Abstract
Endotoxin is a potent microbial mediator implicated in sepsis. We investigated the anti-inflammatory effect of leaf essential oil from Cinnamomum osmophloeum Kanehira (CO) of the linalool chemotype on endotoxin-injected mice. Mice were administered CO or vehicle by gavage before endotoxin injection and were killed 12 h after injection. Neither growth nor the organ weight or tissue weight to body weight ratio was affected by CO treatment. CO significantly lowered peripheral levels of tumor necrosis factor-α, interleukin (IL)-1β, IL-18, interferon-γ, and nitric oxide and inhibited the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response gene (88), myeloid differentiation factor 2, apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC), caspase-1, and Nod-like receptor family, pyrin domain containing 3 (NLRP3). CO also inhibited the activation of nuclear factor-ĸB, inhibited the activity of caspase-1 in small intestine, and ameliorated intestinal edema. Our data provide strong evidence for a protective effect of CO of the linalool chemotype in the endotoxin-induced systemic inflammatory response in close association with suppression of the TLR4 and NLRP3 signaling pathways in intestine.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Anti-Inflammatory Agents / pharmacology
-
Body Weight
-
Carrier Proteins / metabolism*
-
Cinnamomum / chemistry*
-
Cytokines / metabolism
-
Disease Models, Animal
-
Endotoxins / adverse effects
-
Ileum / metabolism
-
Ileum / pathology
-
Inflammation Mediators / metabolism
-
Intestinal Mucosa / metabolism*
-
Intestinal Mucosa / pathology
-
Intestines / pathology
-
Lymph Nodes / metabolism
-
Male
-
Mesentery
-
Mice
-
NF-kappa B / metabolism
-
NLR Family, Pyrin Domain-Containing 3 Protein
-
Nitrates / metabolism
-
Nitrites / metabolism
-
Oils, Volatile / pharmacology*
-
Organ Size
-
Plant Leaves / chemistry*
-
Protective Agents / pharmacology*
-
Signal Transduction / drug effects
-
Systemic Inflammatory Response Syndrome / chemically induced
-
Systemic Inflammatory Response Syndrome / metabolism*
-
Systemic Inflammatory Response Syndrome / pathology
-
Toll-Like Receptor 4 / metabolism*
-
Xanthine Oxidase / metabolism
Substances
-
Anti-Inflammatory Agents
-
Carrier Proteins
-
Cytokines
-
Endotoxins
-
Inflammation Mediators
-
NF-kappa B
-
NLR Family, Pyrin Domain-Containing 3 Protein
-
Nitrates
-
Nitrites
-
Nlrp3 protein, mouse
-
Oils, Volatile
-
Protective Agents
-
Toll-Like Receptor 4
-
Xanthine Oxidase
Grants and funding
This work was supported by a grant from the Ministry of Science and Technology, Taiwan, ROC (NSC 101-2313-B-040 -008 -MY3). The website of the funder is
http://www.most.gov.tw/mp.aspx. This funding was provided to CTL. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.