Electroacupuncture activates enteric glial cells and protects the gut barrier in hemorrhaged rats

AIM:To investigate whether electroacupuncture ST36 activates enteric glial cells,and alleviates gut inflammation and barrier dysfunction following hemorrhagic shock.METHODS:Sprague-Dawley rats were subjected to approximately 45% total blood loss and randomly divided into seven groups:(1) sham:cannulation,but no hemorrhage;(2) subjected to hemorrhagic shock(HS);(3) electroacupuncture(EA) ST36 after hemorrhage;(4) vagotomy(VGX)/EA:VGX before hemorrhage,then EA ST36;(5) VGX:VGX before hemorrhage;(6) a-bungarotoxin(BGT)/EA:intraperitoneal injection of a-BGT before hemorrhage,then EA ST36; and(7) a-BGT group:a-BGT injection before hemorrhage.Morphological changes in enteric glial cells(EGCs) were observed by immunofluorescence,and glial fibrillary acidic protein(GFAP; a protein marker of enteric glial activation) was evaluated using reverse transcriptase polymerase chain reaction and western blot analysis.Intestinal cytokine levels,gut permeability to 4-k Da fluorescein isothiocyanate(FITC)-dextran,and the expression and distribution of tight junction protein zona occludens(ZO)-1 were also determined.RESULTS:EGCs were distorted following hemorrhage and showed morphological abnormalities.EA ST36 attenuated the morphological changes in EGCs at 6 h,as compared with the VGX,a-BGT and HS groups.EA ST36 increased GFAP expression to a greater degree than in the other groups.EA ST36 decreased intestinal permeability to FITC-dextran(760.5 ± 96.43 ng/m L vs 2466.7 ± 131.60 ng/m L,P < 0.05) and preserved ZO-1 protein expression and localization at 6 h afterhemorrhage compared with the HS group.However,abdominal VGX and a-BGT treatment weakened or eliminated the effects of EA ST36.EA ST36 reduced tumor necrosis factor-a levels in intestinal homogenates after blood loss,while vagotomy or intraperitoneal injection of a-BGT before EA ST36 abolished its antiinflammatory effects.CONCLUSION:EA ST36 attenuates hemorrhageinduced intestinal inflammatory insult,and protects the intestinal barrier integrity,partly via activation of EGCs.

Dimethyl sulfoxide inhibits zymosan-induced intestinal inflammation and barrier dysfunction

AIM: To investigate whether dimethyl sulfoxide(DMSO) inhibits gut inflammation and barrier dysfunction following zymosan-induced systemic inflammatoryresponse syndrome and multiple organ dysfunction syndrome.METHODS: Sprague-Dawley rats were randomly divided into four groups: sham with administration of normal saline(SS group); sham with administration of DMSO(SD group); zymosan with administration of normal saline(ZS group); and zymosan with administration of DMSO(ZD group). Each group contained three subgroups according to 4 h,8 h,and 24 h after surgery. At 4 h,8 h,and 24 h after intraperitoneal injection of zymosan(750 mg/kg),the levels of intestinal inflammatory cytokines [tumor necrosis factor-alpha(TNF-α) and interleukin(IL)-10] and oxides(myeloperoxidase,malonaldehyde,and superoxide dismutase) were examined. The levels of diamine oxidase(DAO) in plasma and intestinal mucosal blood flow(IMBF) were determined. Intestinal injury was also evaluated using an intestinal histological score and apoptosis of intestinal epithelial cells was determined by deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay. The intestinal epithelial tight junction protein,ZO-1,was observed by immunofluorescence.RESULTS: DMSO decreased TNF-α and increased IL-10 levels in the intestine compared with the ZS group at the corresponding time points. The activity of intestinal myeloperoxidase in the ZS group was higher than that in the ZD group 24 h after zymosan administration(P < 0.05). DMSO decreased the content of malondialdehyde(MDA) and increased the activity of superoxide dehydrogenase(SOD) 24 h after zymosan administration. The IMBF was lowest at 24 h and was 49.34% and 58.26% in the ZS group and ZD group,respectively(P < 0.05). DMSO alleviated injury in intestinal villi,and the gut injury score was significantly lower than the ZS group(3.6 ± 0.2 vs 4.2 ± 0.3,P < 0.05). DMSO decreased the level of DAO in plasma compared with the ZS group(65.1 ± 4.7 U/L vs 81.1 ± 5.0 U/L,P < 0.05). DMSO significantly preserved ZO-1 protein expression and localization 24 h after zymosan administration. The TUNEL analysis indicated that the number of apoptotic intestinal cells in the ZS group was much higher than the ZD group(P < 0.05).CONCLUSION: DMSO inhibited intestinal cytokines and protected against zymosan-induced gut barrier dysfunction.