1.Clinical value of laparoscopic surgery by pull through technique for anterior resection of rectum in patient with rectal cancer
Hengjun LIN ; Xueke QIU ; Hang YUAN
China Journal of Endoscopy 2017;23(1):1-5
Objective To compare the clinical values of laparoscopic surgery and laparoscopic surgery by pull through technique for anterior of rectum in patients with rectal cancer. Methods From Jan, 2013 to Jan, 2014, 120 patients with low rectal cancer were prospectively collected. The patients were randomly divided into study group (n= 60) and control group (n= 60). Patients in the study group were treated with laparoscopic surgery by pull through technique for anterior resection of rectum, while patients in the control group were treated with laparoscopic surgery. The primary outcomes were intraoperative situations, postoperative complications and recovery. Results When compared with the control group, patients in the study group got a significantly shorter operative duration [(132.32±14.92) vs (154.73±17.65) min, P=0.000];a signiifcantly lower postoperative drainage volume [(299.93±56.49) vs (365.24±68.94) ml, P= 0.000]; a significantly shorter gastrointestinal function recovery time [(57.42±5.84) vs (61.85±7.40) h, P=0.002]; and a signiifcantly less of length of hospital stay [(12.54±2.76) vs (14.75±2.10) d, P= 0.000]. There was no significant difference between the two groups in the amount of bleeding, the number of lymph node dissection, pneumonia, lower extremity arteriovenous thrombosis, incision infection, anastomotic leakage, intestinal obstruction, 2-year recurrence rate and mortality rate (P> 0.05). Conclusion laparoscopic surgery by pull through technique for anterior resection of rectum can accelerate postoperative recovery.
2.The inhibitory effect of Sulindac on human pancreatic cancer cells' proliferation by targeting survivin/ Aurora B pathway
Xueke FAN ; Yusheng LIAO ; Cuifang ZHANG ; Fen CHEN ; Huitao GAO ; Hua QIN ; Demin LI ; Qiu ZHAO
Chinese Journal of Pancreatology 2008;8(5):315-318
Objective To observe the expression of survivin and Aurora B in human pancreatic cancer BXPC3 cells after the treatment of sulindac and to explore the potential mechanism. Methods MTr assay was used to determine the effect of sulindac on the proliferation of the BXPC3 cells. RT-PCR was used to detect the expression of mRNA level of survivin and Aurora B, western blot was used to detect protein expression of survivin and Aurora B Thr-232. Cell cycle and apoptosis were detected by flow eytometry (FCM). Results The BXPC3 cells were inhibited by sulindac in a dose and time-dependent manner; the expression of mRNA of survivin and Aurora B were both significantly decreased from 1.5644 and 0.6554 to 0. 4372 and 0.1132 (P< 0.01), the expression of survivin protein and the phosphorylation of Aurora B Thr-232 were also decreased from 1.2735 and 0.4680 to 0.2126 and 0.2546 (P<0.01); the proportion of cells in the G0/G1 phase was increased from (56.65±1.93)% to (70.58±3.21)% (P<0.01). Conclusions Sulindac had inhibitory effects on the growth of BXPC3 cells, the possible mechanism was via decreasing the expression of survivin which depressed the activity of Aurora B, then the CPC was influenced. The most of the cells were blocked in the G0/G1 phase, and the cells' mitosis was inhibited.
3.Genistein down-regulates Notch-1 expression and inactivates Hedgehog signaling pathway in pancreatic cancer cells
Yusheng LIAO ; Xueke FAN ; Hua QING ; Cuifang ZHANG ; Fen CHEN ; Huitao GAO ; Qiu ZHAO
Chinese Journal of Pancreatology 2008;8(4):230-233
Objective To investigate the effect of genistein on Notch-1, SHH and HHIP gene expression and on the cell cycle and proliferation of of BxPC3 cells. Methods Human pancreatic cancer cell line BxPC3 was cultured. The BxPC3 cells were treated with genistein and then the total RNA and protein were extracted. RT-PCR was used to detect the expression of Notch-1 mRNA, SHH mRNA and HHIP mRNA. Noteh-1 and SHH protein was determined by western blotting. MTT assay was used to detect proliferation of BxPC3 cells. The cell cycle of BxPC3 cells was measured by Propidium iodide (PI) and flow cytometry. Results The inhibiting rate was 67.17%±2.32% when BxPC3 cell lines were treated by 20μg/ml genistein for 48 hours. Notch-1 mRNA was down-regulated from 2.454±0.068 to 1.304±O.169 ; SHH mRNA was down-regulated from 0.959±0.023 to O.472±0.077 ; HHIP mRNA was up-regulated from 0.625±O.158 to 1.761±0.121. Notch-1 protein expression was down-regulated from 1.361±0.109 to 0.760±0.114; SHH protein expression was down-regulated from 0.265±0.018 to 0.129±0.013. (52.77±9.47)% cells were hindered in G2/M stage. Conclusions Genistein could down-regulate Notch-1 expression and inactivate Hedgehog signaling pathway and inhibit the proliferation of pancreatic cancer cells.
4.Involvement of p38-p53 signal pathway in neuroprotective effects of DGMI on SH-SY5 Y cells damaged by oxygen-glucose deprivation
Xueke LI ; Qiu LIU ; Zhiliang XU ; Jun ZHOU ; Liang CAO ; Gang DING ; Zhenzhong WANG ; Wei XIAO
Chinese Pharmacological Bulletin 2016;32(12):1699-1704
Aim To investigate the protective effects of Diterpene Ginkgolides Meglumine Injection(DGMI)on SY5 Y cells damaged by oxygen-glucose deprivation and its functional mechanisms.Methods After 4 h of OGD,the cells were treated with 25 mg·L-1 drugs for 1 h.Subsequently,cell viabilities were measured by cell counting kit-8(CCK-8 kit)and cell apoptosis was measured by flow cytometric analysis.Furthermore, the mitochondrial membrane potential was detected by rhodamine123 staining.The levels of phospho-p38, phospho-p53,Bcl-2,Bax and cleaved caspase-9/3 were evaluated by western blot.Results DGMI signif-icantly increased the cell viabilities of SY5 Y cells dam-aged by OGD,and reduced OGD-elicited dissipation of mitochondrial membrane potential and cell apoptosis. Furthermore,DGMI also reduced p-p38,p-p53,Bax/Bcl-2 ratio,cleaved caspase-9 and cleaved caspase-3. Conclusion DGMI shows good neuroprotective effects on SY5 Y cells after oxygen-glucose deprivation.The underlying mechanisms may be associated with the sup-pression of p38/p53/Bcl-2 /caspase-9/caspase-3 sig-naling pathway.