BACKGROUND:Ethyl linoleate has been proved to attenuate the inflammatory-cytokines release induced by lipopolysaccharide, but whether it can inhibit titanium-induced osteolysis and the underlying mechanism remain unclear. OBJECTIVE:To observe the effect of ethyl linoleate on the expression of inflammatory-related factors induced by titanium particles and explore its mechanism. METHODS:Forty-eight Kunming mice were randomly divided into blank control, titanium, dimethylsulfoxide (DMSO) and experimental groups. The back air pouch Inflammatory models were established in the mice of the titanium, DMSO and experimental groups, in which the 200 μL menstruum of DMSO (0.5%) and 200 μL ethyl linoleate (0.5%) were respectively administered into the pouch of the mice at 12 hours. Mice in the blank control group received no intervention. Fourteen days later, the inflammatory cel infiltration in the skin was examined through hematoxylin-eosin staining;the expression levels of inhibitorκB-α, nuclear factor-κB, inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-αand interleukin-6 as wel as ERK, p-ERK, JNK, p-JNK, p38 and p-p38 in MAPK signaling pathways were evaluated by western blot assay. RESULTS AND CONCLUSION:In the titanium group and DMSO group, there were numerous inflammatory cel s and vacuole-like necrotic tissues in the hair fol icle lacuna of dermis and loose connective tissues of hypodermis. The experiment group showed significant reduction in inflammatory cel infiltration and vacuole-like necrosis. Compared with the blank control group, the expression levels of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κB, tumor necrosis factor-α, interleukin-6, ERK, JNK and p38 in the DMSO and titanium groups were significantly increased, while inhibitorκB-αsignificantly decreased (P<0.05). Compared with the DMSO and titanium groups, there were significantly down-regulated levels of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κB, tumor necrosis factor-α, interleukin-6, ERK, JNK and p38, and up-regulated inhibitorκB-αlevel in the experimental group (P<0.05). In conclusion, ethyl linoleate can remarkably suppress the expressions of titanium-induced inflammatory factors associated with the inhibition of nuclear factor-κB and MAPK signaling pathway activation.

Objective: Using ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) and microPET-CT to test the feasibility of ¹⁸F-FDG PET-CT for validation of olfactory function of rats with standard phenethyl alcohol (PEA) and isovaleric acid (IVA) odors stimulation. To verify the possibility of ¹⁸F-FDG PET-CT as a new objective examination method for olfactory function. Methods: Six healthy Sprague-Dawley (SD) male rats were selected with a weight of 250-300 g. First of all, buried food pellet test (BFT) was used to confirm the normal olfactory function of rats. Then in the next 3 days, after the intravenous injection of ¹⁸F-FDG (18 MBq/100 g), awaken rats were placed in a ventilated plexiglas cage for 30 min. Subsequently, pure air (the first day), PEA (the second day) and IVA (the third day) were delivered. After odor stimulation for 30 min, rats were performed by a static PET-CT under anesthesia. Images reconstructed were assessed by SPM method and analyzed by VBM method. Data was analysied by paired t test. Results: Activation regions of rat′s brain after PEA stimulation included bed nucleus and insula. Activation regions of rat′s brain after IVA stimulation included olfactory bulb, anterior olfactory nucleus, amygdala, entorhinal cortex, olfactory cortex, piriform cortex, insula, prefrontal cortex, cingulate cortex and bed nucleus (P<0.005, Ke>20 voxels). Conclusions Through microPET-CT, we can observe that olfactory stimulation with different odors can induce metabolic activation in different regions of rat′s brain, which was in concordance with olfactory regions. The olfactory related brain regions of rats have strong responses to odor stimulation of IVA.