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Propofol attenuates LPS-induced tumor necrosis factor-α, interleukin-6 and nitric oxide expression in canine peripheral blood mononuclear cells possibly through down-regulation of nuclear factor (NF)-κB activation.

Pei Z, Wang J - J. Vet. Med. Sci. (2014)

Bottom Line: However, propofol's anti-inflammatory effects upon canine peripheral blood mononuclear cells (PBMCs) have not yet been clarified.Through real-time quantitative PCR and the Griess reagent system, we found that non-cytotoxic levels of propofol significantly inhibited the release of NO and IL-6 and TNF-α gene expression in LPS-induced canine PBMCs.Western blotting revealed that LPS does significantly increase the expression of inducible NO synthase (iNOS) protein in canine PBMCs, while pretreatment with propofol significantly decreases the LPS-induced iNOS protein expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, PR China.

ABSTRACT
Sepsis is a major cause of mortality in intensive care medicine. Propofol, an intravenous general anesthetic, has been suggested to have anti-inflammatory properties and able to prevent sepsis induced by Gram-positive and Gram-negative bacteria by down-regulating the gene expression of pro-inflammatory cytokines. However, propofol's anti-inflammatory effects upon canine peripheral blood mononuclear cells (PBMCs) have not yet been clarified. Here, we isolate canine PBMCs and investigate the effects of propofol on the gene expressions of both lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α and upon the production of nitric oxide (NO). Through real-time quantitative PCR and the Griess reagent system, we found that non-cytotoxic levels of propofol significantly inhibited the release of NO and IL-6 and TNF-α gene expression in LPS-induced canine PBMCs. Western blotting revealed that LPS does significantly increase the expression of inducible NO synthase (iNOS) protein in canine PBMCs, while pretreatment with propofol significantly decreases the LPS-induced iNOS protein expression. Propofol, at concentration of 25 µM and 50 µM, also significantly inhibited the LPS-induced nuclear translocation of nuclear factor (NF)-κB p65 protein in canine PBMCs. This diminished TNF-α, IL-6 and iNOS expression, and NO production was in parallel to the respective decreased NF-κB p65 protein nuclear translocation in the LPS-activated canine PBMCs pretreated with 25 µM and 50 µM propofol. This suggests that non-cytotoxic levels of propofol pretreatment can down-regulate LPS-induced inflammatory responses in canine PBMCs, possibly by inhibiting the nuclear translocation of the NF-κB p65 protein.

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Effects of propofol on the cell viability of canine PBMCs after LPS treatment. Canine PBMCs were pretreated for 6 hr with different concentrations of propofol (0, 25 or 50 µM), and then, cells were treated with LPS (100 ng/ml) for 24 hr. Cell viability was measured by MTT assay. Results are expressed as means ± S.D. from three independent experiments.
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fig_001: Effects of propofol on the cell viability of canine PBMCs after LPS treatment. Canine PBMCs were pretreated for 6 hr with different concentrations of propofol (0, 25 or 50 µM), and then, cells were treated with LPS (100 ng/ml) for 24 hr. Cell viability was measured by MTT assay. Results are expressed as means ± S.D. from three independent experiments.

Mentions: Toxicity of propofol and LPS to canine PBMCs: To avoid any cytotoxic effects caused by propofol, we investigated the effects of propofol on cell survival and cytotoxicity in canine PBMCs. Exposure of canine PBMCs to propofol (25 or 50 µM) in the presence or absence of 100 ng/ml LPS for 24 hr did not cause any significant change in MTT absorbance (Fig. 1Fig. 1.


Propofol attenuates LPS-induced tumor necrosis factor-α, interleukin-6 and nitric oxide expression in canine peripheral blood mononuclear cells possibly through down-regulation of nuclear factor (NF)-κB activation.

Pei Z, Wang J - J. Vet. Med. Sci. (2014)

Effects of propofol on the cell viability of canine PBMCs after LPS treatment. Canine PBMCs were pretreated for 6 hr with different concentrations of propofol (0, 25 or 50 µM), and then, cells were treated with LPS (100 ng/ml) for 24 hr. Cell viability was measured by MTT assay. Results are expressed as means ± S.D. from three independent experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4363014&req=5

fig_001: Effects of propofol on the cell viability of canine PBMCs after LPS treatment. Canine PBMCs were pretreated for 6 hr with different concentrations of propofol (0, 25 or 50 µM), and then, cells were treated with LPS (100 ng/ml) for 24 hr. Cell viability was measured by MTT assay. Results are expressed as means ± S.D. from three independent experiments.
Mentions: Toxicity of propofol and LPS to canine PBMCs: To avoid any cytotoxic effects caused by propofol, we investigated the effects of propofol on cell survival and cytotoxicity in canine PBMCs. Exposure of canine PBMCs to propofol (25 or 50 µM) in the presence or absence of 100 ng/ml LPS for 24 hr did not cause any significant change in MTT absorbance (Fig. 1Fig. 1.

Bottom Line: However, propofol's anti-inflammatory effects upon canine peripheral blood mononuclear cells (PBMCs) have not yet been clarified.Through real-time quantitative PCR and the Griess reagent system, we found that non-cytotoxic levels of propofol significantly inhibited the release of NO and IL-6 and TNF-α gene expression in LPS-induced canine PBMCs.Western blotting revealed that LPS does significantly increase the expression of inducible NO synthase (iNOS) protein in canine PBMCs, while pretreatment with propofol significantly decreases the LPS-induced iNOS protein expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, PR China.

ABSTRACT
Sepsis is a major cause of mortality in intensive care medicine. Propofol, an intravenous general anesthetic, has been suggested to have anti-inflammatory properties and able to prevent sepsis induced by Gram-positive and Gram-negative bacteria by down-regulating the gene expression of pro-inflammatory cytokines. However, propofol's anti-inflammatory effects upon canine peripheral blood mononuclear cells (PBMCs) have not yet been clarified. Here, we isolate canine PBMCs and investigate the effects of propofol on the gene expressions of both lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α and upon the production of nitric oxide (NO). Through real-time quantitative PCR and the Griess reagent system, we found that non-cytotoxic levels of propofol significantly inhibited the release of NO and IL-6 and TNF-α gene expression in LPS-induced canine PBMCs. Western blotting revealed that LPS does significantly increase the expression of inducible NO synthase (iNOS) protein in canine PBMCs, while pretreatment with propofol significantly decreases the LPS-induced iNOS protein expression. Propofol, at concentration of 25 µM and 50 µM, also significantly inhibited the LPS-induced nuclear translocation of nuclear factor (NF)-κB p65 protein in canine PBMCs. This diminished TNF-α, IL-6 and iNOS expression, and NO production was in parallel to the respective decreased NF-κB p65 protein nuclear translocation in the LPS-activated canine PBMCs pretreated with 25 µM and 50 µM propofol. This suggests that non-cytotoxic levels of propofol pretreatment can down-regulate LPS-induced inflammatory responses in canine PBMCs, possibly by inhibiting the nuclear translocation of the NF-κB p65 protein.

Show MeSH
Related in: MedlinePlus