The effect of prehabilitation on the postoperative outcomes of patients undergoing colorectal surgery: A systematic review and meta-analysis

Study objectivePrehabilitation is analogous to marathon training and includes preoperative preparation for exercise, as well as nutrition and psychology. However, evidence-based recommendations to guide prehabilitation before colorectal surgery are limited. We aimed to evaluate the effect of prehabilitation on the postoperative outcomes of patients undergoing colorectal surgery.DesignThis study is a systematic review and meta-analysis.MethodsThe PubMed, Embase, and Cochrane databases were searched for studies reporting the effect of prehabilitation strategies versus standard care or rehabilitation in patients undergoing colorectal surgery. The primary outcomes were overall postoperative complications and length of hospital stay (LOS), and the secondary outcome was functional capacity (measured using the 6-min walk test [6MWT]) at 4 and 8 weeks after surgery.Main resultsFifteen studies with 1,306 participants were included in this meta-analysis. The results showed no significant reduction in the number of overall postoperative complications (risk ratio = 1.02; 95% confidence interval [CI] = 0.79–1.31; p = 0.878) or LOS (standardized mean difference = 0.04; 95% CI = −0.11 to 0.20; p = 0.589) in patients who underwent colorectal surgery with or without prehabilitation strategy. Additionally, there were no significant differences in the functional capacity estimated using the 6MWT at 4 and 8 weeks postoperatively.ConclusionsPrehabilitation did not significantly affect the number of postoperative complications, LOS, or functional capacity of patients undergoing colorectal surgery. Whether prehabilitation should be recommended deserves further consideration.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=290108, identifier CRD4202129010

Restorative effects of Lactobacillus rhamnosus LR-32 on the gut microbiota, barrier integrity, and 5-HT metabolism in reducing feather-pecking behavior in laying hens with antibiotic-induced dysbiosis

The development of abnormal feather-pecking (FP) behavior, where laying hens display harmful pecks in conspecifics, is multifactorial and has been linked to the microbiota-gut-brain axis. Antibiotics affect the gut microbial composition, leading to gut-brain axis imbalance and behavior and physiology changes in many species. However, it is not clear whether intestinal dysbacteriosis can induce the development of damaging behavior, such as FP. The restorative effects of Lactobacillus rhamnosus LR-32 against intestinal dysbacteriosis-induced alternations need to be determined either. The current investigation aimed to induce intestinal dysbacteriosis in laying hens by supplementing their diet with the antibiotic lincomycin hydrochloride. The study revealed that antibiotic exposure resulted in decreased egg production performance and an increased tendency toward severe feather-pecking (SFP) behavior in laying hens. Moreover, intestinal and blood-brain barrier functions were impaired, and 5-HT metabolism was inhibited. However, treatment with Lactobacillus rhamnosus LR-32 following antibiotic exposure significantly alleviated the decline in egg production performance and reduced SFP behavior. Lactobacillus rhamnosus LR-32 supplementation restored the profile of the gut microbial community, and showed a strong positive effect by increasing the expression of tight junction proteins in the ileum and hypothalamus and promoting the expression of genes related to central 5-HT metabolism. The correlation analysis revealed that probiotic-enhanced bacteria were positively correlated, and probiotic-reduced bacteria were negatively correlated with tight junction-related gene expression, and 5-HT metabolism, and butyric acid levels. Overall, our findings indicate that dietary supplementation with Lactobacillus rhamnosus LR-32 can reduce antibiotic-induced FP in laying hens and is a promising treatment to improve the welfare of domestic birds

Punicalin attenuates LPS-induced acute lung injury by inhibiting inflammatory cytokine production and MAPK/NF-κB signaling in mice

Background: Acute lung injury (ALI) remains a significant cause of morbidity and mortality in critically ill patients. Novel therapies interfering with the inflammatory response has been an area of focus for infectious disease treatment. Punicalin has shown strong anti-inflammatory and antioxidative properties; however, its effect in ALI has not been previously explored. Purpose: To investigate the effects of punicalin in lipopolysaccharide (LPS)-induced ALI and explore the underlying mechanisms. Methods: LPS (10 mg/kg) was administered intratracheally to create the ALI model in mice. Punicalin (10 mg/kg) was administered intraperitoneally shortly after LPS to investigate survival rate, lung tissue pathological injury, oxidative stress, levels of inflammatory cytokines in BALF and lung tissue, neutrophil extracellular trap (NET) formation and its effects on NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways. In vitro studies were performed to evaluate the inflammatory cytokine release and NET formation in LPS-induced (1 μg/ml) and punicalin-treated mouse neutrophils derived from the bone marrow. Results: In vivo, punicalin reduced mortality, lung injury score, lung wet-to-dry (W/D) weight ratio, protein concentrations in BALF and malondialdehyde (MDA) levels in lung tissues, and increased superoxide dismutase (SOD) levels in lung tissues of LPS-induced ALI mice. Increased secretion of TNF-α, IL-1β, and IL-6 in the BALF and the lungs of ALI mice was reversed by punicalin, whereas IL-10 was upregulated. Neutrophil recruitment and NET formation were also decreased by punicalin. Inhibition of NF-κB and MAPK signaling pathways was observed in punicalin-treated ALI mice. In vitro co-incubation with punicalin (50 μg/ml) inhibited the production of inflammatory cytokines and NET formation in LPS-treated neutrophils derived from mouse bone marrow. Conclusion: Punicalin reduces inflammatory cytokine production, prevents neutrophil recruitment and NET formation, and inhibits the activation of NF-κB and MAPK signaling pathways in LPS-induced ALI