BackgroundIn recent years, the prevalence of chronic constipation among adults worldwide has shown a yearly increasing trend, with most patients experiencing varying degrees of emotional disorders. Understanding the underlying mechanisms linking chronic constipation, gut microbiota, and emotional status is crucial for developing effective therapeutic strategies.ObjectivesTo investigate the clinical efficacy of surgical intervention for slow-transit constipation and evaluate its postoperative impacts on bowel function, gut microbiota composition and function, and host immune status.MethodsThis study aimed to explore the relationship between gut microbiota and emotional status by collecting preoperative and postoperative clinical data, psychological conditions, and gut microbiota profiles from 30 patients undergoing total colectomy with ileorectal anastomosis for chronic constipation. Clinical and microbiota data were analysed to evaluate changes in emotional status and gut microbiota composition before and after surgery.ResultsThe results demonstrated that the anxiety and depression levels of patients significantly improved following surgery. Concurrently, gut microbiota diversity noticeably decreased, accompanied by significant alterations in species composition. Postoperative changes revealed that Clostridium sensu stricto and Streptococcus were key species contributing to the differences observed between preoperative and postoperative microbiota profiles. Notably, Streptococcus was negatively correlated with emotional symptoms such as obsession, anxiety, and depression, and positively correlated with the lactose and galactose degradation pathway.ConclusionsThis study suggests that constipation surgery not only improves bowel movements, but also alters the composition of gut microbiota and ameliorates mood disorders in patients. These findings provide novel insights into the interplay between gut microbiota and emotional well-being, highlighting the potential of targeting gut microbiota as a therapeutic approach for managing psychological conditions associated with chronic constipation.

In today's society, with changes in diet structure and living habits, drug abuse, and psychosomatic diseases, the prevalence of constipation is increasing. Currently, there is a lack of unified diagnostic criteria for constipation, and therapeutic approaches lack standardization. This often leads to an inability to select appropriate treatment methods based on the patient's specific condition. Consequently, a significant proportion of constipation patients do not achieve satisfactory therapeutic outcomes. This is particularly true for slow-transit constipation (STC), which is characterized by a protracted course of the disease and significant diagnostic challenges. Therefore, this review aims to delineate the mechanisms, diagnosis, and therapeutic advances in STC, in order to offer insights for clinical diagnosis and treatment.

