Leonurus sibiricus induces nitric oxide and tumor necrosis factor-α in mouse peritoneal macrophages

2008 ◽  
Vol 86 (10) ◽  
pp. 682-690 ◽  
Author(s):  
Hyo-Jin An ◽  
Hong-Kun Rim ◽  
Jong-Hyun Lee ◽  
Se-Eun Suh ◽  
Ji-Hyun Lee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Host Defense ◽  
Tumor Necrosis ◽  
Peritoneal Macrophages ◽  
No Production ◽  
Tnf Α ◽  
Leonurus Sibiricus ◽  
Factor Α ◽  
Mouse Peritoneal Macrophages ◽  
Necrosis Factor

Using mouse peritoneal macrophages, we have examined the mechanism by which Leonurus sibiricus (LS) regulates nitric oxide (NO) production. When LS was used in combination with recombinant interferon-γ (rIFN-γ), there was a marked cooperative induction of NO production; however, LS by itself had no effect on NO production. The increased production of NO from rIFN-γ plus LS-stimulated cells was almost completely inhibited by pretreatment with pyrrolidine dithiocarbamate (PDTC), an inhibitor of nuclear factor κB. Furthermore, treatment of peritoneal macrophages with rIFN-γ plus LS caused a significant increase in tumor necrosis factor-α (TNF-α) production. PDTC also decreased the effect of LS on TNF-α production significantly. Because NO and TNF-α play an important role in immune function and host defense, LS treatment could modulate several aspects of host defense mechanisms as a result of stimulation of the inducible nitric oxide synthase.

Nitric oxide and tumor necrosis factor-α production by Ixeris dentata in mouse peritoneal macrophages

2002 ◽  
Vol 82 (2-3) ◽  
pp. 217-222 ◽  
Author(s):  
Hwan-Suck Chung ◽  
Hyun-Ja Jeong ◽  
Mi-Jung Han ◽  
Seung-Taeck Park ◽  
Kang-Kyung Seong ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Peritoneal Macrophages ◽  
Factor Α ◽  
Mouse Peritoneal Macrophages ◽  
Necrosis Factor ◽  
Ixeris Dentata

The Chloroform Fraction of Solanum nigrum Suppresses Nitric Oxide and Tumor Necrosis Factor-α in LPS-Stimulated Mouse Peritoneal Macrophages Through Inhibition of p38, JNK and ERK1/2

2011 ◽  
Vol 39 (06) ◽  
pp. 1261-1273 ◽  
Author(s):  
Hee Kang ◽  
Ha-Deok Jeong ◽  
Ho-Young Choi
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Peritoneal Macrophages ◽  
Solanum Nigrum ◽  
Chloroform Fraction ◽  
Tnf Α ◽  
Water Fractions ◽  
Factor Α ◽  
Mouse Peritoneal Macrophages ◽  
Necrosis Factor

Solanum nigrum L., commonly known as black nightshade, is used worldwide for the treatment of skin and mucosal ulcers, liver cirrhosis and edema. We aimed to determine the anti-inflammatory active fraction of S. nigrum by serial extractions. S. nigrum was first extracted with methanol, then fractionated with chloroform and water. The effects of S. nigrum fractions, diosgenin and α-solanine on LPS/interferon-gamma-induced nitric oxide (NO) and inducible NO synthase (iNOS), or LPS-induced tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, in mouse peritoneal macrophages were determined. Western blotting analysis was used to detect LPS-induced phosphorylation of p38, JNK and ERK1/2. The chloroform fraction of S. nigrum was cytotoxic in a time and concentration dependent manner; however, the methanol and water fractions were not. The chloroform fraction reduced NO through inhibition of iNOS synthesis and inhibited TNF-α and IL-6 at the level of protein secretion; the methanol and water fractions showed a weak or no effect. The chloroform fraction also suppressed p38, JNK and ERK1/2. Diosgenin and α-solanine were cytotoxic at a high concentration. In particular, diosgenin was able to inhibit TNF-α and IL-6, but both compounds did not affect LPS-induced iNOS expression. These results indicate that the anti-inflammatory compounds of S. nigrum exist preferentially in the nonpolar fraction, ruling out the possibility that diosgenin and α-solanine are the likely candidates. The inhibition of iNOS, TNF-α and IL-6 by the chloroform fraction may be partly due to the suppression of p38, JNK and ERK1/2. Further study is required to identify the active compounds of S. nigrum.

