Bile acids encompass primary bile acids and secondary bile acids,the latter of which are produced from primary bile acids in the gut.In recent years,bile acids,compounds with a steroid structure found in bile,have been shown through extensive clinical investigations and fundamental studies to play a significant role in regulating intestinal and systemic immune homeostasis,inflammatory responses,and neurological disorders.In the gut,primary and secondary bile acids can disrupt the invasion of pathogenic microorganisms into the host due to their unique physical properties.Additional-ly,they regulate downstream signaling pathways by binding to effector receptors,thereby performing vital biological func-tions,including the modulation of immune responses.Consequently,bile acids function as essential small molecules in the pathophysiological processes of various intestinal diseases and extra-intestinal tissue conditions influenced by intestinal homeostasis.This article focuses on the role and regulatory mechanisms of the"microbe-bile acid"axis in intestinal inflam-mation,elucidating the synthesis and metabolism of bile acids and the significance of intestinal microbes in signal trans-duction via bile acids during the inflammatory process.It aims to provide a foundation and reference for the development of drugs and therapeutic strategies targeting diseases related to intestinal inflammation and immune dysregulation.

Bile acids encompass primary bile acids and secondary bile acids,the latter of which are produced from primary bile acids in the gut.In recent years,bile acids,compounds with a steroid structure found in bile,have been shown through extensive clinical investigations and fundamental studies to play a significant role in regulating intestinal and systemic immune homeostasis,inflammatory responses,and neurological disorders.In the gut,primary and secondary bile acids can disrupt the invasion of pathogenic microorganisms into the host due to their unique physical properties.Additional-ly,they regulate downstream signaling pathways by binding to effector receptors,thereby performing vital biological func-tions,including the modulation of immune responses.Consequently,bile acids function as essential small molecules in the pathophysiological processes of various intestinal diseases and extra-intestinal tissue conditions influenced by intestinal homeostasis.This article focuses on the role and regulatory mechanisms of the"microbe-bile acid"axis in intestinal inflam-mation,elucidating the synthesis and metabolism of bile acids and the significance of intestinal microbes in signal trans-duction via bile acids during the inflammatory process.It aims to provide a foundation and reference for the development of drugs and therapeutic strategies targeting diseases related to intestinal inflammation and immune dysregulation.

The gut microbiota of infants is crucial for the establishment and development of immune system tolerance and responsiveness, as well as long-term health.Breast milk, as the only recommended source of nutrition for infants under 6 months old, possesses all the necessary nutrients and functional components for their growth, development, and health promotion.Human milk oligosaccharides (HMOs), as distinctive functional components that distinguish human milk from other mammalian milk, possess natural targeting properties to reach the colorectum in its intact form and are essential for the maturation of the gut microbiota, development of the digestive system and maintenance of the immune system function in infants, providing natural protection for the digestive and immune systems of newborns.This article reviews the latest research on how HMOs affect the development of the immune system and homeostasis in infants, and focuses on the mechanism by which HMOs control the gut microbiota and influence the immune system′s response through the gut microbiota-immune axis.

Objective To explore the effectiveness of FOCUS-PDCA(find,organise,clarify,understand,select,plan,do,check and act)mode in prevention and treatment of incontinence-associated dermatitis(IAD)in emergency intensive care unit(EICU),and to reduce the incidence of IAD.Methods A pre-post control study design was employed in this study.Inpatients admitted to the EICU of the hospital between 1st January and 31st December 2022 were enrolled as study subjects.A total of 169 patients in EICU between January and June 2022 were assigned as a control group,while 197 patients in EICU between July and December 2022 as an trial group.Patients in the control group received conventional quality management,while those in the trial group were treated with the FOCUS-PDCA mode.The two groups were compared in terms of incidence of IAD,the knowledge,trust and behaviour scores of the nurses,and satisfaction from the communications with nurses before and after implementation of the FOCUS-PDCA mode.Results All patients in the two groups had completed the study.Following the implementation of FOCUS-PDCA mode,patients in the trial group exhibited a significantly decrease in incidence of IAD from 10.06%(trial group)to 1.52%(control group),significant increase of scores on the IAD knowledge,behaviour and satisfaction from communications with the nurses,from(36.07±3.98),(16.56±2.15)and(25.15±5.21),to(38.59±3.72),(18.07±1.66),and(30.67±5.84),respectively(all P<0.05).Conclusion FOCUS-PDCA mode can effectively decrease the incidence of IAD,enhance the IAD knowledge and behaviour of nurses and gain satisfactions from communication with nursing staff and clinical quality,thereby improving therapeutic outcomes.