Slow transit constipation (STC) is a prevalent functional gastrointestinal disorder that significantly affects people's quality of life. Aurantii Fructus Immaturus (Zhishi, ZS) and Atractylodis Macrocephalae Rhizoma (Baizhu, BZ) are a classic herbal pair in traditional Chinese medicine (TCM) for regulating spleen-stomach function, respectively recognized for their properties of "replenishing qi and fortifying the spleen" and "dispersing stagnation and promoting digestion". This study aimed to elucidate the mechanisms by which ZSBZ ameliorates STC through regulating mitophagy in ICCs and restructuring gut microbiota composition. A rat model of STC was established by oral gavage administration of loperamide hydrochloride (3 mg/kg·day). The therapeutic effects of ZSBZ were evaluated by assessing rat body weight, 6-h fecal number, fecal water content, and intestinal transit rate. Histopathological changes in the colon were observed using hematoxylin-eosin (HE) staining and Alcian blue-periodic acid Schiff (AB-PAS) staining. The ultrastructure of colon tissues was observed by transmission electron microscopy (TEM). Immunohistochemistry (IHC) was used to detect the expression of c-Kit, SCF, and autophagy-related markers (p62, Beclin1, and LC3II/I) in colon tissues. The expression levels of α-KGDHC and PDH were measured by ELISA. Combined with biochemical assays for SOD, MDA, respiratory chain complexes I and II, and ATP levels, a comprehensive assessment of cellular mitochondrial oxidative stress status and energy metabolism function was performed. Flow cytometry was used to quantify intracellular Ca2+ concentration and mitochondrial membrane potential (MMP) in cells isolated from colonic tissues. Mitophagy-related protein and mRNA expression were analyzed by Western blotting and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Apoptosis in rat colonic tissues was detected using TUNEL assay. Gut microbiota composition was analyzed by 16S rRNA gene sequencing, and its metabolic functional potential was predicted. Our results showed that ZSBZ significantly ameliorated defecation function and enhanced intestinal motility in a rat model of STC. Histopathological and ultrastructural analyses revealed that ZSBZ effectively restored colonic mucosal damage, increased goblet cell numbers, and attenuated mitochondrial swelling with cristae disruption in ICCs of STC rats. Meanwhile, ZSBZ improved mitochondrial dysfunction by reducing MDA levels and increasing SOD activity in colonic tissues. Furthermore, ZSBZ improved mitochondrial energy metabolism by increasing ATP content, restoring respiratory chain complex I and II activities, and elevating α-KGDHC and PDH activities, thereby reversing the decline in mitochondrial membrane potential and the increase in intracellular Ca2+ concentration in cells isolated from colonic tissues. Mechanistically, ZSBZ attenuated excessive mitophagy in colonic ICCs by downregulating autophagy-related genes and proteins, restoring p62 expression, and suppressing the elevated mRNA and protein expression of the mitophagy-related markers PINK1 and Parkin. In addition, 16S rRNA gene sequencing demonstrated that ZSBZ reshaped the gut microbiota in STC rats, characterized by a decreased abundance of Proteobacteria and an increased abundance of Bacteroidota. KEGG functional prediction further indicated that ZSBZ regulated mitochondrial metabolism-related pathways, possibly contributing to the amelioration of colonic dysmotility. ZSBZ significantly alleviated constipation symptoms in STC rats. The mechanism may involve inhibition of excessive mitophagy in ICCs and restructuring of gut microbiota composition. This study provides compelling theoretical support for ZSBZ as a therapeutic strategy against STC and offers novel insights into intestinal motility restoration in humans.

Chronic constipation (CC) is associated with increased cardiovascular events, and trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite, has been recently shown to correlate with this risk. We examined how constipation status affects serum TMAO and how treatment modifies it. This prospective observational study (July 2023-September 2024), conducted at three Japanese centers. Healthy controls (HCs) were recruited during health checkups, and patients with CC recruited from outpatient clinics. Serum TMAO was measured using liquid chromatography-tandem mass spectrometry at baseline and at 4 and 12 weeks after treatment with magnesium oxide (MgO) or elobixibat. CC was classified as normal transit constipation (NTC) or slow-transit constipation (STC) by colonic transit time. Overall, 72 HCs and 165 patients with CC (NTC, n = 110; STC, n = 55) were included. Mean serum TMAO levels were 1.8 [± 1.1] µM and 9.0 [± 8.1] µM in the HC and CC groups, respectively (p<0.01). Serum TMAO levels were significantly higher in the STC group than in the NTC group (p<0.01). Constipation treatment reduced serum TMAO levels to 5.5 ± 7.6 µM (n = 165, p<0.01) at 4weeks and 4.5 ± 7.6 µM (n = 165, p<0.01) at 12 weeks. Elobixibat lowered serum TMAO at 4 and 12 weeks in both NTC and STC. Conversely, MgO lowered TMAO only at 12 weeks in NTC and did not affect STC. Constipation status, particularly STC, is associated with elevated serum TMAO levels. MgO or elobixibat significantly reduced serum TMAO, with a greater reduction observed with elobixibat.

