Background:TLR4 can mediate immune and inflammatory responses,TFF3,MUC2 are the intestinal mucosa protection factor and can maintain the intestinal barrier function. Aims:To investigate the effect of Anchang Yuyang decoction on colon tissue TFF3,MUC2 and TLR4 gene expressions in rats with ulcerative colitis. Methods:TNBS was used to establish ulcerative colitis model in rats. Ninety Wistar rats were randomly divided into normal control group,model group,low,moderate and high dose Anchang Yuyang decoction groups and mesalazine group,and distilled water,different concentrations of Anchang Yuyang decoction and mesalazine were given respectively. All the rats were sacrificed after 21 days. Colonic histopathological score was assessed,and RT-PCR was used to detect gene expressions of colon tissue TFF3, MUC2 and TLR4. Results:Compared with model group,histopathological score and TLR4 expression were significantly decreased in moderate,high dose Anchang Yuyang decoction groups and mesalazine group(P < 0. 05),expressions of TFF3 and MUC2 were significantly increased( P < 0. 05). Compared with moderate dose Anchang Yuyang decoction group,histopathological score in high dose Anchang Yuyang decoction group and mesalazine group was significantly decreased(P < 0. 05),and TFF3 expression was significantly increased( P < 0. 01). Compared with moderate dose Anchang Yuyang decoction group and mesalazine group,MUC2 expression in high dose Anchang Yuyang decoction group was significantly increased(P < 0. 01),and TLR4 expression was significantly decreased( P < 0. 01). Conclusions:Anchang Yuyang decoction can promote the repair of colonic mucosa in rats with ulcerative colitis,and its mechanism may be related to the increase of TFF3 and MUC2 gene expressions and down regulation of TLR4 gene expression.

As essential concepts of the traditional Chinese medicine theory,"deficiency"and"toxin"have been enriched and developed continuously since Huangdi Neijing.By tracing back and combing"deficiency"and"toxin",this paper sums up their relationship,analyzes and explains their basic connotation,and discusses their extension.The"deficiency-toxin"theory has two meanings:it covers the pathological state of the human body with deficiency of vital qi and excess of pathogenic toxin,and it also refers to the pathological evolutionary process in which"deficiency"and"toxin"promote each other.Based on the connotation and dynamic pathogenesis of the"deficiency-toxin"theory,it is pointed out that this theory can be applied to the prevention and treatment of infectious diseases and chronic debilitating diseases,including the"inflammation-cancer transformation"of inflammatory bowel disease.Taking inflammatory bowel disease as an example and combining its Western medical background,this paper expounds on the pathogenesis and treatment of the"inflammation-cancer transformation"of inflammatory bowel disease,and provides a paradigm of"deficiency-toxin"theory guiding clinical research.

ObjectiveTo observe the clinical efficacy of Tongfu Kuanzhong decoction （TFKZ） in the treatment of constipation-predominant irritable bowel syndrome （IBS-C） with spleen deficiency and Qi stagnation and its effects on anorectal manometry and colonic electrical activity parameters. MethodsSixty-four patients with IBS-C of the spleen deficiency and Qi stagnation type were included as research subjects and were randomized into the observation group （thirty-two cases） and control group （thirty-two cases）. The control group was orally administered mosapride citrate tablets， and the observation group was orally administered TFKZ. Both groups were treated for 4 weeks. The traditional Chinese medicine （TCM） syndrome scores， patient assessment of constipation symptoms （PAC-SYM） score， general anxiety disorder-7 （GAD-7） score， patient health questionnaire-9（PHQ-9）score， anorectal manometry， and colonic electrical activity parameters were observed before and after treatment in the two groups. ResultsThe total points of TCM syndromes were significantly lower in both groups after treatment （P<0.01） and lower in the observation group （P<0.05）. The fecal symptoms， rectal symptoms， abdominal symptoms， and total symptom scores of the patients in both groups were significantly decreased after treatment （P<0.01）， and the rectal symptoms， abdominal symptoms， and total symptom scores of the observation group were lower （P<0.05，P<0.01）. In both groups， the forced anal residual pressure and the initial rectal sensation threshold decreased after treatment （P<0.05，P<0.01）， and forced anal residual pressure in the control group was lower （P<0.01）. After treatment， the GAD-7 and PHQ-9 scores of patients in both groups decreased significantly （P<0.01）， and the GAD-7 score of the observation group was significantly lower （P<0.01）. After treatment， the average wave amplitude at different time points of each lead increased significantly in both groups， compared with that before treatment （P<0.01）. The average wave amplitude of each lead of the ascending colon， descending colon， sigmoid colon， and rectum in the observation group at 5 min before the meal and 10 min after the meal， as well as that of the ascending colon and rectum at 20 min and 30 min after the meal， was higher than that of the control group （P<0.05）. ConclusionTFKZ is effective in the treatment of IBS-C. Its mechanism may be related to the regulation of colonic function by down-regulating the forced anal residual pressure and the initial rectal sensation threshold and up-regulating the amplitude and frequency of intestinal electrical activity in each intestinal segment of the colon.

