Erratum to “Inhibitory effect of Buthus martensi Karsch extracts on interleukin-1b-induced expression of nitric oxide (NO) synthase and production of NO in human chondrocytes and LPS-induced NO and prostaglandin E2 production in mouse peritoneal macrophages” [Toxicology in Vitro 19 (2005) 757–769]

2010 ◽  
Vol 24 (2) ◽  
pp. 695
Author(s):  
Kap-Sung Kim ◽  
Hyun-Seok Cho ◽  
Seung-Deok Lee ◽  
Kyung-Ho Kim ◽  
Jae-Yong Cho ◽  
...  
2003 ◽  
Vol 47 (6) ◽  
pp. 1895-1901 ◽  
Author(s):  
Maria do Socorro S. Rosa ◽  
Ricardo R. Mendonça-Filho ◽  
Humberto R. Bizzo ◽  
Igor de Almeida Rodrigues ◽  
Rosangela Maria A. Soares ◽  
...  

ABSTRACT The in vitro leishmanicidal effects of a linalool-rich essential oil from the leaves of Croton cajucara against Leishmania amazonensis were investigated. Morphological changes in L. amazonensis promastigotes treated with 15 ng of essential oil per ml were observed by transmission electron microscopy; leishmanial nuclear and kinetoplast chromatin destruction, followed by cell lysis, was observed within 1 h. Pretreatment of mouse peritoneal macrophages with 15 ng of essential oil per ml reduced by 50% the interaction between these macrophages and L. amazonensis, with a concomitant increase by 220% in the level of nitric oxide production by the infected macrophages. Treatment of preinfected macrophages with 15 ng of essential oil per ml reduced by 50% the interaction between these cells and the parasites, which led to a 60% increase in the amount of nitric oxide produced by the preinfected macrophages. These results provide new perspectives on the development of drugs with activities against Leishmania, as linalool-rich essential oil is a strikingly potent leishmanicidal plant extract (50% lethal doses, 8.3 ng/ml for promastigotes and 8.7 ng/ml for amastigotes) which inhibited the growth of L. amazonensis promastigotes at very low concentrations (MIC, 85.0 pg/ml) and which presented no cytotoxic effects against mammalian cells.


FEBS Letters ◽  
2010 ◽  
Vol 584 (19) ◽  
pp. 4227-4232 ◽  
Author(s):  
Yogesh Dahiya ◽  
Rajeev Kumar Pandey ◽  
Kunal H. Bhatt ◽  
Ajit Sodhi

2004 ◽  
Vol 91 (5) ◽  
pp. 733-739 ◽  
Author(s):  
Meijuan Zhang ◽  
Kevin L. Fritsche

Our laboratory has reported that n-3 PUFA can reduce host resistance to Listeria infection, in part, by impairing in vivo IL-12 biosynthesis. Recently, PUFA were shown to be ligands for PPAR, a novel family of nuclear receptors with three isoforms: PPARα, PPARδ/β and PPARγ. PPARγ is expressed in immune cells, such as T cells and macrophages. Two PPARγ agonists, 15-deoxy-Δ12,14-prostaglandin (PG) J2 and rosiglitazone, have been shown to have immunomodulatory activity in vitro, including inhibiting IL-12 biosynthesis. We hypothesized that n-3 PUFA inhibit IL-12 production through activating PPARγ. We used thioglycolate-elicited mouse peritoneal macrophages to study the effect of various fatty acids and their oxidized metabolites on in vitro IL-12 production. Our present results demonstrate that both n-3 and n-6 PUFA can reduce in vitro IL-12 biosynthesis, though less potently than 15-deoxy-PGJ2 and rosiglitazone. GW9662, a PPARγ antagonist, reversed the inhibitory effect of rosiglitazone, but not that of PUFA. Our present findings suggest that fatty acid-mediated inhibition of IL-12 production is independent of PPARγ.


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