Human milk oligosaccharides (HMOs), as the third most abundant solid nutrient in breast milk, are critical for early infants growth. HMOs are not only involved in the development of the immune system, maintaining inflammation balance, regulating gut microbiota, and participating in the maturation of the digestive system, but also in the improvement of the brain's nervous system and the development of advanced cognitive functions such as learning and memory. However, the role of HMOs in regulating neural development remains unclear. Related studies have focused on the mechanism of the microbiota-gut-brain axis, indicating that there is a practical interaction between the gut and brain. The function of HMOs in children's neurocognition and the biological process of disorders via this mechanism has also been preliminary reported. This review aims to review the structural characteristics and species-specific characteristics of HMOs, and analyze the potential pathways of HMOs in infant nervous system development from the perspective of the microbiota-gut-brain axis.

Objective:To investigate the mechanism of 6-sialyllactose (6-SL) in interfering the immune checkpoint inhibitor-induced colitis (ICIC) through the bacterial 16S rDNA sequencing.Methods:BALB/c mice were randomly divided into the normal control (NC) group ( n = 7), dextran sulfate sodium (DSS) group ( n = 6), ICIC group ( n = 6), and ICIC+6-SL group ( n = 6). The DSS group was continuously fed with 3.5% DSS drinking water for 7 days to induce colonic inflammation; the ICIC group was administered cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4, 150 μg) intraperitoneally on days 0 and 4 in addition to 3.5% DSS drinking water to establish the ICIC mouse model; the ICIC+6-SL group was given 6-SL [150 mg/ (kg·d) ] by gavage simultaneously with the establishment of the ICIC model. Changes in mouse body weight and disease activity index (DAI) were statistically analyzed, and all mice were sacrificed on day 7 to observe gross and histopathological morphological changes in the colon and to tally histopathological scores; the fresh colonic feces were collected for 16S rDNA sequencing to statistically analyze the diversity and species differences in the microbiota of mice of each group. Results:The success rate of the ICIC model was 100%, with all mice surviving. At the endpoint of the study (day 7), compared with the NC and DSS groups, the ICIC group had lower mouse body weight ( P < 0.05), higher DAI ( P < 0.05), damaged integrity of colonic mucosal tissue, and typical ulcerative lesions; the ICIC+6-SL group showed significant alleviation of body weight loss, significantly lower DAI scores, and lower pathological scores compared to the ICIC group, with all differences being statistically significant (all P < 0.05). 16S rDNA sequencing of mouse intestinal feces indicated that the alpha diversity of colonic microbiota in the ICIC group was lower than that in the NC and DSS groups (both P < 0.05), while the ICIC+6-SL group had higher alpha diversity than the ICIC group ( P < 0.05). In beta diversity analysis, the ANOSIM statistical value R = 0.376, P = 0.001 for the PCoA analysis of colonic microbiota and a Stress value of 0.125, P = 0.001 for the NMDS analysis indicated differences in the composition of colonic microbiota among the groups, with the greatest difference between the NC and ICIC groups, and the ICIC+6-SL group's microbiota composition was closer to that of the NC group compared to the ICIC group. Lefse analysis and Kruskal-Wallis test-based differential microbiota analysis showed that at the phylum level, compared to the NC group, the abundance of Bacteroidetes was significantly reduced in the ICIC group, while Campilobacterota was increased, and 6-SL administration could increase the abundance of Bacteroidetes and Campilobacterota in the ICIC group. At the genus level, compared to other groups, the abundance of unclassified_f_Lachnospiraceae and norank_f_Muribaculaceae was the lowest in the ICIC group, while Helicobacter, Akkermansia, and Escherichia-Shigella were enriched. Compared to the ICIC group, the abundance of unclassified_f_Lachnospiraceae and norank_f_ Muribaculaceae was increased in the ICIC+6-SL group, while the abundance of Helicobacter and Escherichia-Shigella was significantly suppressed. Conclusions:6-SL, an oligosaccharide derived from human milk, alleviates intestinal inflammatory injury in ICIC mice, reducing disease activity. This beneficial effect may be related to its regulation of gut microbiota profiling, an increased diversity of microbiota, a restoration of Bacteroidetes, and an inhibition of the growth advantage of pathogenic bacteria such as Helicobacter and Escherichia-Shigella.