ObjectiveTo explore the potential mechanism by which Huangqi Baijiang Yiren decoction （HBY） repairs the intestinal mucosal injury in the rat model of ulcerative colitis （UC） via the miR-21/suppressor of cytokine signaling 1 （SOCS1）/Janus kinase 1 （JAK1）/signal transducer and activator of transcription 6 （STAT6） signaling pathway. MethodsSixty SPF-grade male SD rats were randomly assigned into six groups： blank， model， low-dose （3.68 g·kg^-1） HBY， medium-dose （7.35 g·kg^-1） HBY， high-dose （14.5 g·kg^-1） HBY， and mesalazine （0.035 g·kg^-1）， with 10 rats in each group. The rat model of UC was established in other groups except the blank group by 3% dextran sulfate sodium solution. The rats were administrated with corresponding drugs once a day for 7 consecutive days since the 3th day after modeling. The histopathological changes of the colon were observed by hematoxylin-eosin staining， and the Robarts histopathology index （RHI） was scored. Enzyme-linked immunosorbent assay was employed to measure the levels of pro-inflammatory cytokines ［interleukin （IL）-6， IL-18， IL-1β， and tumor necrosis factor-α （TNF-α）］ in the serum. Real-time PCR was employed to determine the mRNA levels of miR-21， SOCS1， JAK1， and STAT6 in the colon tissue. Western blot was employed to determine the protein levels of SOCS1， JAK1， phosphorylated （p）-JAK1， STAT6， p-STAT6， Occludin， and Claudin-1 in the colon tissue. ResultsCompared with the blank group， the model group showed an increase in disease activity index （DAI） （P<0.01）， shortening of colon length （P<0.01）， severe histopathological damage in the colon tissue， and an increase in RHI， rises in serum levels of IL-6， IL-1β， IL-18， and TNF-α （P<0.01）， up-regulation in mRNA levels of miR-21， JAK1， and STAT6 and protein levels of p-JAK1 and p-STAT6 （P<0.01）， and down-regulation in mRNA and protein levels of SOCS1 and protein levels of Occludin and Claudin-1 （P<0.01）. The treatment with HBY reduced the DAI （P<0.01）， alleviated colon shortening and histopathological damage in the colon tissue， decreased the RHI （P<0.01）， lowered the serum levels of IL-6， IL-1β， IL-18， and TNF-α （P<0.01）， down-regulated the mRNA levels of miR-21， JAK1， and STAT6 （P<0.05， P<0.01）， up-regulated the mRNA level of SOCS1 （P<0.05）， up-regulated the protein levels of SOCS1， Occludin， and Claudin-1 （P<0.05， P<0.01）， and down-regulated the protein levels of p-JAK1 and p-STAT6 （P<0.05， P<0.01）. ConclusionHBY may modulate the miR-21/SOCS1/JAK1/STAT6 signaling pathway to suppress inflammatory responses and restore the intestinal mucosal barrier in UC rats.