Purpose:Colonic motility disorders, including diarrhea-predominant irritable bowel syndrome and slow-transit constipation, impose a major clinical burden. Although high-resolution colonic manometry reveals characteristic spatiotemporal motor patterns, such as high-amplitude propagating contractions and cyclic motor pattern in healthy individuals, these patterns are often altered or absent in disease. Understanding how these patterns arise from underlying pacemaker, neural, and mechanical mechanisms is essential for improving treatment strategies.Methods:We developed a biophysical whole-colon model that integrates an Interstitial Cells of Cajal–inspired oscillator network, enteric nervous system reflexes, a pressure-gated modulation element motivated by rectosigmoid brake behavior, and a nonlinear tube law describing colon wall mechanics. The model simulates spatiotemporal pressure patterns along the colon and allows systematic variation of physiological parameters associated with pacemaker activity, neural reflex control, and distal gating.Results:A small set of parameters reproduces three illustrative motility patterns corresponding to healthy motility, diarrhea-predominant irritable bowel syndrome, and slow-transit constipation. The simulated pressure maps recapitulate key features observed in high-resolution manometry, including propagation direction, regional patterning of contractions, and case-specific changes in amplitude and coordination. Sensitivity analysis suggests that proximal excitation strength and waveform morphology strongly influence global motility metrics.Conclusion:Our study presents a simple, biophysical framework for reproducing clinically observed colonic motor patterns and exploring their disruption in disease. More broadly, the model may help interpret clinical manometry in mechanistic terms and support hypothesis-driven in silico studies of colonic motility disorders.

Effects and mechanisms of nobiletin on gut motility by coordinating bile acid signaling via dual ileal-colonic axes in STC model mice.

IntroductionSlow transit constipation (STC) is a chronic disease characterized by delayed intestinal transit and weakened spontaneous contractions of colonic smooth muscle. Current pharmacological treatments are often associated with adverse effects, highlighting the need for safe and more effective therapeutic strategies. This study investigated the potential role of Lactobacillus acidophilus (L. acidophilus) in regulating intestinal motility and alleviating STC, as well as the underlying mechanism.MethodsA humanized mouse model was established by intragastric administration of fecal bacterial suspension from STC patients on alternate days, in order to evaluate the effect of L. acidophilus on constipation. The regulatory effect of L. acidophilus on intestinal motility was evaluated using defecation parameters. Colon histopathology was assessed by hematoxylin-eosin (H&E) staining. Immunohistochemistry (IHC), RT-qPCR, ELISA, and in vitro cell experiments were performed to examine the inflammatory cytokine levels and changes in the 5-hydroxytryptamine (5-HT) signaling pathway. In addition, metagenomic sequencing was used to analyze changes in the intestinal microbial community.ResultsThe results showed L. acidophilus treatment significantly enhanced intestinal peristalsis and maintained the intestinal barrier by up-regulating Occludin expression and down-regulating inflammatory cytokines, including TNF-α and IL-1β, thereby suppressing inflammatory responses. Both in vivo and in vitro experiments showed that L. acidophilus affected the synthesis and release of 5-HT by regulating the expression of TPH1 and the mechanosensitive ion channel Piezo1. Additionally, L. acidophilus reshaped the intestinal microbial community structure and altered the inter-bacterial interaction network, which was closely associated with improved intestinal motility.ConclusionOur current research reveals that constipation symptoms by L. acidophilus through the gut microbiota composition, intestinal barrier, and the 5-HT signaling pathway. These findings provide a strong theoretical basis for the development of L. acidophilus as a potential therapeutic strategy for the treatment of STC.

Dysregulation of complement factor D (CFD) has been associated with various diseases, such as metabolic, cardiovascular, and renal disorders. However, its role in intestinal function has been less studied. Our research found that CFD-deficient (Cfd–/–) mice exhibited spontaneous slow transit constipation (STC) compared to wild-type (WT) mice. Moreover, the fecal weight and water content in Cfd–/– mice were significantly reduced, despite no specific changes in feeding behavior. Reduced C-kit protein expression, colon injury, complement dysfunction and dysbiosis of the fecal microbiota are also observed in Cfd–/– mice. After microbiota transplantation from WT mice into Cfd–/– mice, reduced stool output, water content, decreased C-kit protein expression and colon injury were significantly improved. These results indicate that CFD is critical for controlling microbial homeostasis in the colon and, in its absence, leads to colon injury and promotes slow transit constipation.

