Asghari-Roodsari A.,Basic Medical science Research Center |
Lesani A.,Basic Medical science Research Center |
Javadi-Paydar M.,Basic Medical science Research Center |
Javadi-Paydar M.,Brain and Spinal Injury Repair Research Center |
And 5 more authors.
Reproductive Sciences | Year: 2010
Introduction: In this study, we explained that exogenous cannabinoid, Δ9-tetrahydrocannabinol (THC), has a preventive effect in a murine model of lipopolysaccharide (LPS)-induced preterm delivery and the contribution of nitric oxide (NO) pathway as a mechanism involved in this process. Study Design: Preterm delivery was induced by double dose of 35 μg/kg LPS with 3-hour interval on gestational day (gd) 15. Δ9-tetrahydrocannabinol was administered with (a) double dose (0.02, 0.05, 0.1, 0.5, 1, and 5 mg/kg) 1 hour before each LPS injection, on gd 15 and (b) single administration (0.05, 0.1, and 0.5 mg/kg,) on gds 13 and 14, and the double administration, 1 hour before each LPS injection. To assess the involved mechanism, either AM281 (CB1 receptor antagonist, 2 mg/kg) and AM630 (CB2 receptor antagonist, 5 mg/kg) or Nω-nitro-L-arginine methyl ester (L-NAME, 2 mg/kg) was administered 1 hour before each THC injection on gds 13, 14, and 15. The main outcome measurement was the incidence of preterm delivery after injection of last LPS dose. Any interaction in the incidence and time of preterm delivery was ruled out by administration of AM281, AM630, or L-NAME alone. Results: Chronic THC treatment (0.5 mg/kg) significantly decreased the incidence of LPS-induced premature labor and increased the delivery time. Both AM281 and L-NAME reversed THC-induced attenuation of preterm delivery rate and pregnancy duration. Unlike AM281, AM630 did not influence the rate of preterm delivery in THC-treated mice. Conclusion: Δ9-Tetrahydrocannabinol contributes to the regulation of gestational duration in LPS-induced preterm delivery probably by NO coupling through the CB1 receptor.
Qiu J.-L.,Basic Medical science Research Center |
Zhu W.-L.,shanxi Fourth Peoples Hospital |
Lu Y.-J.,Basic Medical science Research Center |
Bai Z.-F.,Basic Medical science Research Center |
And 6 more authors.
Neurochemistry International | Year: 2015
Sulfur dioxide (SO2) is a common air pollutant and can cause harmful insults on neurons. Microglial activation has been implicated in the signaling cascades that contribute to neuronal cell death in various neurological disorders. In the present study, we found that SO2 derivatives decreased cell viability via inducing oxidative stress, inflammatory responses and apoptotic cell death in BV2 microglial cells. Pretreatment with (RS)-2-chloro-5-hydroxyphenylglycine (CHPG), an mGluR5 agonist, significantly attenuated the SO2-induced cytotoxicity, which was fully prevented by the mGluR5 antagonist MPEP. CHPG increased the expression of TNF-α stimulated gene/protein 6 (TSG-6), but decreased the activation of nuclear factor-κB (NF-κB) after SO2 derivatives treatment in BV2 cells. In addition, knockdown of TSG-6 expression by specific targeted short interfering RNA (siRNA) partially reversed the protection induced by CHPG. Therefore, our findings reveal a mechanistic basis for exploring the association between SO2 exposure and neurological disorders, and also for opening up therapeutic approaches of ameliorating neuronal injury resulting from exposure in atmospheric polluting environment. © 2015 Elsevier Ltd. All rights reserved.