Jianpi Qingchang decoction regulates intestinal motility of dextran sulfate sodium-induced colitis through reducing autophagy of interstitial cells of Cajal

AIM To investigate the underlying effect of Jianpi Qingchang decoction(JQD) regulating intestinal motility of dextran sulfate sodium(DSS)-induced colitis in mice. METHODS C57BL/6 mice were randomly divided into four groups: the control group, the DSS group, the JQD group, and the 5-aminosalicylic acid group. Except for the control group, colitis was induced in other groups by giving distilled water containing 5% DSS. Seven days after modeling, the mice were administered corresponding drugs intragastrically. The mice were sacrificed on the 15^(th) day. The disease activity index, macroscopic and histopathologic lesions, and ultrastructure of colon interstitial cells of Cajal(ICC) were observed. The levels of tumor necrosis factor-alpha(TNF-α), interleukin(IL)-1β, IL-10 and interferon gamma(IFN-γ), the expression of nuclear factor-kappa B(NF-κB) p65, c-kit, microtubule-associated protein 1 light chain 3(LC3-Ⅱ) and Beclin-l m RNA, and the colonic smooth muscle tension were assessed. RESULTS Acute inflammation occurred in the mice administered DSS. Compared with the control group, the levels of IL-1β, TNF-α, IL-10 and IFN-γ, the expression of LC3-Ⅱ, Beclin-1 and NF-κB p65 m RNA, and the contractile frequency increased(P < 0.05), the expression of c-kit m RNA and the colonic smooth muscle contractile amplitude decreased in the DSS group(P < 0.05). Compared with the DSS group, the levels of IL-10 and IFN-γ, the expression of c-kit m RNA, and the colonic smooth muscle contractile amplitude increased(P < 0.05), the levels of TNF-α and IL-1β, the expression of LC3-Ⅱ, Beclin-1 and NF-κB p65 m RNA, and the contractile frequency decreased in the JQD group(P < 0.05).CONCLUSION JQD can regulate the intestinal motility of DSS-induced colitis in mice through suppressing intestinal inflammatory cascade reaction, reducing autophagy of ICC, and regulating the network path of ICC/smooth muscle cells.

Qingchang decoction retention enema may induce clinical and mucosal remission in left-sided ulcerative colitis: A case report

BACKGROUND Ulcerative colitis(UC)is a chronic autoimmune disease characterized by relapsing-remitting abdominal pain,diarrhea,mucopurulent discharge and rectal bleeding.To date,the etiology of the disease remains unknown;therefore,medical therapy is not yet available.Left-sided UC is mainly treated with oral and topical mesalazine.However,due to its modest clinical effect,endoscopic mucosal remission is not achieved in all patients.CASE SUMMARY A 44-year-old man presented to Longhua Hospital with a history of left-sided UC for more than 6 years and slight bloody diarrhea over time.Endoscopy suggested hyperemia,edema,and erosive mucosa involving the rectum and sigmoid colon.The Traditional Chinese medicine Qingchang decoction(QCD)enema treatment was initiated once a day combined with a previous standard dose of mesalazine for 8 wk,and rectal bleeding ceased after 4 wk of treatment.Another QCD enema treatment was provided after symptom relapse due to drug withdrawal for nearly 6 mo.At the 2-mo follow-up,the colonoscopy results indicated mucosal healing with no erosion or ulcers.CONCLUSION The Chinese formula QCD retention enema represents a potential treatment for left-sided UC with predominant rectal bleeding to achieve clinical and mucosal remission.

Jianpi Qingchang Bushen decoction improves inflammatory response and metabolic bone disorder in inflammatory bowel disease-induced bone loss

BACKGROUND Bone loss and osteoporosis are commonly described as extra-intestinal manifestations of inflammatory bowel disease(IBD).Jianpi Qingchang Bushen decoction(JQBD)is a prescription used in clinical practice.However,further studies are needed to determine whether JQBD regulates the receptor activator of nuclear factor kappa B(NF-κB)(RANK)/receptor activator of NF-κB ligand(RANKL)/osteoprotegerin(OPG)pathways and could play a role in treating IBD-induced bone loss.AIM To evaluate the therapeutic effect of JQBD in IBD-induced bone loss and explore the underlying mechanisms.METHODS An IBD-induced bone loss model was constructed by feeding 126-to-8-wk-old interleukin-10(IL-10)-knockout mice with piroxicam for 10 d.The mice were randomly divided into model and JQBD groups.We used wild-type mice as a control.The JQBD group was administered the JQBD suspension for 2 wk by gavage,while the control and model groups were given normal saline at the corresponding time points.All mice were killed after the intervention.The effect of JQBD on body weight,disease activity index(DAI),and colon length was analyzed.Histopathological examination,colon ultrastructure observation,and micro-computed tomographic scanning of the lumbar vertebrae were performed.The gene expression of NF-κB,tumor necrosis factor-α(TNF-α),IL-1β,IL-6,and IL-8 in the colon was evaluated by real-time polymerase chain reaction.Colon samples were assessed by Western blot for the expression of RANKL,OPG,RANK,and NF-κB proteins.RESULTS The model group lost body weight,had a shorter colon,and showed a dramatic increase in DAI score,whereas JQBD had protective and therapeutic effects.Treatment with JQBD significantly improved inflammatory cell infiltration and reduced crypt abscess and ulcer formation.Threedimensional imaging of the vertebral centrum in the model group revealed a lower bone mass,loose trabeculae,and“rod-shaped”changes in the structure compared to the control group and JQBD groups.The bone volume/total volume ratio and bone mineral density were significantly lower in the model group than in the control group.JQBD intervention downregulated the NF-κB,TNF-α,IL-1β,IL-6,and IL-8 m RNA expression levels.The RANKL and OPG protein levels were also improved.CONCLUSION JQBD reduces inflammation of the colonic mucosa and inhibits activation of the RANK/RANKL/OPG signaling pathway,thereby reducing osteoclast activation and bone resorption and improving bone metabolism.

Analysis of underlying mechanism of Qingchang Huashi Decoction in treating ulcerative colitis based on network pharmacology

Objective:To explore the target and signal pathway of Qingchang Huashi Decoction(QCHSD)in the treatment of ulcerative colitis(UC)by using network pharmacology,so as to explain its molecular mechanism of action in the treatment of UC from damp heat.Methods:TCMSP was used to screen the potential active components(OB≥30%,DL≥0.18)and target of QCHSD.The network of"potential active ingredients-target-disease"was constructed by using the database of TCMSP and GeneCards.Using the string platform,the protein protein interaction(PPI)network model was constructed to find the core target.Go and KEGG enrichment of potential targets were analyzed by R software.Results:The results of network analysis showed that quercetin,kaempferol,scutellarin and baicalein were the top four active ingredients in QCHSD.210 gene targets were found in QCHSD,4213 in UC.The key targets of QCHSD in treating UC included AKT1,IL-6,VEGFA,CASP3,etc.GO enrichment analysis showed that these gene targets mainly affected nuclear receptor,steroid receptor,cytokine receptor binding,cytokine activity,etc.KEGG enrichment analysis showed that AGE-RAGE signaling pathway,IL-17 signaling pathway and TNF were more abundant.Conclusion:This study describes the material basis and mechanism of QCHSD in the treatment of UC,which provides theoretical basis and research direction for future research.