Trans-10, cis-12 conjugated linoleic acid and the PPAR-γ agonist rosiglitazone attenuate lipopolysaccharide-induced TNF-α production by bovine immune cells

Perdomo, M.C.; Santos, J.E.P.; Badinga, L.

doi:10.1016/j.domaniend.2011.05.005

Cited by 23 publications

(17 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rosiglitazone (10 µM; Sequoia Research Products, Pangbourne, UK) and 30 µM G3335 (BioVision Incorporated, Milpitas, CA, USA) were used in the presence or absence of oxaliplatin for 2 or 5 days. The chosen concentrations are in accord with previous published data [8], [40], [41] and, as regards oxaliplatin, with plasmatic concentration of treated rats.…”

Section: Methodssupporting

confidence: 70%

Oxaliplatin Neurotoxicity Involves Peroxisome Alterations. PPARγ Agonism as Preventive Pharmacological Approach

et al. 2014

View full text Add to dashboard Cite

The development of neuropathic syndromes is an important, dose limiting side effect of anticancer agents like platinum derivates, taxanes and vinca alkaloids. The causes of neurotoxicity are still unclear but the impairment of the oxidative equilibrium is strictly related to pain. Two intracellular organelles, mitochondria and peroxisomes cooperate to the maintaining of the redox cellular state. Whereas a relationship between chemotherapy-dependent mitochondrial alteration and neuropathy has been established, the role of peroxisome is poor explored. In order to study the mechanisms of oxaliplatin-induced neurotoxicity, peroxisomal involvement was evaluated in vitro and in vivo. In primary rat astrocyte cell culture, oxaliplatin (10 µM for 48 h or 1 µM for 5 days) increased the number of peroxisomes, nevertheless expression and functionality of catalase, the most important antioxidant defense enzyme in mammalian peroxisomes, were significantly reduced. Five day incubation with the selective Peroxisome Proliferator Activated Receptor-γ (PPAR-γ) antagonist G3335 (30 µM) induced a similar peroxisomal impairment suggesting a relationship between PPARγ signaling and oxaliplatin neurotoxicity. The PPARγ agonist rosiglitazone (10 µM) reduced the harmful effects induced both by G3335 and oxaliplatin. In vivo, in a rat model of oxaliplatin induced neuropathy, a repeated treatment with rosiglitazone (3 and 10 mg kg−1 per os) significantly reduced neuropathic pain evoked by noxious (Paw pressure test) and non-noxious (Cold plate test) stimuli. The behavioral effect paralleled with the prevention of catalase impairment induced by oxaliplatin in dorsal root ganglia. In the spinal cord, catalase protection was showed by the lower rosiglitazone dosage without effect on the astrocyte density increase induced by oxaliplatin. Rosiglitazone did not alter the oxaliplatin-induced mortality of the human colon cancer cell line HT-29. These results highlight the role of peroxisomes in oxaliplatin-dependent nervous damage and suggest PPARγ stimulation as a candidate to counteract oxaliplatin neurotoxicity.

show abstract

Section: Methodssupporting

confidence: 70%

Oxaliplatin Neurotoxicity Involves Peroxisome Alterations. PPARγ Agonism as Preventive Pharmacological Approach

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Linoleic acid and cis-9, trans-11 CLA isomer had no detectable effects on lipopolysaccharide (LPS)-induced TNF alpha production in cultured bovine blood. However, trans-10, cis-12 CLA isomer attenuate LPS-induced TNF-alpha production by bovine immune cells (Perdomo et al 2011).…”

Section: Cla and Immune Responsementioning

confidence: 91%

“…There is also a complementary hypothesis that CLA might alter immune function by interaction with peroxisome proliferator-activated receptors (PPARs) which regulate the expression of genes responsible for energy balance and immunity as CLA isomers are potent modulators of PPARs (Moya-Camarena et al 1999, Perdomo et al 2011.…”

Section: Cla and Immune Responsementioning

confidence: 99%

Biological effects of conjugated linoleic acids supplementation

Oleszczuk¹,

Oleszczuk²,

Siwicki³

et al. 2012

Polish Journal of Veterinary Sciences

View full text Add to dashboard Cite

Conjugated linoleic acids (CLA) are a group of polyunsaturated fatty acids (PUFA) with a single pair of conjugated double bonds. The major natural CLA isomer is 18:2 cis-9, trans-11 (c9, t11) linoleic acid, or rumenic acid (RA). Chemically synthesized CLA is also available, mostly as a mixture of RA and 18:2 trans-10, cis-12 (t10, c12) isomers in equal amounts (50:50). Consumption of ruminant meat (beef and lamb) and dairy products (milk and cheese) is the main source of dietary exposure to CLA. Despite numerous studies on animal and human models (tumorigenesis, obesity, immune response) it has not been established whether additional supplementation of CLA is of benefit. Moreover, some studies, conducted both in animals and in humans, reveal that CLA isomers may induce insulin resistance. Presently, balanced diet rich in CLA from natural sources is recommended. The purpose of this review was to sum up the results available in the literature.

show abstract

“…The ability of CLA to reduce inflammation has been recently investigated in a series of detailed in vitro experiments using bovine blood. Such studies have revealed that the t-10,c-12 CLA isomer is able to reduce LPS-induced TNFα production in cultured bovine blood immune cells, whereas linoleic acid and c-9t-11 CLA treatments result in no detectable changes (Perdomo et al, 2011). Another ex vivo study showed decreased NF-κB activation and TNFα mRNA levels after adding t-10,c-12 CLA to endotoxin-stimulated pig peripheral blood mononuclear cells (PBMCs) (Kim et al, 2011).…”

Section: Cla As a Modulator Of Cytokine Expressionmentioning

confidence: 99%