ObjectiveTo compare the clinical effects of laparoscopic cholecystectomy (LC) and open cholecystectomy (OC) in the treatment of gangrenous cholecystitis and their influence on inflammatory mediators. MethodsA total of 82 patients with gangrenous cholecystitis who underwent surgery in 22 Hospital of PLA from January 2012 to June 2015 were enrolled and divided into LC group (42 patients) and OC group (40 patients). The condition of surgery and perioperative levels of inflammatory mediators were compared between the two groups. The t-test was used for comparison between the two groups, and the chi-square test was used for categorical data. ResultsAll the patients underwent the surgery successfully without deaths during the perioperative period, and three patients were converted to laparotomy. The rate of partial cholecystectomy, time of operation, intraoperative blood loss, and hospital costs showed no significant differences between the two groups (all P＞0.05). The LC group had a shorter length of postoperative hospital stay, a lower rate of drainage tube placement, and fewer postoperative complications compared with the OC group, but only the length of postoperative hospital stay showed a significant difference between the two groups (t=7472,P＜0.001). The LC group experienced significant reductions in the serum white blood cell count (WBC), C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNFα) on days 3 and 5 after surgery (all P＜0.05). The OC group experienced significant increases in serum WBC, CRP, IL-6, and TNFα on day 1 after surgery, and significant reductions in these indices on days 3 and 5 after surgery (all P＜0.05). The LC group had significantly lower serum WBC, CRP, IL-6, and TNFα on days 1, 3, and 5 after surgery compared with the OC group (all P＜0.05). ConclusionLC is safe and effective in the treatment of gangrenous cholecystitis. Compared with OC, LC has the advantages of less trauma and faster recovery after surgery and can reduce the release of inflammatory mediators.

Objective To investigate the role of TLR4/NF-κB signal pathway in pathogenesis of brain inju-ry during deep hypothermia circulatory arrest(DHCA). Methods BV2 microglia cells were subjected to oxygen-glucose deprivation/reoxygenation(OGD/R),in vitro model for DHCA. The BV2 were randomly divided into the control group(C group)and the experimental group(O group). BV2 viability was determined by CCK-8 assay. TLR4 and its downstream signaling molecules ,MyD88 and phosphorylated NF-κB (p-p65) expressions were detected by Western blotting. TLR4 mRNA expression in BV2 microglial cells were determined by RT-PCR. Level of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in culture medium was detected by ELASA. Results Compared with the group C,BV2 microglia cell viability in experiment group was obviously weaker(P<0.05). Expressions of TLR4,MyD88 and phosphorylated NF-κB(p-p65)from the experiment group increased remarkedly than those from the group C (P < 0.05). TLR4 mRNA level was higher significantly in the group O than in the group C (P < 0.01). Production of IL-6 and TNF-α in the group O were up-regulated apparently compared to the group C(P<0.01). Conclusion TLR4/NF-κB signaling pathway contributed to activation of BV2 microglia cells treated by OGD/Reoxygenation ,which was probably the exactly way that involved in pathogenesis of brain injury during deep hypothermia circulatory arrest.