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IntroductionInterleukin-17 is a pro-inflammatory cytokine with a wide range of protective and destructive effects in periodontitis. The role of IL-23 is stabilisation and expansion of Th-17. The aim of this study was to assess whether patients with aggressive and chronic periodontitis exhibit different gingival crevicular fluid (GCF) concentrations of IL-17 and IL-23 compared with clinically healthy subjects.Material and methodsGCF samples were obtained from 32 patients: 10 with chronic periodontitis (CP), 12 with aggressive periodontitis (AgP), and 10 healthy controls (HC). IL-23 and IL-17 concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Comparison of study groups was performed with ANOVA and Tukey HSD tests. Spearman’s correlation coefficient was used to assess correlations between the variables.ResultsIL-17 concentration was significantly higher in the healthy group compared to the AgP and CP groups (p < 0.001), but there were no significant differences between the CP and AgP groups. IL-23 levels in the healthy group were significantly higher than that in the AgP group (p < 0.001). Cytokine concentrations did not correlate significantly with probing depths and clinical attachment levels.ConclusionsGingival crevicular fluid concentrations of IL-17 and IL-23 were significantly higher in the healthy group compared to periodontitis groups.

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The present study was designed to explore whether administration of estrogen affects brain cytokine levels in TBI. We also sought determine which one of type of classical estrogen receptors (ERs) is involved. Ovariectomized female rats were divided in to eight groups. Estrogen or vehicle was administered following TBI (E2 and oil groups). Antagonist of ER(ICI 182, 780) or vehicle was also administered following TBI (ICI and DMSO groups). The ICI or vehicle was administered either before induction of TBI and administration of estrogen (ICI+E2 and DMSO+E2 groups). TBI was induced by Marmarou's method. In addition to brain water content, the levels of brain proinflammatory and anti-inflammatory cytokines were measured 24 hours post- TBI. Present results demonstrated that, estrogen reduced TBI- induced brain edema. The antiedema effect of estrogen was attenuated by ICI. The brain measures of IL-1β, IL-6 and TNF-α in TBI were also reduced by estrogen. The anti-inflammatory effect of estrogen was attenuated by ICI. The inhibition level of estrogen by ICI was 53.2%, 12.09% and 48.45% for IL-1β, IL-6 and TNF-α, respectively. Estrogen also elevated IL-10 in TBI. ICI inversely controlled the effect of estrogen on IL-10, by 33.84%. This effect was not observed once ICI was used alone. The estrogen administration following TBI probably results in proinflammatory cytokines reduction, and inversely enhancement of anti-inflammatory cytokines. In our study, the neuroprotective effect of estrogen is proposed to be mediated by both ERα and ERα, and accordingly the inhibition of neuroprotective effect of estrogen by ICI.

Traumatic brain injury (TBI) is a major health concern affecting the general public as well as military personnel. However, there is no FDA-approved therapy for the treatment of TBIs. In this work, we investigated the neurotherapeutic effects of the well-known natural Iranian medicine Satureja Khuzistanica Jamzad (SKJ) essential oil (SKEO) on the outcomes of diffused experimental TBI, with particular attention paid to its anti-inflammatory and anti-apoptotic effects. Male Wistar rats were treated with doses of 50, 100 and 200 (mg/kg, i.p) SKEO after induction of diffused TBIs. The results showed that injecting SKEO (200 mg/kg) 30 minutes after TBI significantly reduced brain oedema and damage to the blood-brain barrier (BBB) and limited the post-TBI increase in intracranial pressure. The veterinary coma scale (VCS) scores significantly improved in the treatment group. Also, inflammatory marker assays showed reduced levels of TNF-α, IL-1β, and IL-6 and increased IL-10 in the treated groups. Moreover, the immunohistochemical results indicated that SKEO not only reduced neuronal death and BBB permeability but also affected astrocytic activation. Overall, our data indicate potential clinical neurological applications for SKEO.

Increased levels of inflammatory cytokines after traumatic brain injury (TBI) can lead to brain edema and neuronal death. In this study, the effect of melatonin on pro-inflammatory (IL-1ß, IL-6, and TNF-α) and anti-inflammatory (IL-10) cytokines following TBI was investigated considering anti-inflammatory effect of melatonin. Male Wistar rats were divided into five groups: Sham, TBI, TBI + VEH (vehicle), TBI + 5 mg dose of melatonin (MEL5), TBI + 20 mg dose of melatonin (MEL20). Diffuse TBI was induced by Marmarou method. Melatonin was administered 1, 24, 48 and 72 h after TBI through i.p. Brain water content and brain levels of pro-inflammatory (IL-1ß, IL-6 and TNF-α) and anti-inflammatory (IL-10) cytokines were measured 72 h after TBI. The IL-1ß levels decreased in the TBI + MEL5 and TBI + MEL20 groups in comparison to TBI + VEH group (p < 0.001). The levels of IL-6 and TNF-α also decreased in melatonin-treated groups compared to control group (p < 0.001). The amount of IL-10 decreased after TBI. But melatonin administration increased the IL-10 levels in comparison with TBI + VEH group (p < 0.001). The results showed that melatonin administration affected the brain levels of pro-inflammatory and anti-inflammatory cytokines involving in brain edema led to neuronal protection after TBI.

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