production by both
strains was reduced in the presence of specific inhibitors of mitogen-activated protein kinase kinase-1 (PD98059), p38 (SB203580),
and NF-κB (BAY 11-7082). Furthermore, inhibition of NF-κB was accompanied by an increase in strain-induced extracellular-signal
regulated kinase 1/2 phosphorylation. Collectively, these results indicate for the first time that the production of Bcl-2
and TNF-α by M. tuberculosis H37Rv/H37Ra-infected THP-1 human monocytes is mediated through mitogen-activated protein kinases and NF-κB. 相似文献
10.
Daneshmandi S Pourfathollah AA Pourpak Z Heidarnazhad H Kalvanagh PA 《Molecular biology reports》2012,39(2):1845-1853
Asthma is a multifactor inflammatory disorder, and its management requires understanding of its various pathogenesis and control
mechanisms. Cytokines and other inflammatory mediators are important factors in asthma pathophysiology. In this study, we
evaluated the role of cytokine polymorphisms in the asthma susceptibility, progress, control, and lung functions. IL-4-C590T
polymorphism by PCR-RFLP method, IFN-γ T+874A, TNF-α-A308G, IL-6 G−174C and TGF-β T+869C variants by ARMS-PCR method and IgE
serum level by ELISA technique were determined in 81 asthmatic patients and 124 normal subjects. Asthma diagnosis, treatment
and control levels were considered using standard schemes and criteria. TNF-α−308GA genotype was more frequent in asthmatics
(P = 0.025, OR 3.352), and polymorphisms between different asthma control levels (P > 0.05) were not different. IFN-γ+874AT genotype had a positive correlation with the familial history of asthma (P = 0.034, OR 2.688). IL-6−174C allele (P = 0.045), TNF-α−308GG genotype (P = 0.002) and TNF-α−308G allele (P = 0.004) showed reduced values, and TNF-α−308GA genotype (P = 0.002) increased FEF25-75 value in asthmatics. IFN-γ+874AA genotype caused a decrease in FVC factor (P = 0.045). This study showed that TNF-α−308GA is a risk factor for asthma, but cytokine gene variants do not affect asthma
control and IgE serum levels. Variants producing lower levels of IL-6, TNF-α and IFN-γ are associated with reduced pulmonary
capacities. To achieve an appropriate schema for asthma management, further studies with consideration of different aspects
in a larger group of patients would be more elucidative. 相似文献
11.
AK Zgair 《World journal of microbiology & biotechnology》2012,28(5):2139-2146
Flagellin, a principal component of bacterial flagella, is a virulence factor that is recognized by the innate immune system.
Recognition of flagellin by innate immune receptors stimulates the production of cytokines necessary for the development of
effective immunity. Here, we demonstrated that the intranasal (i.n.) instillation of different amount of Escherichia coli K-12 flagellin preparation (0.5, 1, 2, 4 μg) in BALB/c mice induced pro-inflammatory immune response. Instillation i.n. of
1 μg of flagellin induced the maximum expression of interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α) and interleukin
6 (IL-6) mRNA and production of pro-inflammatory cytokines (IL-1β, TNF-α and IL-6) in mice lungs. The same dose of flagellin
induced neutrophil polymorphonuclear cells infiltration in peribronchial and perivascular regions. High number of neutrophil
in bronchoalveolar lavage fluid was found at 24 h after i.n. instillation of flagellin (1 μg). These findings were concomitant
with the maximum production of myeloperoxidase and nitric oxide in mice lungs. Present study showed that the maximum pro-inflammatory
mediator levels were found when mice instilled i.n. with 1 μg E. coli flagellin. The amount of flagellin of E. coli K-12 that achieve the maximum stimulation of mucosal pro-inflammatory immune response in mice lungs was explored in this
study. 相似文献
12.
Long-term alcohol consumption can cause oxidative stress and cytokines induction, which are associated with free radicals.
