Dataset Information

Shenhuang Plaster Application Improves Gastrointestinal Motility in Mice with Postoperative Ileus through Intestinal Microbiota.

ABSTRACT: Postoperative ileus (POI) is a common surgical complication, and its incidence remains high. Shenhuang Plaster (SHP) is a famous traditional Chinese medicine with a definite curative effect on postoperative intestinal dysfunction; however, the mechanisms involved in these effects are unclear. Accordingly, in this study, we constructed a POI mouse model and used the intestinal flora as the target to explore the regulatory effect of SHP on gastrointestinal motility. The results illustrated that SHP applied at the Shenque acupoint promoted the recovery of gastrointestinal motility, relieved intestinal villus atrophy and basal damage caused by POI, protected the integrity of intestinal tissue morphology, and alleviated the inflammatory response in the intestinal tissue of POI model mice. In addition, we clarified the role of the intestinal flora in the occurrence and development of POI, further evaluated the changes in the intestinal flora in each group of mice, and analysed the regulatory effect of SHP on the intestinal flora in mice with POI. The results suggested that SHP might improve gastrointestinal motility disorder in POI mice by effectively regulating intestinal flora.

SUBMITTER: Shi Y

PROVIDER: S-EPMC9377883 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Shenhuang Plaster Application Improves Gastrointestinal Motility in Mice with Postoperative Ileus through Intestinal Microbiota.

Shi Yanan Y Xu Xiao X Liu Ting T Wang Rongyun R Xu Jingming J Wu Yujing Y Ding Bin B Sun Qiuhua Q

Evidence-based complementary and alternative medicine : eCAM 20220808

Postoperative ileus (POI) is a common surgical complication, and its incidence remains high. Shenhuang Plaster (SHP) is a famous traditional Chinese medicine with a definite curative effect on postoperative intestinal dysfunction; however, the mechanisms involved in these effects are unclear. Accordingly, in this study, we constructed a POI mouse model and used the intestinal flora as the target to explore the regulatory effect of SHP on gastrointestinal motility. The results illustrated that SH ...[more]

PMID: 35979003

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Project description:AimTo explore the effects of abdominal surgery and interleukin-1 signaling on antimicrobial defense in a model of postoperative ileus.MethodsC57BL/6 and Interleukin-1 receptor type I (IL-1R1) deficient mice underwent intestinal manipulation to induce POI. Expression of mucosal IL-1α, IL-1β and IL-1R1 and several antimicrobial peptides and enzymes were measured by quantitative PCR or ELISA, western blotting or immunohistochemistry. Bacterial overgrowth was determined by fluorescent in-situ hybridization and counting of jejunal luminal bacteria. Translocation of aerobic and anaerobic bacteria into the intestinal wall, mesenteric lymph nodes, liver and spleen was determined by counting bacterial colonies on agar plates 48h after plating of tissue homogenates. Antimicrobial activity against E. coli and B. vulgatus was analyzed in total and cationic fractions of small bowel mucosal tissue homogenates by a flow cytometry-based bacterial depolarization assay.ResultsJejunal bacterial overgrowth was detected 24h after surgery. At the same time point, but not in the early phase 3h after surgery, bacterial translocation into the liver and mesenteric lymph nodes was observed. Increased antimicrobial activity against E. coli was induced within early phase of POI. Basal antimicrobial peptide and enzyme gene expression was higher in the ileal compared to the jejunal mucosa. The expression of lysozyme 1, cryptdin 1, cryptdin 4 and mucin 2 were reduced 24h after surgery in the ileal mucosa and mucin 2 was also reduced in the jejunum. Postoperative IL-1α and IL-1β were increased in the postoperative mucosa. Deficiency of IL-1R1 affected the expression of antimicrobial peptides during homeostasis and POI.ConclusionSmall bowel antimicrobial capacity is disturbed during POI which is accompanied by bacterial overgrowth and translocation. IL-1R1 is partially involved in the gene expression of mucosal antimicrobial peptides. Altered small bowel antimicrobial activity may contribute also to POI development and manifestation in patients undergoing abdominal surgery.

