Abstract
Citral is a mixture of monoterpenes present in the essential oil of several plants, such as Cymbopogon citratus and Zingiber officinale, possessing anti-inflammatory, anti-ulcerogenic, and antipyretic actions. We investigated the action of citral on body temperature (Tb) and inflammatory signaling in eutrophic and obese mice during Systemic Inflammation (SI) induced by Lipopolysaccharide (LPS). Thus, we assessed the effect of citral (25, 100, and 300 mg/kg) and ibuprofen in LPS-induced SI in Swiss male mice fed a standard diet (SD) or high-fat diet (HFD) for 12 weeks. Following SI induction, we measured Tb and collected the serum, hypothalamus, and gastric mucosa for biochemical measurements. Acute treatment with citral decreased the Tb of both SD and HFD-fed animals. Citral (300 mg/kg) treatment caused a significantly lower Tb variation in HFD-fed animals than in those fed the SD. Citral reduced peripheral levels of tumor necrosis factor (TNF)-α in SD and HFD mice and decreased serum leptin concentration in HFD mice 90 min after the LPS challenge. Furthermore, citral also reduced interleukin (IL)-6 levels in the hypothalamus of obese mice. In summary, citral effectively reduced Tb during SI by reducing inflammatory mediators with a distinct action profile in HFD mice when compared with SD.
Highlights
Obesity is a chronic disease that has been affecting different countries worldwide [1]
We observed that, in high-fat diet (HFD) mice, the increased gross organ weights were accompanied by an increase in relative weight of adipose tissues and decrease in relative weight of kidney and heart when compared with standard diet (SD) mice (p < 0.05)
During LPS-induced Systemic Inflammation (SI), our results demonstrated a significant increase in serum tumor necrosis factor (TNF)-α and IL-6 levels in both eutrophic and obese mice, corroborating with the validation of systemic inflammation induced by LPS in our model
Summary
Obesity is a chronic disease that has been affecting different countries worldwide [1]. It is a complex and multifactorial disease that involves genetic, behavioral, socioeconomic, and environmental variables. Ingestion of a high-fat diet (HFD) results in progressive body alterations and fat accumulation, triggering changes in the immune system characterized by an increase in systemic biomarkers such as interleukin (IL)-6, tumor necrosis factor (TNF)-α, and leptin [2,3,4]. The low-grade systemic inflammatory status increases the levels of proinflammatory mediators, resulting in a greater susceptibility to infections caused by alterations in the host’s homeostasis [5,6]
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