Integration of network pharmacology and gut microbiota analysis to uncover the molecular mechanisms of Zengye decoction against slow transit constipation.

IntroductionSlow transit constipation (STC) is a prevalent gastrointestinal disorder characterized by impaired intestinal motility, metabolic dysregulation, and gut microbial dysbiosis. Zingiber mioga (Thunb.) Rosc. (RH), a traditional medicinal-edible plant, is empirically used to alleviate gastrointestinal dysfunction, but its therapeutic mechanisms in STC remain unclear. Herein, we investigated the laxative efficacy and mechanism of RH in a rat STC model via integrated untargeted metabolomic and metagenomic analyses, providing experimental evidence for its clinical use.MethodsA rat STC model was established by intragastric loperamide hydrochloride (5 mg/kg) for 35 consecutive days. Thirty-six SD rats were randomly divided into six groups (n = 6): normal control, STC model, mosapride-positive control (2 mg/kg), and low- (1350 mg/kg), medium- (2700 mg/kg), high-dose (3400 mg/kg) RH groups, with concurrent drug intervention. Serum concentrations of SP, MTL, and GAS (key gastrointestinal motility regulators) were quantified. Colonic pathological damage was histopathologically evaluated, and intestinal propulsive rate was measured. Untargeted serum metabolomics and fecalmetagenomics identified differential metabolites and gut microbiota alterations.ResultsCompared with the STC model, RH significantly reduced serum SP (intestinal motility inhibitor) and increased MTL/GAS (motility promoters). It also dose-dependently ameliorated colonic lesions and improved intestinal propulsive rate. Serum metabolomics identified 15 differential metabolites, mainly enriched in nitrogen metabolism, neuroactive ligand–receptor interaction, and amino acid metabolism. Fecal metagenomics showed RH restored the Eubacteriales/Lachnospirales ratio (a STC dysbiosis marker) and increased beneficial genera (e.g., Ruminococcus sp., Eubacterium sp.).Discussion and conclusionOur findings show RH effectively ameliorates colonic injury and gastrointestinal motility in STC rats, associated with regulating gastrointestinal hormone secretion. Its benefits are likely mediated by improving dysregulated amino acid/nitrogen metabolism and modulating gut microbiota composition. This study provides mechanistic evidence for RH as a natural functional agent for STC management, laying a foundation for exploring its active components and clinical translation.

To explore the mechanism of Huayu Tongbian Decoction (HYTBD) for relieving slow transit constipation (STC) in rats. Sixty SD rat models of STC induced by intragastric administration of loperamide hydrochloride suspension were randomized equally into 5 groups for treatment with daily gavage with saline (STC model group), low-, medium-, or high-dose HYTBD, or mosapride (positive control group), with another 12 normal rats receiving saline gavage as the blank control group. The first black stool time, fecal water content and intestinal propulsion rate of the rats were measured, and the ultrastructure of interstitial Cajal cells (ICCs) was observed using transmission electron microscopy to calculate the mitochondrial vacuolar rate. The phagocytosis rate of macrophages was detected using immunofluorescence assay, and colonic pathologies were examined using HE staining. The colonic expression levels of c-Kit, CD47, PI3K and Akt were detected with immunohistochemistry or Western Blotting, and their correlations with efferocytosis were analyzed. The rat models of STC showed significant ultrastructural damage of the ICCs with increased first black stool time, mitochondrial vacuolar rate, and colonic expression levels of CD47, p-PI3K/PI3K and p-Akt/Akt proteins, lowered fecal water content, intestinal propulsion rate and c-Kit expression level, without significant changes in phagocytic rate. Treatment with HYTBD, especially at the high dose, significantly increased fecal water content, intestinal propulsion rate, phagocytosis rate and colonic c-Kit expression, and decreased the first black stool time, mitochondrial vacuolar rate, and colonic expressions of CD47, p-PI3K/PI3K and p-Akt/Akt in the mouse models. HYTBD improves STC in rats possibly by down-regulating colonic CD47 expression and improving macrophage phagocytosis rate via inhibiting PI3K and Akt phosphorylation, thereby promoting efferocytosis of the ICCs.