Objective:To investigate the mechanism of 6-sialyllactose (6-SL) in interfering the immune checkpoint inhibitor-induced colitis (ICIC) through the bacterial 16S rDNA sequencing.Methods:BALB/c mice were randomly divided into the normal control (NC) group ( n = 7), dextran sulfate sodium (DSS) group ( n = 6), ICIC group ( n = 6), and ICIC+6-SL group ( n = 6). The DSS group was continuously fed with 3.5% DSS drinking water for 7 days to induce colonic inflammation; the ICIC group was administered cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4, 150 μg) intraperitoneally on days 0 and 4 in addition to 3.5% DSS drinking water to establish the ICIC mouse model; the ICIC+6-SL group was given 6-SL [150 mg/ (kg·d) ] by gavage simultaneously with the establishment of the ICIC model. Changes in mouse body weight and disease activity index (DAI) were statistically analyzed, and all mice were sacrificed on day 7 to observe gross and histopathological morphological changes in the colon and to tally histopathological scores; the fresh colonic feces were collected for 16S rDNA sequencing to statistically analyze the diversity and species differences in the microbiota of mice of each group. Results:The success rate of the ICIC model was 100%, with all mice surviving. At the endpoint of the study (day 7), compared with the NC and DSS groups, the ICIC group had lower mouse body weight ( P < 0.05), higher DAI ( P < 0.05), damaged integrity of colonic mucosal tissue, and typical ulcerative lesions; the ICIC+6-SL group showed significant alleviation of body weight loss, significantly lower DAI scores, and lower pathological scores compared to the ICIC group, with all differences being statistically significant (all P < 0.05). 16S rDNA sequencing of mouse intestinal feces indicated that the alpha diversity of colonic microbiota in the ICIC group was lower than that in the NC and DSS groups (both P < 0.05), while the ICIC+6-SL group had higher alpha diversity than the ICIC group ( P < 0.05). In beta diversity analysis, the ANOSIM statistical value R = 0.376, P = 0.001 for the PCoA analysis of colonic microbiota and a Stress value of 0.125, P = 0.001 for the NMDS analysis indicated differences in the composition of colonic microbiota among the groups, with the greatest difference between the NC and ICIC groups, and the ICIC+6-SL group's microbiota composition was closer to that of the NC group compared to the ICIC group. Lefse analysis and Kruskal-Wallis test-based differential microbiota analysis showed that at the phylum level, compared to the NC group, the abundance of Bacteroidetes was significantly reduced in the ICIC group, while Campilobacterota was increased, and 6-SL administration could increase the abundance of Bacteroidetes and Campilobacterota in the ICIC group. At the genus level, compared to other groups, the abundance of unclassified_f_Lachnospiraceae and norank_f_Muribaculaceae was the lowest in the ICIC group, while Helicobacter, Akkermansia, and Escherichia-Shigella were enriched. Compared to the ICIC group, the abundance of unclassified_f_Lachnospiraceae and norank_f_ Muribaculaceae was increased in the ICIC+6-SL group, while the abundance of Helicobacter and Escherichia-Shigella was significantly suppressed. Conclusions:6-SL, an oligosaccharide derived from human milk, alleviates intestinal inflammatory injury in ICIC mice, reducing disease activity. This beneficial effect may be related to its regulation of gut microbiota profiling, an increased diversity of microbiota, a restoration of Bacteroidetes, and an inhibition of the growth advantage of pathogenic bacteria such as Helicobacter and Escherichia-Shigella.

