Electroacupuncture ST36 prevents postoperative intra-abdominal adhesions formation.

BACKGROUND: We have recently proved electroacupuncture (EA) ST36 exerted an anti-inflammatory effect in the early phase of intra-abdominal adhesion formation. Evidences indicate that the anti-inflammatory effect of EA ST36 involves a cholinergic anti-inflammatory pathway-dependent mechanism via the vagus nerve. However, the exact effects and accurate vagal modulation of acupuncture in prevention of postoperative intra-abdominal adhesion formation has not been thoroughly evaluated. MATERIALS AND METHODS: Sprague-Dawley rats subjected to abdominal adhesion lesions operation at the cecum and abdominal wall were randomly divided into six groups as follows: (a) EAN: EA non-channel acupoints; (b) EA: EA ST36 after abdominal lesions; (c) VGX/EA: vagotomy (VGX) after abdominal lesions, then EA ST36; (d) VGX/EAN: VGX after abdominal lesions, then EAN; (e) α-BGT/EA: intraperitoneal injection of α-bungarotoxin (α-BGT, an antagonist of α7 subunit of cholinergic nicotinic receptor) before EA ST36, and (f) α-BGT/EAN group: α-BGT injection before EAN. Seven days after abdominal surgical lesions, the levels of tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) in the adhesive tissue were evaluated, macroscopic observation and histopathologic evaluation of adhesion formation and assessment of angiogenesis by immunohistochemical staining of platelet endothelial cell adhesion molecule-1 (CD31) were performed. RESULTS: EA ST36 reduced TNF-α and VEGF levels in adhesive tissue homogenates 7 d after surgery, whereas vagotomy or intraperitoneal injection of α-BGT before EA ST36 reversed its suppressive effects. EA at non-channel acupoints with or without vagotomy or intraperitoneal injection of α-BGT before EA had no suppressive effects on TNF-α and VEGF levels. EA ST36 alleviated the adhesion formation, with both of macroscopic and histopathologic adhesion scores significantly lower than those of the EAN group (1.56 ± 0.29 versus 3.00 ± 0.82, 1.35 ± 0.4 versus 3.91 ± 0.8, respectively, both P < 0.05). Compared with the EAN group, EA ST36 significantly decreased angiogenesis evidenced by reduced CD31 positive microvessel density in adhesive tissue. CONCLUSIONS: EA ST36 might reduce the postoperative local inflammatory response, attenuate the angiogenesis, and alleviate the adhesion formation partly via activating the cholinergic anti-inflammatory mechanism.

Pyruvate Is Superior to Citrate in Oral Rehydration Solution in the Protection of Intestine via Hypoxia-Inducible Factor-1 Activation in Rats With Burn Injury.

BACKGROUND: Recent studies have suggested that pyruvate-enriched oral rehydration solution (Pyr-ORS) may be superior to the standard bicarbonate-based ORS in the protection of intestine from ischemic injury. The aim of this study was to compare the effects of Pyr-ORS with citrate-enriched ORS (Cit-ORS) on the intestinal hypoxia-inducible factor-1 (HIF-1)-erythropoietin (EPO) signaling pathway for enteral rehydration in a rat model of burn injury. METHODS: Rats were randomly assigned to 4 groups (N = 20, 2 subgroups each: n = 10): scald sham (group SS), scald with no fluid resuscitation (group SN), scald and resuscitation with enteral Cit-ORS (group SC), and scald and resuscitation with enteral Pyr-ORS (group SP). At 2.5 and 4.5 hours after a 35% total body surface area (TBSA) scald, intestinal mucosal blood flow (IMBF), contents of HIF-1, EPO, endothelial nitric oxide synthase (eNOS), nitric oxide (NO), barrier protein (ZO-1), levels of serum diamine oxidase (DAO), and intestinal mucosal histology injury score were determined. RESULTS: Serum DAO activities in the scalded groups were significantly elevated, but less raised in group SP than in group SC, at 2.5 hours and at 4.5 hours after the scald. Further, group SP more profoundly preserved intestinal HIF-1 expression compared with group SC at the 2 time points. Compared with group SC, group SP had markedly elevated intestinal EPO, eNOS, and NO levels at the same time points, respectively (P < .05). Similarly, IMBF and ZO-1 levels were significantly higher in group SP than in group SC. Intestinal mucosal histopathological scores were statistically higher at 2.5 hours and 4.5 hours after scalding but were more attenuated in group SP than in group SC (P < .05). Immunofluorescence expression of intestinal mucosal ZO-1 was consistent with the above changes. The above parameters were also significantly different between groups SC and SN (all P < .05). CONCLUSION: Pyr-ORS provides a superior option to Cit-ORS for the preservation of intestinal blood flow and barrier function and the attenuation of histopathological alterations in enteral resuscitation of rats with burn injury. Its underlying mechanism may be closely related to the pyruvate in activation of intestinal HIF-1-EPO signaling cascades.

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 inflammatory response 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 dUTP 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.

Electroacupuncture at Zusanli (ST36) promotes gastric emptying and mucosal blood flow during oral resuscitation of scalded rats with a pyruvate-enriched ORS.

AIM: The aim of this study was to investigate the effect of electroacupuncture at ST36 (EA ST36) on gastric emptying and mucosal blood flow during intragastric resuscitation with pyruvate-enriched oral rehydration solution (Pyr-ORS) in scalded rats. METHODS: The rats were subjected to a 35% total body surface area (TBSA) of scald injury and randomly divided into five groups (N=24) and two subgroups (n=12) in each group. The Pyr-ORS was delivered intragastrically according to the Parkland formula immediately after scalding at a dose of 1 mL kg(-1) %TBSA(-1) in 1 h. In these animals, the bilateral Zusanli points (ST36) were electroacupunctured at a constant voltage (2 mA and 2-100 HZ) for 0.5 h immediately after intragastric resuscitation. At 2 and 4 h after scalding, the gastric emptying rate (GER) and gastric mucosal blood flow (GMBF) were determined, and the motilin levels of the plasma and gastric tissues were also analyzed at two time points, respectively. RESULTS: GER and GMBF were markedly decreased in groups with scalding and resuscitation, compared with the sham groups at two time points (P<0.05), but they were greatly improved in groups byEAST36 at 2 and 4 h after sustaining scald injuries (P<0.05). Bilateral vagotomy further aggravated the reduction of GER and GMBF in scalded rats. EA after gastric vagotomy failed to raise GER and GMBF. Neither EA nor vagotomy had effects on the reduced motilin levels of plasma and gastric tissues in animals after scalding. CONCLUSION: EA ST36 has a significant effect on improving gastric emptying and mucosal ischemia in the oral resuscitation of burn injury, possibly through the activation of a cholinergic nerve-dependent mechanism. In addition, EA ST36 showed no effects on motilin levels, but requires further investigations.

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) α-bungarotoxin (BGT)/EA: intraperitoneal injection of α-BGT before hemorrhage, then EA ST36; and (7) α-BGT group: α-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-kDa 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, α-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/mL vs 2466.7 ± 131.60 ng/mL, P < 0.05) and preserved ZO-1 protein expression and localization at 6 h after hemorrhage compared with the HS group. However, abdominal VGX and α-BGT treatment weakened or eliminated the effects of EA ST36. EA ST36 reduced tumor necrosis factor-α levels in intestinal homogenates after blood loss, while vagotomy or intraperitoneal injection of α-BGT before EA ST36 abolished its anti-inflammatory effects. CONCLUSION: EA ST36 attenuates hemorrhage-induced intestinal inflammatory insult, and protects the intestinal barrier integrity, partly via activation of EGCs.