This study investigated the efficacy differences of Atractylodis Macrocephalae Rhizoma with different growth years in treating slow transit constipation(STC) and explored its potential mechanism of action. Thirty-six male KM mice were randomly assigned to six groups(n=6): blank control group, STC model group, two-year Atractylodis Macrocephalae Rhizoma group, four-year Atractylodis Macrocephalae Rhizoma group, ten-year Atractylodis Macrocephalae Rhizoma group, and mosapride group. The STC model was established via loperamide hydrochloride suspension gavage. Efficacy indicators including defecation function, intestinal transit rate, histopathology, and serum levels of gastrointestinal hormones were measured to evaluate the effectiveness of Atractylodis Macrocephalae Rhizoma with different growth years in improving STC. Untargeted metabolomics was used to analyze differential metabolites in mouse feces, and related metabolic pathways were enriched. Immunohistochemistry and Western blot(WB) were used to verify the proteins related to the key pathways. In comparison to the model group, all Atractylodis Macrocephalae Rhizoma-treated groups significantly alleviated STC symptoms to varying degrees. Notably, the ten-year Atractylodis Macrocephalae Rhizoma group demonstrated the most pronounced ameliorative effects: defecation function and intestinal transit rate were significantly enhanced; histopathological damage in colon tissue was reduced; serum levels of motilin(MTL) and gastrin(GAS) were markedly increased; the level of total bile acids(TBA) in the colon decreased. A total of 45 differential metabolites were identified in metabonomics study, of which 20 had a pullback after the ten-year Atractylodis Macrocephalae Rhizoma intervention. Pathway enrichment analysis revealed that the differential metabolites primarily involved primary bile acid biosynthesis, biosynthesis of phenylalanine, tyrosine, and tryptophan, and phenylalanine metabolism. Immunohistochemistry and WB results showed that ten-year Atractylodis Macrocephalae Rhizoma influenced bile acid metabolism probably by modulating the farnesoid X receptor(FXR) and G protein-coupled bile acid receptor 5(TGR5), thereby restoring the intestinal mucosal barrier(upregulating the expression of occludin and claudin-1). This study provides an experimental foundation for further clarifying the effectiveness of genuine Atractylodis Macrocephalae Rhizoma in treating STC.

Slow transit constipation (STC) is a prevalent functional gastrointestinal disorder. Gastrodin (GAS), a natural compound, has demonstrated protective effects in intestinal contexts; however, its therapeutic potential and mechanisms of action in STC remain largely unexplored. A total of 30 male C57BL/6 mice (6weeks old) were used in this study. An STC model was established using loperamide. The therapeutic effects of GAS were systematically evaluated by measuring several parameters: stool output (fecal pellet count and moisture content), intestinal transit rate, and colon histopathology. Furthermore, we analyzed serum and colonic levels of inflammatory cytokines, key neurotransmitters, and aquaporins (AQPs). The integrity of interstitial cells of Cajal (ICC) in the colon was assessed via immunohistochemistry. Finally, the expression levels of proteins associated with the mitogen-activated protein kinase (MAPK) signaling pathway were examined. GAS administration significantly improved STC symptoms by promoting defecation, enhancing gastrointestinal motility, and ameliorating histopathological damage in the colon. It also markedly attenuated intestinal inflammation, normalized the expression of neurotransmitters and AQPs, and restored the loperamide-induced depletion of ICC networks. Mechanistically, the protective effects of GAS were associated with the suppression of the MAPK signaling pathway, as evidenced by reduced phosphorylation of its key components: extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. Our findings indicate that GAS possesses significant therapeutic potential for STC by mediating its beneficial effects through the regulation of intestinal inflammation, motility, and water transport, ultimately via the inhibition of the MAPK signaling pathway.

