Clinical Observation And Related Mechanism Study Of Sanbai Enteric Enema Solution In Treating Ulcerative Colitis

Objective: Ulcerative colitis(Ulcerative Colitis,UC)is a chronic inflammatory bowel disease with unclear etiology and very low cure rate and recurrence rate.A large number of clinical trials show that the etiology factors of inflammatory bowel disease are complex.UC mainly causes mucosal erosion,congestion,edema and other injuries in the intestinal cavity.There are many kinds of clinical drugs.TCM treatment has the unique advantages of promoting immune mechanism response to ulcerative colitis and maintaining the normal balance of intestinal flora,and has the advantages of small side effects and quick effect.UC large intestine damp-heat syndrome is relatively common in clinical practice,mainly including mucus pus and bloody stool,and anal fever.Sanbai enema solution is a pure traditional Chinese medicine preparation for the treatment of UC,consisting of five traditional Chinese medicines: Fangfeng,Baiji,Bailian,Baizhi,and Danggui.Currently,it has been developed as a hospital preparation called Wuwei Xiaopi Lotion.The entire formula adheres to the pathogenesis and has the effects of clearing heat,resolving blood stasis,relieving pain,dispelling dampness,and stopping diarrhea.Fangfeng,as the main medicine of Sanbai enema solution,has been proven to have a significant inhibitory effect on lung inflammation through research.At present,it has been developed into a hospital preparation.The whole prescription is strictly responsible for the pathogenesis of the disease,and has the effects of clearing heat,removing blood stasis,relieving pain,removing dampness and stopping diarrhea.Besides,Fangfeng is the sovereign medicine of Sanbai enema.Relevant studies have also shown that Fangfeng has obvious anti-inflammatory effects.So we conducted the following five aspects of research: 1,observe the clinical application of Sanbai enema in UC(large intestine damp-heat syndrome).2,To analyze the effect of the active component of Fangfeng in Sanbai enema on the inflammatory factor response of DSS-induced UC mice model.3,Clarify the effect of Prim-O-glucosylcimifugin(POG)on NF-κ B.Regulation of AKT and MAPK signaling pathways and improvement and remission of UC.4,To elucidate the positive regulatory effect of POG on the homeostasis of UC intestinal flora.5,To investigate the effect of cimetin glycoside on LPS induced inflammatory response in RAW264.7 cells.Methods: Clinically,patients with UC(large intestine damp-heat type)were selected and treated with Sanbai enema liquid on the basis of a controlled treatment with mesalazine enema.The clinical efficacy and mechanism of the two groups of patients were objectively evaluated by comparing their TCM symptom scores,TCM syndrome efficacy,and changes in modified Mayo scores,colonoscopy scores,and blood ESR,CRP levels before and after taking the medicine.In the experiment,36 mice were randomly divided into 6 groups.After successful modeling of UC induced by DSS,colon HE staining results and flora sequencing results were analyzed;Detection of inflammatory factor IL-1β、 IL-6 and TNF-α Expression level and detection of the fluorescent expression content of barrier proteins Occludin,Cludin-3,and ZO-1,followed by WB detection of NF-κ B.Phosphorylation expression of AKT and MAPK signaling pathway related proteins.Results: Chapter 1 showed 93.3% in the control group and 76.9%.The effective rate of the treatment group was significantly higher than that of the control group,and the TCM syndrome score,Mayo score,colonoscopy score,ESR and CRP expression inhibition also had significant effects compared with the control group,which had significant statistical significance.Chapter 2 shows that POG reduces the clinical and pathological tissue scores of the mouse UC model induced by DSS,and significantly inhibits the inflammatory factor IL-1 β,IL-6,TNF-α Expression level;By inhibiting MAPK and NF-κB Protein P38,ERK1/2,JNK1/2,P65,IκB-α and AKT signaling pathway κ B-α And AKT phosphorylation to inhibit the occurrence of inflammation;POG can maintain intestinal flora homeostasis and resist intestinal tissue damage by up-regulating the content of intestinal barrier proteins Occludin,Claudin-3 and ZO-1 and regulating the fixed value of intestinal beneficial bacteria(Lactobacillus,Firmicute)and harmful bacteria(Enterobacillus,Helicobacteraceae,Gamma-proteobacteria).chapter 3 shows that POG inhibited the inflammatory development of macrophages RAW264.7 induced by LPS,and blocked MAPK and NF-κ B and AKT signal transduction process,inhibit inflammation and collaterals,and also down-regulate inflammatory factor IL-1 β,IL-6,TNF-α m RNA content effect.Reducing the expression content of the inflammatory proteins COX-2 and i NOS,hindering the combined interaction of the two signaling proteins and forming protection against RAW264.7 inflammation.Conclusion: The clinical application results show that the treatment group has a better therapeutic effect on UC patients with damp-heat type of large intestine than the control group,with fewer side effects and higher acceptance.The experimental results show that cimetin glycosides inhibit the occurrence of inflammation by blocking the formation of inflammatory signaling pathways and downregulating the expression of related inflammatory factors,thereby achieving protection against intestinal tissue damage in UC mouse models and inhibiting the development of LPS-induced RAW264.7 cell inflammation.