Objective: To evaluate the clinical efficacy and safety of low-intensity extracorporeal shock wave therapy (LI-ESWT) in the treatment of ED based on the available clinical evidence. METHODS: We searched PubMed, MEDLINE, EMBASE, Cochrane Library, CNKI, VIP, CBM and Wanfang Database up to June 2018 for published randomized controlled trials on the treatment of ED by LI-ESWT. We performed literature screening, data extraction and quality evaluation according to inclusion and exclusion criteria, and conducted a meta-analysis of the data obtained using the RevMan 5.3 software. RESULTS: A total of 595 ED cases in 8 double-blind randomized controlled trials (RCT) were included in this study, 362 in the LI-ESWT and 233 in the control group. Compared with the controls, the patients treated by LI-ESWT showed significantly improved IIEF (WMD = 1.70, 95% CI: 0.44－2.96, P = 0.008) and erection hardness score (EHS) (RR = 11.72, 95% CI: 5.13－26.80, P < 0.01). The IIEF scores of the patients were markedly increased at 4 and 24 weeks after LI-ESWT (WMD = 1.43, 95% CI: 0.10－2.75, P = 0.03; WMD = 3.09, 95% CI: 1.49－4.68, P = 0.0002), as well as after the 10th to 12th treatment (WMD = 1.81, 95% CI: 0.31－3.31, P = 0.02) though not after the 5th to 6th (WMD = 1.88, 95% CI: －2.10 to 5.86, P = 0.35). LI-ESWT also significantly increased the IIEF scores in the patients with the baseline IIEF ≥12 (WMD = 2.13, 95% CI: 0.51－3.75, P = 0.01) but not in those with the baseline IIEF ≤11 (WMD = 1.04, 95% CI: －0.96 to 3.03, P = 0.31). No significant adverse events were reported in the 8 RCTs. CONCLUSIONS As a non-invasive treatment, LI-ESWT is safe and effective and can significantly improve IIEF and EHS in ED patients.

ObjectiveTo investigate the effects of fosfomycin tromethamine (FT) on the expressions of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), and interleukin-6 (IL-6) in the prostate tissue of the rats with chronic bacterial prostatitis (CBP).

METHODSWe randomly divided 70 male SD rats into 7 groups of equal number: blank control, CBP model control, positive control, 14 d low-dose FT, 7 d low-dose FT, 14 d high-dose FT, and 7 d high-dose FT. The CBP model rats in the latter five groups were treated intragastrically with levofloxacin at 100 mg/kg/d for 30 days and FT at 200 mg/kg/d for 14 and 7 days and at 300 mg/kg/d for 14 and 7 days, respectively. Then we collected the prostate tissue from the animals for determination of the levels of TNF-α, IL-8 and IL-6 by ELISA.

RESULTSCompared with the blank controls, the CBP model rats showed significantly increased levels of TNF-α (［19.83 ± 6.1］ vs ［32.93 ± 6.21］ ng/g prot, P <0.01), IL-8 (［8.26 ± 0.52］ vs ［16.2 ± 2.84］ ng/g prot, P <0.01) and IL-6 (［1.55 ± 0.11］ vs ［2.51 ± 1.06］ ng/g prot, P <0.05) in the prostate tissue. In comparison with the CBP model controls, the levels of TNF-α and IL-8 were remarkably decreased in the groups of positive control (［20.54 ± 5.78］ ng/g prot, P <0.01; ［12.43 ± 4.02］ ng/g prot, P <0.05), 14 d low-dose FT (［21.95 ± 6.48］ ng/g prot, P <0.01; ［11.11 ± 2.86］ ng/g prot, P <0.01), 7 d low-dose FT (［23.8 ± 6.93］ ng/g prot, P <0.05; ［12.43 ± 4.02］ ng/g prot, P <0.05), 14 d high-dose FT (［19.97 ± 2.58］ ng/g prot, P <0.01; ［8.83 ± 1.32］ ng/g prot, P <0.01), and 7 d high-dose FT (［21.97 ± 3.38］ ng/g prot, P <0.01; ［12.68±1.97］ ng/g prot, P <0.05). No statistically significant differences were observed between the positive control and FT groups in the contents of TNF-α, IL-8 or IL-6 (P >0.05). The expression of IL-6 was markedly reduced in the 14 d high-dose FT group as compared with the model controls (［1.76 ± 0.46］ vs ［2.51 ± 1.06］ ng/g prot, P<0.05) but exhibited no significant difference between the CBP model control and the other groups (P >0.05).