Slow transit constipation (STC) is a prevalent functional gastrointestinal disorder characterized by a reduced frequency of bowel movements, the presence of dry and hard stools, and abdominal pain. However, the underlying mechanisms contributing to its pathogenesis have not yet been fully clarified. This study aims to investigate the effects of METTL3 on loperamide (LOP)-induced STC mice and glutamic acid-induced interstitial cells of Cajal (ICCs). METTL3-knock down adeno-associated virus (AAV) was used to treat LOP-induced mice, and the effect of METTL3 down-regulation was assessed by the stool parameters, histological analysis, transmission electron microscopy (TEM), TdT-mediated dUTP nick end labeling (TUNEL) staining, immunohistochemistry, Immunofluorescence staining, and Western blotting. METTL3 small interfering RNA (siRNA) was transfected into ICCs before glutamic acid, PI3K inhibitor (LY294002), and AKT inhibitor (GSK690693) treatment alone or in combination. EdU assays, flow cytometry, TEM, and Western blot were used to investigate the relationship between METTL3 and PI3K/AKT pathway. METTL3 deletion alleviated constipation symptoms and promoted intestinal motility in STC mice. METTL3 knockdown suppressed apoptosis and autophagy, accompanied by increased proliferation of glutamic acid-induced ICCs. More importantly, the effect of METTL3 knockdown on proliferation and autophagy was significantly reversed in glutamic acid-induced ICCs treated with LY294002 or GSK690693. Mechanistically, METTL3 deletion exerts its STC-repressive influence through the activation of the PI3K/AKT pathway. Collectively, the findings indicate that METTL3 modulates PI3K/AKT-mediated autophagy following LOP and highlight the potential of METTL3 as a therapeutic target in STC treatment.

Background Dendrobium officinale (DOF), a highly valued traditional Chinese medicinal herb and functional food, boasts a millennia‐long history of medicinal use. Our previous research has demonstrated its efficacy in alleviating acute constipation, primarily attributed to its polysaccharide (DOP). Nevertheless, the therapeutic potential of DOP in addressing slow transit constipation (STC) and its underlying mechanisms remain unexplored. This research seeks to elucidate the protective effects and underlying mechanistic pathways of DOP in loperamide‐induced STC. Methods KM mice were administered loperamide to establish the STC model, followed by DOP intervention. After treatment, gastrointestinal motility, fecal output, and key gastrointestinal regulatory hormones were all detected. The 5‐hydroxytryptamine (5‐HT) pathway was further analyzed by analyzing enterochromaffin cells (ECs), serotonin transport (SERT), and 5‐HT receptors (5‐HTRs). Additionally, 16S rDNA sequencing was performed to evaluate gut microbiota composition. Changes in levels of short‐chain fatty acids (SCFAs) and their receptor were also quantified. Results DOP significantly ameliorated defecation dysfunction in STC mice, enhancing gastrointestinal motility and increasing 24‐h fecal output. Additionally, DOP treatment restored the colonic levels of key gastrointestinal hormones, especially in 5‐HT concentration. This effect may be attributed to the expansion of ECs and suppression of SERT expression. Moreover, DOP selectively upregulated 5‐HT 4 R expression without affecting 5‐HT 3 R. Beyond neurotransmitter regulation, DOP modulated gut microbiota composition by increasing microbial diversity and altering the community structure, particularly through shifts in the Bacteroidetes/Firmicutes ratio. Furthermore, DOP elevated SCFA levels and activated their downstream receptor G Protein–Coupled Receptor 43 (GPR43), which may contribute to the observed 5‐HT system modulation. Conclusions DOP demonstrates significant efficacy in ameliorating constipation symptoms in STC mice through the dual modulation of the 5‐HT system and gut microbiota composition. These results furnish robust scientific support, substantiating the therapeutic potential of DOP in the daily health care or management of STC.

