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. 2014 Oct 22:1:1062-1067.
doi: 10.1016/j.toxrep.2014.10.006. eCollection 2014.

The effect of capsaicin on circulating biomarkers, soluble tumor necrosis factor and soluble tumor necrosis factor-receptor-1 and -2 levels in vivo using lipopolysaccharide-treated mice

Affiliations

The effect of capsaicin on circulating biomarkers, soluble tumor necrosis factor and soluble tumor necrosis factor-receptor-1 and -2 levels in vivo using lipopolysaccharide-treated mice

Yoshio Ijiri et al. Toxicol Rep. .

Abstract

The circulating soluble tumor necrosis factor (sTNF) and sTNF-receptor (R) 1 and -R2 have known as septic biomarker. The pungent component of capsicum, capsaicin (Cap), has several associated physiological activities, including anti-oxidant, anti-bacterial and anti-inflammatory effects. The aim of this study was to elucidate the effect of Cap on circulating sTNF and sTNF-R1 and -R2 in vivo using lipopolysaccharide (LPS)-treated mice. LPS (20 mg/kg, ip)-treated group was significantly increased circulating sTNF, sTNF-R1, and -R2 and TNF-α mRNA expression levels compared to the vehicle group. Treatment with LPS (20 mg/kg, ip) + Cap (4 mg/kg, sc)-treated group was significantly decreased both circulating sTNF levels (after 1 h only) and TNF-α mRNA expression (after 6 h) compared to the LPS-treated group. There is an early increase in circulating sTNF, sTNR-R1, and -R2 observed in the LPS-treated mice. Since Cap inhibits this initial increase as biomarkers, circulating sTNF, it is considered a potent treatment option for TNF-α-related diseases, such as septicemia. In conclusion, Cap interferes with TNF-α mRNA transcription and exerts an inhibiting effect on TNF-α release from macrophages in the early phase after LPS stimulation. Thus, Cap is considered a potent agent for the treatment of TNF-α-related diseases, such as septicemia.

Keywords: ADAM-17; Cap, capsaicin; Capsaicin; LPS, lipopolysaccharide; Lipopolysaccharide (LPS); NO, nitric oxide; PBS, phosphate buffered saline; Soluble tumor necrosis (sTNF); Soluble tumor necrosis factor-receptor 1 and 2 (TNF-R 1 and 2); TACE, TNF-converting enzyme; TNF-R, tumor necrosis factor-receptor; TNF-converting enzyme (TACE); TNF-α, tumor necrosis factor-alpha.

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Figures

Fig. 1
Fig. 1
The chronological changes in circulating soluble tumor necrosis factor (sTNF), sTNF-receptor 1 (R1), and sTNF-R2 levels. Mice were treated with or without lipopolysaccharide (LPS) 20 mg/kg, and were treated with LPS 20 mg/kg and capsaicin (Cap) 4 mg/kg. (A) Circulating sTNF level mice. Data shows mean ± SD (n = 3–4). (B) Circulating sTNF-R1 level in mice. Data shows mean ± SD (n = 3–4). (C) Circulating sTNF-R2 level in mice. Data shows mean ± SD (n = 3–4). *P < 0.05, compared to the vehicle group. **P < 0.01, compared to the vehicle group. P < 0.05, ††P < 0.01, compared with LPS group.
Fig. 2
Fig. 2
The chronological changes in circulating tumor necrosis factor (TNF)-α, TNF-receptor (TNF-R) 1 and TNF-R2 mRNA expression levels. Mice were treated with or without lipopolysaccharide (LPS) 20 mg/kg, and were treated with LPS 20 mg/kg and capsaicin (Cap) 4 mg/kg. (A) Circulating TNF-α mRNA expression level in mice. Data shows mean ± SD (n = 3). (B) Circulating TNF-R1 mRNA expression level in mice. Data shows mean ± SD (n = 3). (C) Circulating TNF-R1 mRNA expression level in mice. Data shows mean ± SD (n = 3). *P < 0.05, compared to the vehicle group (without LPS administration), **P < 0.01, compared to the vehicle group (without LPS administration), P < 0.05, compared to the LPS group, ††P < 0.01, compared to the LPS group.

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