Anti-inflammatory activity of four Bolivian Baccharis species (Compositae)

Abad, María J. F.; Bessa, Ana Latourrette; Ballarin, B.; Aragón, O.; Gonzales, Eduardo; Bermejo, Paulina

doi:10.1016/j.jep.2005.08.024

Cited by 41 publications

(32 citation statements)

References 21 publications

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“…The phytochemical analysis of many Baccharis species indicates the presence of flavonoids, diterpenes and triterpenes, which have been associated with antimicrobial, antinflammatory, antioxidant and gastroprotector properties (Heral et al, 1998;Baggio et al, 2003;Abad et al, 2006;Morales et al, 2008). EOs obtained from B. notosergila Griseb.…”

Section: Research Articlementioning

confidence: 99%

Sedative effects of essential oils obtained fromBaccharis uncinella

Ascari

Sens²,

Nunes

et al. 2011

Pharmaceutical Biology

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Section: Research Articlementioning

confidence: 99%

Sedative effects of essential oils obtained fromBaccharis uncinella

Ascari

Sens²,

Nunes

et al. 2011

Pharmaceutical Biology

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“…PKC δ activation and translocation are induced by a variety of inflammatory stimuli (Abad et al, 2006). However, some recent studies showed that rottlerin was not effective at inhibiting PKC δ activity in vitro and that may display non-specific effects (Soltoff, 2007; (5 ng/ml) for 12 h. The cells were lysed and the lysates were analyzed using immunoblotting with anti-COX-2 antibody.…”

Section: Introductionmentioning

confidence: 99%

Rottlerin enhances IL-1β-induced COX-2 expression through sustained p38 MAPK activation in MDA-MB-231 human breast cancer cells

Park

Kwon

2011

Exp Mol Med

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Cyclooxygenase-2 (COX-2) is an important enzyme in inflammation. In this study, we investigated the underlying molecular mechanism of the synergistic effect of rottlerin on interleukin1β (IL-1β)-induced COX-2 expression in MDA-MB-231 human breast cancer cell line. Treatment with rottlerin enhanced IL-1β-induced COX-2 expression at both the protein and mRNA levels. Combined treatment with rottlerin and IL-1β significantly induced COX-2 expression, at least in part, through the enhancement of COX-2 mRNA stability. In addition, rottlerin and IL-1β treatment drove sustained activation of p38 Mitogen-activated protein kinase (MAPK), which is involved in induced COX-2 expression. Also, a pharmacological inhibitor of p38 MAPK (SB 203580) and transient transfection with inactive p38 MAPK inhibited rottlerin and IL-1β-induced COX-2 upregulation. However, suppression of protein kinase C δ (PKC δ) expression by siRNA or overexpression of dominant-negative PKC δ (DN-PKC-δ) did not abrogate the rottlerin plus IL-1β-induced COX-2 expression. Furthermore, rottlerin also enhanced tumor necrosis factor-α (TNF-α), phorbol myristate acetate (PMA), and lipopolysaccharide (LPS)-induced COX-2 expression. Taken together, our results suggest that rottlerin causes IL-1β-induced COX-2 upregulation through sustained p38 MAPK activation in MDA-MB-231 human breast cancer cells.

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“…4) LPS can directly activate macrophages, which trigger the production of inflammatory mediators, such as NO, cyclooxygenase (COX)-2, pro-inflammatory cytokines and leukotrienes. 21) Therefore the pharmacological reduction of LPS-induced inflammatory mediators is regarded as one of the essential events to a variety of disorders caused by excessive activation of macrophages. 22) In this study, we confirmed the inhibitory effect of gallotannin 15 and newly defined the activity of gallotannin 23 on the LPSstimulated macrophages.…”

Section: Discussionmentioning

confidence: 99%