Slow transit constipation (STC) is a chronic colonic motility disorder characterized by markedly delayed transit, leading to reduced bowel movements, abdominal discomfort, and significant quality-of-life impairment. It predominantly affects women and is associated with abnormalities in enteric neuronal signaling, smooth muscle contractility, interstitial cells of Cajal, gut peptides, bile acid homeostasis, and autonomic regulation. Secondary causes of constipation and structural lesions must be excluded before the diagnosis of STC, with colonic transit studies serving as the gold standard. Complementary investigations such as anorectal manometry and defecography help detect coexisting outlet obstruction, which can alter management. The treatment of STC should follow a stepwise approach, beginning with dietary and lifestyle modification, osmotic and stimulant laxatives, and prokinetics such as prucalopride. Secretagogues and bile acid modulators may offer additional benefit. Biofeedback therapy is primarily indicated for overlapping dyssynergic defecation. For refractory STC, interventional therapies, such as fecal microbiota transplantation, acupuncture, sacral nerve stimulation, and transanal irrigation, are found to have equivocal outcomes. Antegrade continence enema procedures can be an alternative for patients unsuitable for colectomy. Surgical options, including subtotal colectomy with ileosigmoid or cecorectal anastomosis, and total colectomy with ileorectal anastomosis, are reserved for carefully selected patients with medically intractable symptoms, following thorough physiological evaluation. Although advances in understanding STC pathophysiology are guiding novel therapeutic development, robust randomized controlled trials remain scarce. Optimal care requires multidisciplinary collaboration between gastroenterologists, colorectal surgeons, and pelvic floor specialists to ensure accurate diagnosis, tailored treatment, and improved long-term outcomes.

Batatasin III alleviates slow transit constipation by regulating gut microbiota and inhibiting the NLRP3-IL-1β pathway.

Mechanistic insights into the effects of Norisoboldine on intestinal immunity and neuroinflammation in a mouse model of slow transit constipation with depression.

Objective: To investigate the feasibility of employing high-resolution colon manometry (HRCM) in conjunction with natural orifice specimen extraction surgery (NOSES) during laparoscopic Jinling surgery for the treatment of colonic slow transit constipation (STC). Methods: This study retrospectively analyzed data from nine patients with STC who underwent HRCM preoperative evaluation and subsequently received NOSES Jinling surgery at Tianjin Union Medical Center between October 2016 and March 2023. The general intraoperative conditions and postoperative evaluation indicators were recorded. Results: All 9 patients underwent HRCM examination before surgery. High amplitude propagation contraction (HAPC) was observed in the ascending colon segment of all patients. The occurrence frequency of HAPC was 4.22±1.86 (times/day). The operation time of 9 patients was 200.0 (167.5, 250.0) minutes, the intraoperative blood loss was 100 (50, 150) ml, the postoperative hospitalization time was 13.0 (12.5, 24.0) days, and the first postoperative exhaust time was 3.0 (2.0, 3.5) days, the first postoperative defecation time was 5.0 (4.5, 5.5) days, the first postoperative eating time was 5.0 (5.0, 5.5) days, and the first postoperative time out of bed was 5.0 (5.0, 8.0) days. Notably, none of the 9 patients experienced postoperative complications. The Wexner scores at 6 months [5 (4, 7)], and 12 months [4 (3, 5)] post-surgery were significantly lower than the preoperative score [20 (16, 21)] (P<0.05). Additionally, the patient assessment of constipation quality of life (PAC-QOL) scores at 6 months [22 (20, 25)], and 12 months [18 (12, 45)] after surgery showed a significant decrease compared to preoperative scores [79 (72, 82)] (P<0.05). Conclusions: The combination of HRCM preoperative assessment and NOSES Jinling surgery is both safe and feasible for the treatment of slow transit constipation, warranting further development and promotion.

