Protective effect of leaf essential oil from Cinnamomum osmophloeum Kanehira on endotoxin-induced intestinal injury in mice associated with suppressed local expression of molecules in the signaling pathways of TLR4 and NLRP3

Shih-Chieh Lee; Jie-Sheng Hsu; Chien-Chun Li; Ke-Ming Chen; Cheng-Tzu Liu

doi:10.1371/journal.pone.0120700

Protective effect of leaf essential oil from Cinnamomum osmophloeum Kanehira on endotoxin-induced intestinal injury in mice associated with suppressed local expression of molecules in the signaling pathways of TLR4 and NLRP3

PLoS One. 2015 Mar 20;10(3):e0120700. doi: 10.1371/journal.pone.0120700. eCollection 2015.

Authors

Shih-Chieh Lee¹, Jie-Sheng Hsu², Chien-Chun Li², Ke-Ming Chen³, Cheng-Tzu Liu⁴

Affiliations

¹ Department of BioIndustry Technology, Da-Yeh University, No. 168, University Rd., Dacun, Changhua, Taiwan, Republic of China.
² School of Nutrition, Chung Shan Medical University, No. 110, Sec. 1, Chien Kuo N. Rd., Taichung, Taiwan, Republic of China.
³ Department of Parasitology, Chung Shan Medical University, No. 110, Sec. 1, Chien Kuo N. Rd., Taichung, Taiwan, Republic of China.
⁴ School of Nutrition, Chung Shan Medical University, No. 110, Sec. 1, Chien Kuo N. Rd., Taichung, Taiwan, Republic of China; Department of Nutrition, Chung Shan Medical University Hospital, No. 110, Sec. 1, Chien Kuo N. Rd., Taichung, Taiwan, Republic of China.

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.