scholarly journals Nitric Oxide and Tumor Necrosis Factor-Alpha Inhibitory Substances from the Rhizomes of Kaempferia Marginata

2013 ◽  
Vol 8 (9) ◽  
pp. 1934578X1300800 ◽  
Author(s):  
Kanidta Kaewkroek ◽  
Chatchai Wattanapiromsakul ◽  
Palangpon Kongsaeree ◽  
Supinya Tewtrakul
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
No Production ◽  
Significant Activity ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

The ethanol extract of the rhizomes of Kaempferia marginata showed a potent inhibitory effect against lipopolysaccharide (LPS)-induced nitric oxide (NO) and tumor necrosis factor-alpha (TNF-α) release in RAW264.7 cells. Moreover, the partition with various organic solvents also inhibited NO production. One new pimarane-type diterpene, 1α-acetoxysandaracopimaradien-2α-ol (5), along with four known diterpenes (1–4), were isolated from the n-hexane and chloroform layers, respectively. Among these metabolites, compounds 1 and 4 were isolated for the first time from K. marginata. Compounds 1–5 showed significant inhibitory effects on NO production, with IC50 values ranging from 38.6 to 51.9 μM. Furthermore, compound 2 also exhibited significant activity against TNF-α release (IC50 = 48.3 μM). These findings may support the use of K. marginata by traditional doctors for treatment of inflammatory-related diseases.

scholarly journals Lipopolysaccharide-induced selective priming effects on tumor necrosis factor alpha and nitric oxide production in mouse peritoneal macrophages.

1993 ◽  
Vol 177 (2) ◽  
pp. 511-516 ◽  
Author(s):  
X Zhang ◽  
D C Morrison
Keyword(s):  
Tumor Necrosis ◽  
Peritoneal Macrophages ◽  
Tnf Alpha ◽  
No Production ◽  
Necrosis Factor Alpha ◽  
Priming Effects ◽  
Alpha Production ◽  
Factor Alpha ◽  
Mouse Peritoneal Macrophages ◽  
Necrosis Factor

Preculture of thioglycollate-elicited C3HeB/FeJ mouse peritoneal macrophages in vitro with subthreshold stimulatory concentrations of lipopolysaccharide (LPS) can induce hyporesponsiveness (desensitization) to both tumor necrosis factor alpha (TNF-alpha) and nitric oxide (NO) production when these cells are subsequently stimulated with 100 ng/ml of LPS. We have established, however, that the primary dose of LPS required for inducing downregulation of NO production is significantly lower than that required for inducing downregulation of TNF-alpha production. Further, when LPS-pretreated macrophages become refractory to subsequent LPS stimulation for NO production, the secondary LPS-stimulated TNF-alpha production is markedly enhanced, and vice versa. These results indicate that LPS-induced TNF-alpha and NO production by macrophages are differentially regulated, and that the observed desensitization process may not reflect a state in which macrophages are totally refractory to subsequent LPS stimulation. Rather, our data suggest that LPS-pretreated macrophages become selectively primed for differential responses to LPS. The LPS-induced selective priming effects are not restricted to LPS stimulation, but extend as well to stimuli such as zymosan, Staphylococcus aureus, and heat-killed Listeria monocytogenes.