Quercetin, one of the most widely distributed flavonoids in plants, is a natural antioxidant. We investigated the hypothesis
that quercetin could prevent the ethanol-induced oxidative stress and decreases tumor necrosis factor-α (TNF-α) and interferon-γ
(INF-γ) as pro-inflammatory cytokines. Twenty-eight rats were randomly divided into control group (C), ethanol treatment group
(EtOH) (~1 ml/day, 80%; 2 g/kg body wt), intragastrically (i.g.), quercetin treatment group (Q), (100 mg/kg-body wt per 3 days)
i.g. and ethanol plus quercetin treatment group (EtOH + Q) (1 ml/day, 80% of ethanol and 100 mg/kg-body wt of quercetin per
3 days) i.g. for 30 days Plasma thiobarbituric acid reactive substance (TBARS) levels and protein carbonyl content were significantly
higher in the EtOH group than the C group (P < 0.01). On the other hand, TBARS level and protein carbonyl content in the EtOH + Q group was decreased significantly by
quercetin (P < 0.05, P < 0.01; respectively). While GSH levels in whole blood decreased in EtOH group compared to C group, they increased significantly
by quercetin (P < 0.05). Plasma ALT, TNF-α and IFN-γ levels increased significantly in the EtOH group compared to control group (P < 0.05, P < 0.01, P < 0.01, respectively), but they decreased significantly in the EtOH + Q group in comparison with EtOH group (P < 0.05, P < 0.01, P < 0.01, respectively). Our results demonstrate that quercetin treatment may provide a protection as reflected by decreased
plasma TBARS, protein carbonyls, TNF-α, INF-γ and ALT levels against ethanol-induced oxidative damage. 相似文献
13.
14.
Yeo Dae Yoon Eun Sook Lee Jong Pil Park Mee Ree Kim Jun Won Lee Tae Hoon Kim Min Kyun Na Jin Hee Kim 《Biotechnology and Bioprocess Engineering》2011,16(6):1099-1105
Hizikia fusiforme is a commonly used food that possesses potent anti-bacterial, anti-fungal, and anti-inflammatory activities. The immunostimulatory
activities of aqueous extract of Hizikia fusiforme (HFAE) in RAW 264.7 macrophages and whole spleen cells were investigated. HFAE activated RAW 264.7 macrophages to produce
cytokines such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in
a dose-dependent manner. In addition, HFAE induced the mRNA expression of TNF-α, IL-1β, and IL-6 in RAW 264.7 macrophages.
Moreover, HFAE stimulated proliferation of whole spleen cells and reference mitogen. Taken together, the results demonstrate
that HFAE potently activates the immune function by regulating NO, TNF-α, IL-1β, and IL-6 in RAW 264.7 macrophage and promoting
spleen cell proliferation. 相似文献
15.
16.
Angiotensin II is able to trigger inflammatory responses through an angiotensin II type 1 (AT1) receptor. The role of AT1 receptor in acute lung injury (ALI) is poorly understood. Mice were randomly divided into three groups (n = 40 each groups): NS group; LPS group (2 mg/kg LPS intratracheally); and LPS + ZD 7155 group, 10 mg/kg ZD 7155 (an AT1 receptor antagonist) intraperitoneally 30 min prior to LPS exposure. Samples from the lung were isolated and assayed for histopathology analyses or proinflammatory gene expressions, angiotensin II receptors expressions and nuclear factors activities. LPS exposure resulted in severe ALI, elevated levels of TNF-α and IL-1β mRNA expressions, and increased activities of NF-κB and activated protein (AP)-1. Upregulation of AT1 receptor and down-regulation of AT2 receptor were also observed after LPS challenge. Pretreatment with ZD 7155 significantly inhibited the increase of AT1 receptor expression and upregulated AT2 receptor expression. ZD 7155 also reduced the mRNA expression of TNF-α and IL-1β, inhibited the activation of NF-κB and AP-1, and improved lung histopathology. These findings suggest that antagonism of AT1 receptor inhibits the activation of NF-κB and AP-1 in the lung, which may mediate the release of TNF-α and IL-1β and contribute to LPS-induced ALI. 相似文献
17.
