Intervention of Traditional Chinese and Western Medicine in NLRP3 Inflammasome-mediated Digestive System Diseases： A Review / 中国实验方剂学杂志

The aberrant activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 （NLRP3） inflammasome as an essential component of the innate system is implicated in the pathogenesis of several human inflammatory diseases. Studies have confirmed its association with digestive system diseases such as ulcerative colitis， Crohn's disease， and acute pancreatitis， suggesting that the NLRP3 inflammasome plays a role in the initiation and progression of these diseases. Based on the mechanism of NLRP3 inflammasome activation and the pathways that mediate the inflammatory response， this article introduced the relationship between the NLRP3 inflammasome and the pathogenesis of multiple digestive system diseases and the Chinese and western medical therapies. Traditional Chinese medicine （TCM） has demonstrated definite effects on the NLRP3 inflammasome-mediated digestive system diseases. Some single Chinese medicines or TCM prescriptions can treat digestive system diseases by activating or inhibiting NLRP3 inflammasome activation. NLRP3 inflammasome can receive a variety of endogenous and exogenous stimulatory signals， which can initiate， activate， and mediate inflammatory responses. The inflammasome formation and downstream inflammatory cytokines are involved in not only the inflammatory responses but also the development and progression of multiple digestive system diseases. Therefore， the NLRP3 inflammasome can serve as an ideal target for disease treatment. The future rediscovery and in-depth studies of multiple inflammasomes will shed new light on the treatment of multiple digestive system diseases.

Effects and mechanism of Biglycan and FAK signaling pathway on the invasion and metastasis of colon cancer cells / 实用肿瘤学杂志

Objective To observe the influence of Biglycan on the focal adhesion kinase( FAK) activa-tion and to explore whether it regulates the invasion and metastasis of colon cancer through FAK signaling path-way.Methods The overexpressive plasmid of Biglycan was constructed and then transfected into the colon canc-er cell line HCT116.Meanwhile,FAK inhibitor was used to treat cells.Control group(HCT116),empty plasmid group(Vector),empty plasmid and inhibitor treatment group(Vector +PF -562271),Biglycan overexpression group( Biglycan) ,Biglycan overexpression and inhibitor treatment group( Biglycan+PF-562271) were set.Twen-ty four hours after exposure to inhibitor,the expression of FAK and p-FAK in each group was detected by West-ern Blot.The invasion and metastasis of colon cancer cells was detected by transwell assay.Results Overexpres-sion of Biglycan significantly enhanced the phosphorylation level of FAK and promoted the invasion and metastasis of HCT116(P<0.01).The inhibitor of FAK PF-562271 could significantly reduce the expression of p-FAK and reverse the effect of Biglycan on the invasion and metastasis of colon cancer cells.Conclusion Biglycan reg-ulates the invasion and metastasis of colon cancer cells through activation FAK signaling pathway.

Effect of Biglycan and FAK signal pathway on the proliferation of colon cancer cells and its mechanisms / 实用肿瘤学杂志

Objective To investigate the effect of Biglycan and FAK signal pathway on the proliferation of colon cancer cells in vitro and its possible mechanisms.Methods Biglycan expression vector was constructed and transfected into the colon cancer cell line HCT116.FAK inhibitor was used for cell treatment as well.Cells were divided into 5 groups:control group(HCT116),control group transfected with empty plasmid(Vector),con-trol group with empty plasmid transfected and inhibitor treatment(Vector+PF-562271),group transfected with Biglycan expression vector(Biglycan),group with Biglycan expression vector transfected and inhibitor treatment ( Biglycan+PF-562271) .Treatment duration was 24 hours.The expressions of FAK,p-FAK,PCNA and p53 were detected by Western Blot.The proliferation of cells was detected by MTT.Results The overexpression of Biglycan significantly promoted the proliferation of HCT116 and the phosphorylation of FAK(P<0.01).It signif-icantly up-regulated PCNA and down-regulated p53(P<0.01).The FAK inhibitor PF-562271 treatment could obviously inhibit the proliferation of HCT116,and the regulation of Biglycan on the expression of p-FAK, PCNA.p53 proteins was reversed(P<0.01).Conclusion Biglycan regulates the proliferation of colon cancer cells by promoting the activation of FAK signal pathway.

Therapeutic of anastomotic leakage in post-esophagogastrectomy / 中国基层医药

Objective To study the therapeutic of anastomotic leakage in post-esophagogastrectomy. Meth-ods There were 18 cases of anastomotic leakage in 127 cases with cancer of the thoracic esophagus who underwent esophagectomy were retrospectively studied. There were ten cases had anastomotic leakage of 67 cases of esophagogas-trectomy from 1995 to 2001 (first phase),the intestines nutrition sustain treatment taked rice water,fish soup and broth, there were eight cases had anastomotic leakage of 60 cases of esophagogastrectomy from 2002 to 2007 (second phase) ,the intestines nutrition sustain treatment taked supportan,fresubin. Results There were six cases death of 10 cases of anastomotic leakage at first phase, and there was any not death in the second phase. Conclusion When anastomotic leakage of esophagogastreetomy,it can elevate the cure rate with early diagncsis and treatment and intes-tines nutrition sustain treatment choose by supportan or fresubin.