Probiotics have been widely used in maintaining intestinal health and one of their benefits is to enhance host antioxidant capacity. However, the involved molecular mechanisms require further investigated. Autophagy is a self-protection process in response to diverse stresses. We hypothesized that probiotics could modulate intestinal autophagy to alleviate oxidative stress. Sprague-Dawley (SD) rats were orally administered Bacillus SC06 or SC08 daily for 24 days and thereafter received an intraperitoneal injection of diquat (DQ) to induce oxidative stress. We found that rats administered Bacillus SC06 showed more significant intestinal tissue repair and antioxidant properties than those administered SC08, which suggests a strain-specific effect of probiotics. Moreover, SC06 alleviated apoptosis by regulating the expression of Bcl2, Bax and cleaved caspase-3. Further investigations revealed that SC06 triggered autophagy, indicated by the upregulation of LC3 and Beclin1 and the degradation of p62 in rat jejunum and IEC-6 cells. Preincubation with autophagy inhibitor 3-methyladenine (3-MA) significantly aggravated reactive oxygen species (ROS) production and apoptotic cell formation. Furthermore, we demonstrated that p38 MAPK (mitogen-activated protein kinase), not AKT (alpha serine/threonine kinase)/mTOR (mammalian target of rapamycin), was involved in SC06-induced autophagy. Taken together, Bacillus SC06 can alleviate oxidative stress-induced disorders and apoptosis via p38-mediated autophagy. The above findings highlight a novel mechanism underlying the beneficial effects of probiotics as functional food and provide a new perspective on the prevention and treatment of oxidative damages.

Oxidative stress is a state of imbalance between oxidation and antioxidation. It is caused by excess levels of free radicals and leads to the damage of DNA, proteins, and lipids. The crucial role of gut microbiota in regulating oxidative stress has been widely demonstrated. Studies have suggested that the redox regulatory effects of gut microbiota are related to gut microbiota metabolites, including fatty acids, lipopolysaccharides, tryptophan metabolites, trimethylamine-N-oxide and polyphenolic metabolites. In recent years, the potential benefits of probiotics have been gaining increasing scientific interest owing to their ability to modulate gut microbiota and oxidative stress. In this review, we summarise the adverse health effects of oxidative stress and discuss the role of the gut microbiota and its metabolites in redox regulation. Based on the influence of gut microbiota metabolites, the roles of probiotics in preventing oxidative stress are highlighted.

The objective of this study was to evaluate effects of probiotic Bacillus amyloliquefaciens (Ba) as a substitute for antibiotics on growth performance, antioxidant ability and intestinal autophagy of piglets. Ninety piglets were divided into three groups: G1 (containing 150 mg/Kg aureomycin in the diet); G2 (containing 75 mg/Kg aureomycin and 1 × 108 cfu/Kg Ba in the diet); G3 (containing 2 × 108 cfu/Kg Ba in the diet without any antibiotics). Each treatment had three replications of ten pigs per pen. Results showed that Ba replacement significantly increased the daily weight gain of piglets. Moreover, improved antioxidant status in serum and jejunum was noted in Ba-fed groups as compared with aureomycin group. Increased gene expression of antioxidant enzymes and elevated nuclear factor erythroid 2 related factor 2 (Nrf2) in jejunum was also observed in Ba-fed groups. Besides, Ba replacement significantly decreased jejunal c-Jun N-terminal kinase (JNK) phosphorylation compared with antibiotic group. Western blotting results also revealed that replacing all antibiotics with Ba initiated autophagy in the jejunum as evidenced by increased microtubule-associated protein 1 light chain 3 II (LC3-II) abundance. Taken together, these results indicate that replacing aureomycin with Ba can improve growth performance and antioxidant status of piglets via increasing antioxidant capacity and intestinal autophagy, suggesting a good potential for Ba as an alternative to antibiotics in feed.

