Shirin Torkestani; Alireza Zamani; Mehrdokht Mazdeh; Elahe Talebi-Ghane; Ghodratoallah Roshanaie; Mohammad Mahdi Eftekharian
Abstract
Background: Abnormal humoral and cellular immune responses have been reported in immune-mediated polyneuropathies. CD137, as a costimulatory molecule and a TNF receptor superfamily member, has been demonstrated to have a key role in the pathogenesis of many autoimmune as well as inflammatory disorders.Objective: ...
Read More
Background: Abnormal humoral and cellular immune responses have been reported in immune-mediated polyneuropathies. CD137, as a costimulatory molecule and a TNF receptor superfamily member, has been demonstrated to have a key role in the pathogenesis of many autoimmune as well as inflammatory disorders.Objective: To evaluate the transcripts levels of CD137, its ligand (CD137L), and the serum levels of soluble CD137 (sCD137) in patients with immune-mediated polyneuropathy.Methods: A total of 45 patients and 46 sex and age-matched healthy individuals were enrolled in the study. CD137 and CD137L transcript levels were assessed by the Real-Time PCR, and the serum level of sCD137 was measured using the ELISA technique. The Bayesian regression model was used for statistical analysis at the 0.05 significance level in R 4.1.0 statistical environment. Results: Transcript levels of the CD137 and CD137L were higher in polyneuropathy patients in comparison with the healthy subjects (P=0.006 for both). Conversely, the mean level of sCD137 was significantly lower in the sera of patients compared to the controls (P<0.001).Conclusion: Our findings point to the possible role of CD137 and CD137L in immune-mediated polyneuropathy pathogenesis. More investigations are required to clarify the exact contributions of the mentioned molecules to the pathogenesis of immune-mediated polyneuropathies.
Shahriar Shahriari; Aliasghar Rezaei; Seyed Mohsen Jalazadeh; Khosro Mani; Alireza Zamani
Volume 8, Issue 3 , September 2011, , Pages 176-182
Abstract
Background: Bone resorption is one of the main features of inflammatory periapical lesions and is mainly mediated by interleukin-1 beta (IL-1β), tumor necrosis factoralpha (TNF-α) and prostaglandin-E2 (PGE2). Recent investigations of these lesions revealed that pharmacological modulation may ...
Read More
Background: Bone resorption is one of the main features of inflammatory periapical lesions and is mainly mediated by interleukin-1 beta (IL-1β), tumor necrosis factoralpha (TNF-α) and prostaglandin-E2 (PGE2). Recent investigations of these lesions revealed that pharmacological modulation may be possible. Objective: The aim of this study was to evaluate the effect of Ibuprofen on IL-1β, TNF-α and PGE2 levels in periapical exudates and compare the results with a group of placebo control. Methods: Thirty patients with non vital teeth and radiographic lesions were divided into two groups of case and control according to their entrance to the study. Periapical exudates were taken from root canals using absorbent paper points and followed by 400 mg Ibuprofen and placebo prescribed one tablet every 6 hour for three days and in the fourth day second samples were taken, then final cleaning, shaping and obturation of the canals were completed. IL-1β, TNF-α and PGE2 levels were determined by enzymelinked immunosorbent assays (ELISA). Data were analyzed using paired t-test and student's t-test. Results: The results showed that PGE2 levels were decreased significantly in the case group to 86.92 ± 72.42 Pg/ml following Ibuprofen treatment comparing with the pre-treatment (164.96 ± 12.255 Pg/ml) (p=0.02) and placebo group (154.2 ± 97.13 Pg/ml) (p=0.001). But there were no significant differences in IL-1β and TNF-α level between the two groups and in each group before and after treatment. Conclusion: The data indicate that Ibuprofen, as a non-steroidal anti-inflammatory drug (NSAID), can be used to block PGE2 release, enhance healing of inflammatory periapical lesions and possibly to inhibit bone resorption.