Factors mediating the hemodynamic effects of tumor necrosis factor-α in portal hypertensive rats

1999 ◽  
Vol 276 (3) ◽  
pp. G687-G693 ◽  
Author(s):  
Javier Muñoz ◽  
Agustín Albillos ◽  
María Pérez-Páramo ◽  
Irma Rossi ◽  
Melchor Alvarez-Mon
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Portal Pressure ◽  
Systemic Resistance ◽  
Short Term ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Nitric oxide, prostacyclin, and glucagon have been implicated in promoting the hyperdynamic circulatory state of portal hypertension. Recent evidence also indicates that increased tumor necrosis factor-α (TNF-α) production is involved in the pathogenesis of this hemodynamic abnormality. This study was aimed at investigating in rats with portal vein stenosis (PVS) the effects on splanchnic hemodynamics of blocking circulating TNF-α and the factors mediating the vascular action of this cytokine in this setting. Anti-TNF-α polyclonal antibodies or placebo was injected into rats ( n = 96) before and 4 days after PVS (short-term inhibition) and at 24 h and 4, 7, 10 days after PVS (long-term inhibition). Short-term TNF-α inhibition reduced portal venous inflow and cardiac index and increased splanchnic and systemic resistance. Portal pressure was unchanged, but portal-systemic shunting was decreased. After long-term TNF-α inhibition, portal venous inflow and portal pressure were unchanged, but arterial pressure and systemic resistance rose significantly. Anti-TNF-α PVS rats exhibited lower increments of systemic resistance after N ω-nitro-l-arginine methyl ester and indomethacin administration and lower serum levels of TNF-α, nitrates-nitrites, and 6-keto-PGF1α, both over the short and the long term. Serum glucagon levels rose after long-term inhibition. In conclusion, the specific role played by TNF-α in the development of the hyperdynamic state of portal hypertension appears to be mainly mediated through an increased release of nitric oxide and prostacyclin. Maintenance of the splanchnic hyperemia after long-term TNF-α inhibition could be due to a compensatory release of glucagon.

Comparisons of the Effects of Anesthesia and Stress on Release of Tumor Necrosis Factor-α, Leptin, and Nitric Oxide in Adult Male Rats

2001 ◽  
Vol 226 (4) ◽  
pp. 296-300 ◽  
Author(s):  
Claudio A. Mastronardi ◽  
Wen H. Yu ◽  
Samuel M. McCann
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Adult Male ◽  
Tumor Necrosis ◽  
Fold Increase ◽  
Male Rats ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Bacterial lipopolysaccharide (LPS) stimulates massive release of tumor necrosis factor-alpha (TNF-α) together with nitric oxide (NO) and a lessor release of leptin. We hypothesized that other types of stress such as that of surgery might also release these cytokines and NO. Adult male rats were anesthetized with ketamine/acepromazine/xylazine anesthesia (90 + 2 + 6 mg/ml, respectively) and an external jugular catheter was inserted for removal of blood samples (0.6 ml) at various times postoperatively. Plasma TNF-α was almost undetectable in decapitated rats and was near zero immediately following the placement of the jugular catheter (time zero [to]). As the rats awakened from anesthesia, there was a rise in TNF-α at 30 min that peaked at 2 hr with a 400-fold increase and then precipitously declined 40-fold to a level still greater than zero at 3 hr. At 6 hr on the following morning, TNF-α values were near zero, but following connection of tubing and withdrawal of the initial blood sample, there was a 100-fold increase 1 hr later, followed by a decline over the next 3 hr. In contrast, plasma [NO3/NO2] from decapitated rats was 117 μM. Values at t0 were decreased and plummeted 4-fold within 30 min, then rose slightly in the ensuing 3 hr. At 6 hr on the next day [NO3/NO2] values were lower than at t0 and declined gradually during the next 4 hr. Leptin gradually declined from pre-operative concentrations, reaching a minimum at 3 hr and its concentration was unaffected by the bleeding stress of the second day. We conclude that release of TNF-α, [NO3/NO2], and leptin are neurally controlled since plasma levels of all three declined as a result of anesthesia. TNF-α secretion was remarkably stress responsive, whereas NO release appeared to be suppressed by the combined operative and bleeding stress, and leptin was stress unresponsive.

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