CONCLUSIONSFosfomycin tromethamine inhibits the expressions of TNF-α, IL-8 and IL-6 in the prostate tissue, suppresses its inflammatory reaction, promotes the repair of damaged prostatic structure, and thus contributes to the treatment of chronic bacterial prostatitis in rats.

Animals ; Anti-Bacterial Agents ; pharmacology ; Bacterial Infections ; drug therapy ; microbiology ; Fosfomycin ; pharmacology ; Interleukin-6 ; metabolism ; Interleukin-8 ; metabolism ; Levofloxacin ; pharmacology ; Male ; Prostate ; drug effects ; metabolism ; Prostatitis ; drug therapy ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism

Objective: To explore the effects of Xialiqi Capsules(XLQ) on the expressions of the proliferating cell nuclear antigen (PCNA) and caspase-3 in the prostate tissue of the BPH rat model. METHODS: Fifty male SD ratswereequally randomized into groups A (sham operation control), B (BPH model control), C (high-dose XLQ), D (low-dose XLQ), and E (finasteridecontrol) andthe BPH modelswere established by subcutaneous injection of testosterone propionate at 0.5 mg per kilogram of the body weight per day for 30 days after castration. After modeling, the animals in groups A and B were treated intragastricallywith normal saline, while those in C, D, and E with XLQ at 1.20 and 0.61 g per kilogram of the body weight per day or finasterideat 0.8 mg per kilogram of the body weight per day, respectively, all for 30 days. Then,the bilateral prostates were harvestedfrom the rats for calculation of the prostatic index (prostate wet weight/ body weight) and determination of the expressions of PCNA and caspase-3 in the prostate tissue by immunohistochemistry and immunofluorescence staining, respectively. RESULTS: The prostate wet weight and prostate index were significantly increased in group B as compared with group A, (［1326±60］ vs［471±17］ g, P<0.01; ［2.89±0.18］ vs ［1.06±0.06］ mg/g, P<0.01), but decreased in groups C (［914±36］ g;［2.02±0.08］ mg/g), D (［1 099±46］g;［2.39±0.11］ mg/g), and E (［817±53］ g;［1.83±0.10］ mg/g)in comparison with B (P<0.01), with statistically significant differences among groups C, D, and E(P<0.01) and most significantly in E.The PCNA level in the prostate tissue wasremarkably higher in group B than in A, but lower in groups C, D and E than in B. The expression of caspase-3 was down-regulatedin group B as compared with A, but up-regulated in groups C, D and E in comparison with B, most significantly in E. CONCLUSIONS Xialiqi Capsules can effectively reduce the prostate wet weight and prostatic index of in rats with BPH by inhibiting the level of PCNA and promoting the expression of caspase-3.
Animals ; Capsules ; Caspase 3 ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; Finasteride ; administration & dosage ; pharmacology ; Male ; Orchiectomy ; Organ Size ; drug effects ; Proliferating Cell Nuclear Antigen ; metabolism ; Prostate ; drug effects ; metabolism ; pathology ; Prostatic Hyperplasia ; drug therapy ; metabolism ; pathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Urological Agents ; administration & dosage ; pharmacology