Project description:Postoperative ileus (POI) and postoperative gastrointestinal tract dysfunction (POGD) are well-known complications affecting patients undergoing intestinal surgery. GI symptoms include nausea, vomiting, pain, abdominal distention, bloating, and constipation. These iatrogenic disorders are associated with extended hospitalizations, increased morbidity, and health care costs into the billions and current therapeutic strategies are limited. This is a narrative review focused on recent concepts in the pathogenesis of POI and POGD, pipeline drugs or approaches to treatment. Mechanisms, cellular targets and pathways implicated in the pathogenesis include gut surgical manipulation and surgical trauma, neuroinflammation, reactive enteric glia, macrophages, mast cells, monocytes, neutrophils and ICC’s. The precise interactions between immune, inflammatory, neural and glial cells are not well understood. Reactive enteric glial cells are an emerging therapeutic target that is under intense investigation for enteric neuropathies, GI dysmotility and POI. Our review emphasizes current therapeutic strategies, starting with the implementation of colorectal enhanced recovery after surgery protocols to protect against POI and POGD. However, despite colorectal enhanced recovery after surgery, it remains a significant medical problem and burden on the healthcare system. Over 100 pipeline drugs or treatments are listed in Clin.Trials.gov. These include 5HT4R agonists (Prucalopride and TAK 954), vagus nerve stimulation of the ENS—macrophage nAChR cholinergic pathway, acupuncture, herbal medications, peripheral acting opioid antagonists (Alvimopen, Methlnaltexone, Naldemedine), anti-bloating/flatulence drugs (Simethiocone), a ghreline prokinetic agonist (Ulimovelin), drinking coffee, and nicotine chewing gum. A better understanding of the pathogenic mechanisms for short and long-term outcomes is necessary before we can develop better prophylactic and treatment strategies.

Project description:Inflammatory cytokines produced by muscularis macrophages largely contribute to the pathological signs of postoperative ileus (POI). Electroacupuncture (EA) can suppress inflammation, mainly or partly via activation of vagal efferent. The goal of this study was to investigate the mechanisms by which EA stimulation at an hindlimb region ameliorates inflammation in POI. Methods: Intestinal motility and inflammation were examined after 24 h after intestinal manipulation (IM)-induced POI in mice. Local immune response in the intestinal muscularis, expression of macrophages, α7 nicotinic acetylcholine receptor (α7nAChR), Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) were determined by flow cytometry, Western Blot, qPCR and immunofluorescence. The effects of α7nAChR antagonists (methyllycaconitine and α-bungarotoxin) and JAK2/STAT3 inhibitors (AG490 and WP1066) were also administered in a subset of mice prior to EA. In the parasympathetic pathways, intestinal motility and inflammation were determined after cervical vagotomy and sub-diaphragmatic vagotomy. The expression of gamma absorptiometry aminobutyric acid (GABAA) receptor in dorsal motor nucleus of vagal (DMV) cholinergic neurons was assessed by immunofluorescence and the response to DMV microinjection of bicuculine (antagonist of GABAA receptor) or muscimol (agonist of GABAA receptor) were assessed. Results: EA suppressed intestinal inflammation and promoted gastrointestinal motility. Mechanistically, EA activated the α7nAChR-mediated JAK2/STAT3 signaling pathway in macrophages which reduced the production of inflammatory cytokines. Furthermore, we also demonstrated that hindlimb region stimulation drove vagal efferent output by inhibiting the expression of GABAA receptor in DMV to ameliorate inflammation. Conclusions: The present study revealed that EA of hindlimb regions inhibited the expression of GABAA receptor in DMV neurons, whose excited vagal nerve, in turn suppressed IM-induced inflammation via activation of α7nAChR-mediated JAK2/STAT3 signaling pathway.

Dataset Information

Shenhuang Plaster Application Improves Gastrointestinal Motility in Mice with Postoperative Ileus through Intestinal Microbiota.

Publications

Shenhuang Plaster Application Improves Gastrointestinal Motility in Mice with Postoperative Ileus through Intestinal Microbiota.

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