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
نویسندگان
چکیده
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.
منابع مشابه
TLR2 and TLR4 Signaling Pathways and Gastric Cancer: Insights from Transcriptomics and Sample Validation
Background: Pattern recognition receptors, especially toll-like receptors (TLRs), as the first line of defense for pathogen detection, were found to be associated with H. pylori infection and gastric cancer (GC). However, the expression levels of TLRs, i.e. TLR2 and TLR4, as the main receptors sensed by H. pylori, still remain largely ambiguous. We aimed to investigate the patterns of key tra...
متن کاملSoluble uric acid induces inflammation via TLR4/NLRP3 pathway in intestinal epithelial cells
Objective(s): Hyperuricemia is a risk for cardiovascular and metabolic diseases, but the mechanism is ambiguous. Increased intestinal permeability is correlated with metabolic syndrome risk factors. Intestinal epithelial cells play a pivotal role in maintaining intestinal permeability. Uric acid is directly eliminated into intestinal lumen, however, the mechanism and e...
متن کاملFiltered Kombucha Tea Rings the Bell for TLR2, TLR4, MYD88, and Dectin-1 in Mice Model of Colitis
Background and objectives: TLR2, TLR4, and Dectin-1 (Clec7) are pattern recognition receptors (PRRs) expressed by intestinal epithelia cells and MYD88 is a signaling molecule of TLR2 and TLR4. They warn immune system about the presence of invading pathogens promoting initiation of inflammatory response. Because of colonic cancer risk, therapy of intestinal inflammation is of h...
متن کاملP 147: Role of Sparstolonin B in Intracerebral Hemorrhage-Induced Inflammatory Brain Injury: Blocking the Formation of TLR2/TLR4 Heterodimer
Intra-cerebral hemorrhage (ICH) is a particularly severe type of stroke accounting for 10–15 % of all strokes and is associated with a mortality rate of 30–50%. Neuroinflammation contributes to ICH-induced secondary brain injury and understanding the mechanisms causing neuroinflammation can be helpful to find new treatments of ICH. Recent studies demonstrated that toll like receptor...
متن کاملHyperin protects against LPS-induced acute kidney injury by inhibiting TLR4 and NLRP3 signaling pathways
Hyperin is a flavonoid compound derived from Ericaceae, Guttifera, and Celastraceae that has been shown to have various biological effects, such as anti-inflammatory and anti-oxidant effects. However, there is no evidence to show the protective effects of hyperin on lipopolysaccharide (LPS)-induced acute kidney injury (AKI). Therefore, we investigated the protective effects and mechanism of hyp...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 10 شماره
صفحات -
تاریخ انتشار 2015