Objective: To compare postoperative anal function recovery between laparoscopic subtotal colectomy with antiperistaltic cecorectal anastomosis and laparoscopic total colectomy with ileorectal anastomosis for slow transit constipation. Methods: This multicenter retrospective cohort study enrolled patients meeting the following criteria: (1) severe constipation symptoms (<2 bowel movements/week), absent or insignificant defecation urge, abdominal distension, requiring laxatives to maintain bowel movements or laxatives being ineffective; (2) constipation symptoms for over 5 years, ineffective after >2 years of medical treatment, with strong desire for surgery; (3) significantly prolonged colon transit time (>72 hours) without significant gastric or small intestinal transit dysfunction; (4) no organic colonic lesions confirmed by colonoscopy and abdominal CT. Exclusion criteria: (1) patients undergoing open surgery; (2) exclusion of outlet obstruction constipation (e.g., rectocele, rectal prolapse, puborectalis spasm) by functional defecation MRI; (3) comorbid psychiatric disorders; (4) missing clinical data or loss to follow-up (postoperative follow-up <24 months). Based on these criteria, clinical and follow-up data were collected from 220 patients who underwent either laparoscopic subtotal colectomy with antiperistaltic cecorectal anastomosis (LSC group, n = 115) or laparoscopic total colectomy with ileorectal anastomosis (LTC group, n = 105) for slow transit constipation between January 2013 and December 2022. Subjective anal function (Constipation Severity Score and Wexner Fecal Incontinence Score) and objective anal function (positive rate of rectoanal inhibitory reflex [RAIR] and anorectal manometry) were observed preoperatively and at 6, 12, and 24 months postoperatively. Results: No significant differences were found in baseline characteristics between the two groups (all P >0.05). All surgeries were completed successfully without major significant complications. Subjective anal function assessment: At 24 months postoperatively, Constipation Severity Scores decreased significantly compared to preoperative scores in both groups [LSC group: (25.2±2.8) vs. (2.9±1.8), P <0.001; LTC group: (25.8±2.9) vs. (2.8±1.9), P<0.001]. No significant differences were found between the groups at 6, 12, and 24 months postoperatively (all P>0.05). Wexner Fecal Incontinence Scores at 24 months were significantly lower than those at 6 months in both groups [LSC group: (12.9±1.8) vs. (3.9±2.5), P<0.001; LTC group: (12.6±1.8) vs. (5.4±2.4), P<0.001]. Although no significant difference was found at 6 months (P = 0.190), the LSC group had significantly lower Wexner scores than the LTC group at 12 and 24 months postoperatively (both P < 0.001). Objective anal function assessment: (1) Positive RAIR rate: Preoperative positive RAIR rates were 33.0% (38/115) in the LSC group and 25.7% (27/105) in the LTC group (P > 0.05). At 24 months, positive rates increased significantly in both groups [LSC: 66.1% (76/115); LTC: 63.8% (67/105)] compared to preoperative rates (both P<0.001), but no significant differences were found between groups at 6, 12, and 24 months (all P>0.05). (2) Resting pressure (RP) and squeeze pressure (SP): No significant differences were found in preoperative RP and SP between groups (all P>0.05). The LSC group had significantly higher RP and SP than the LTC group at 6 and 12 months postoperatively (all P<0.05), but no significant differences were found at 24 months (P>0.05). Conclusion: Both laparoscopic subtotal colectomy with antiperistaltic cecorectal anastomosis and laparoscopic total colectomy with ileorectal anastomosis are safe for patients with slow transit constipation. However, laparoscopic subtotal colectomy with antiperistaltic cecorectal anastomosis offers superior postoperative anal function recovery.