Guanghai Yu Xiaoqiang Jia Jianping Wen Guoying Wang Yunlin Chen 《World journal of microbiology & biotechnology》2011,27(8):1859-1868
The effects of eight cofactors of enzymes on daptomycin production were investigated in this work, which included nicotinic
acid (VPP), riboflavin (VB2), heme, thiamine (VB1), biotin (VH), cyanocobalamin (VB12), tetrahydrofolic acid (THF) and pyridoxal 5-phosphate (VB6). The dry cell weight (DCW), consumption of glucose, and daptomycin production were obviously improved when proper amount
of exogenous cofactors were supplemented in the medium. The effects of heme, THF, VB12 and VB6 on daptomycin production were especially notable. The daptomycin yield enhanced 363, 104, 53 and 46%, respectively, when
optimized amount of these four cofactors were supplemented in the broth. Moreover, the daptomycin yield further increased
to 632 mg/l, which was over 4.5-fold higher than that of the control (without cofactors), at 132 h in a 7.5-l fermenter, by
supplementation all of the eight cofactors at optimized concentrations (VPP 4 mg/l, VB2 0.5 mg/l, heme 9 mg/l, VB1 0.4 mg/l, VH 0.1 mg/l, VB12 0.04 mg/l, THF 6 mg/l and VB6 0.4 mg/l). Further, the effects of cofactors on the corresponding key enzymes and important intracellular metabolites were
studied in order to elucidate the mechanism of enhancement of daptomycin production by manipulation of cofactors concentration
in the fermentation culture. It is suggested that this strategy for increasing the daptomycin production in Streptomyces roseosporus LC-51 by manipulation of cofactors concentration in the fermentation culture may provide an alternative approach to enhance
the production of metabolites in other Streptomyces. 相似文献
18.
Semiha Erisen Mustafa Yorgancilar Emine Atalay Mehmet Babaoglu 《Plant Cell, Tissue and Organ Culture》2010,100(2):229-233
Prolific shoot regeneration via organogenesis was induced from leaf and leaf petiole explants of the endemic Astragalus cariensis species on Murashige and Skoog (MS) medium with α-naphthaleneacetic acid (NAA) and benzyladenine (BA) within 8 week. The
highest number of shoots (23/explants) was obtained from leaf explants cultured on MS with 0.5 mg/l NAA and 4 mg/l BA. Elongated
shoots were successfully rooted in MS medium with 0.5 mg/l indole-3-butyric acid. Rooted plantlets were acclimatized in pots
containing 1:1 mixture of peat and perlite. 相似文献
19.
20.
Kitanaka J Kitanaka N Hall FS Uhl GR Tatsuta T Morita Y Tanaka K Nishiyama N Takemura M 《Neurochemical research》2011,36(10):1824-1833
The effects of the histamine H3 receptor agonists (R)-α-methylhistamine, imetit and immepip on methamphetamine (METH)-induced stereotypical behavior were examined in mice. The
administration of METH (10 mg/kg, i.p.) to male ddY mice induced behaviors including persistent locomotion and stereotypical
behaviors, which were classified into four categories: stereotypical head-bobbing (1.9%), circling (1.7%), sniffing (14.3%),
and biting (82.1%). Pretreatment with (R)-α-methylhistamine (3 and 10 mg/kg, i.p.) significantly decreased stereotypical sniffing, but increased stereotypical biting
induced by METH, in a dose-dependent manner. This effect of (R)-α-methylhistamine on behavior was mimicked by imetit or immepip (brain-penetrating selective histamine H3 receptor agonists; 10 mg/kg, i.p. for each drug). Hypothalamic histamine levels 1 h after METH challenge were significantly
increased in mice pretreated with saline. These increases in histamine levels were significantly decreased by pretreatment
with histamine H3 receptor agonists, effects which would appear to underlie the shift from METH-induced stereotypical sniffing to biting. 相似文献