, 2006, Pan et al., 2007, Pan et al., 2010 and Pan et al., 2013). It reduces inflammation

induced by serotonin (Bianchi et al., 1994) and inhibits NF-κB signaling in intestinal epithelial cells exposed to dextran sulfate sodium (Koh et al., 2011). Furthermore, fluoxetine decreases microglial release of glutamate and D-serine to promote cortical neuronal viability following ischemic insult (Dhami et al., 2013), prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced loss of dopaminergic neurons by inhibiting microglial activation (Chung et al., 2011), and reduces inflammatory response in lipopolysaccharides-stimulated microglial selleck compound cells (Liu et al., 2011), indicating that fluoxetine may have the anti-inflammatory

action in glial cells. We therefore investigated the effects of fluoxetine on CUMS-induced these inflammatory alterations in rats. This study may further support the hypothesis that microglial NLRP3 inflammasome activation may be a mediator of IL-1β-related CNS inflammation in depression. Male Wistar rats, weighting 180–220 g were purchased from the Suzhou Industrial Park AyeMatt Technology Co., Ltd. (Suzhou, China, Certificate No. SCXK(Su)2009-0001) and housed in plastic cages with a 12:12-h light–dark cycle under constant temperature of 22–24 °C and relative humidity (50–60%). They were fed standard chow ad libitum and allowed 4 weeks of Trametinib acclimatization to the laboratory environment. The mean body weight was about 300 g before experiments.

PLEKHB2 All the procedures were in strict accordance with China legislation on the use and care of laboratory animals and with the guidelines established by the Institute for Experimental Animals of Nanjing University. All rats were trained to consume 1% sucrose solution before CUMS procedure. This training consisted of initial 72 h sucrose solution exposure without any food or water available. Baseline test of sucrose solution intake was performed 3 times over 7 days. Sucrose intake was tested a 14 h period of food and water deprivation followed by the offering of a sucrose solution for 1 h. At the end of each test, sucrose intake was calculated and expressed as relative sucrose intake in relation to animal body weight (g/kg), respectively. Subsequently, sucrose solution intake test was monitored under similar condition in 1 h test (11:00–12:00 h) at 2-week intervals for the subsequent 12 weeks of CUMS procedure, respectively. On the basis of sucrose intake in the final baseline test, rats were discarded due to extraordinary variations in baseline. Remained rats were randomly divided Non-CUMS, CUMS and CUMS + Fluoxetine groups, having average intake ranges. The diagrammatic experimental procedure of CUMS was presented in Fig. 1. All of the stressors were shown in Table 1 as previously described by Pan et al.