Oxidation is a major cause of meat quality deterioration during broiler production, which leads to undesirable meat color and impaired water holding capacity (WHC), thereby impacting consumer appeal and satisfaction. Chlorogenic acid (CGA), a natural phenolic acid, is regarded as a potential, safer and healthier antioxidant to improve meat quality. To investigate the protective effects of CGA on the meat quality of oxidatively stressed broilers, 240 one-day-old male Cobb broiler chickens were allocated to four treatments: basal diet (control group), basal diet + dexamethasone (DEX) injection (DEX group), basal diet containing 500 mg kg⁻¹ CGA (CGA group), and basal diet containing 500 mg kg⁻¹ CGA + DEX injection (DEX_CGA group). Meat quality, antioxidant capacity, the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, and metabolomic profile were detected in the breast muscle of broilers. Then, correlation analysis between meat quality and antioxidant capacity, antioxidant-related genes, and metabolites was performed. The results indicated that CGA supplementation improved the growth performance and meat quality traits (pH, WHC, and meat color) and enhanced the antioxidant enzyme activity by activating the Nrf2 pathway in the breast muscle of oxidatively stressed broilers. A total of 619 metabolites were identified, among which 93 differential metabolites were found between control and DEX groups, and 65 differential metabolites were observed between DEX and DEX_CGA groups. Breast metabolic profiles were changed by DEX treatment, while CGA supplementation could normalize the metabolic changes in DEX-challenged broilers. Metabolic pathway analysis revealed that most of the differential metabolites between DEX and DEX_CGA groups were involved in pyrimidine/purine, propanoate and phenylalanine metabolism, primary bile acid biosynthesis, and lysine metabolism, which may contribute to explain the protective effects of CGA on meat quality. Moreover, according to the correlation analysis, four metabolites were identified as potential biomarkers to predict the meat quality. In conclusion, our findings demonstrate that CGA is an effective, natural and safe antioxidant to enhance the quality of meat from intensive industrial poultry production.

Intensive production can cause immunological stress in commercial broilers. Chlorogenic acid (CGA) regulates the intestinal microbiota, barrier function, and immune function in chickens. As complex interrelations regulate the dynamic interplay between gut microbiota, the host, and diverse health outcomes, the aim of this study was to elucidate the immunoregulatory mechanisms of CGA using multi-omics approaches. A total of 240 one-day-old male broilers were assigned to a 2 × 2 factorial design with 2 CGA levels (0 or 500 mg/kg) either with or without dexamethasone (DEX) injection for a 21-day experimental period. Therefore, there were 4 dietary treatments: control, DEX, CGA, and DEX + CGA, with 6 replicates per treatment. CGA supplementation improved (P < 0.05) growth performance, jejunal morphology, jejunal barrier function, and immune function in DEX-treated broilers. Moreover, in DEX + CGA-treated broilers, the increase in gut microbiome diversity (P < 0.05) was consistent with a change in taxonomic composition, especially in the Clostridiales vadin BB60_group. Additionally, the levels of short-chain fatty acids increased remarkably (P < 0.01) after CGA supplementation. This was consistent with the Kyoto Encyclopedia of Genes and Genomes analysis results that the “pyruvate fermentation to butanoate” pathway was more enriched (P < 0.01) in the DEX + CGA group than in the DEX group. Proteomics revealed that CGA treatment increased the expression of several health-promoting proteins, thymosin beta (TMSB4X) and legumain (LGMN), which were verified by multiple reaction monitoring. Metabolomics revealed that CGA treatment increased the expression of health-promoting metabolites (2,4-dihydroxy benzoic acid and homogentisic acid). Proteomic and metabolic analyses showed that CGA treatment regulated the peroxisome proliferator-activated receptor (PPAR) and mitogen-activated protein kinase (MAPK) pathways. Western blotting results support these findings. Pearson’s correlation analyses showed correlations (P < 0.01) between altered immune function, jejunal barrier function, different microbiota, proteins, and metabolites parameters. Overall, our data indicate that CGA treatment increased growth performance and improved the immunological functions of DEX-treated broilers by regulating gut microbiota and the PPAR and MAPK pathways. The results offer novel insights into a CGA-mediated improvement in immune function and intestinal health.