Probiotics are microbial strains that are beneficial to health, and their potential has recently led to a significant increase in research interest in their use to modulate the gut microbiota. The animal gut is a complex ecosystem of host cells, microbiota, and available nutrients, and the microbiota prevents several degenerative diseases in humans and animals via immunomodulation. The gut microbiota and its influence on human nutrition, metabolism, physiology, and immunity are addressed, and several probiotic species and strains are discussed to improve the understanding of modulation of gut microbiota. This paper provides a broad review of several Lactobacillus spp., Bifidobacterium spp., and other coliform bacteria as the most promising probiotic species and their role in the prevention of degenerative diseases, such as obesity, diabetes, cancer, cardiovascular diseases, malignancy, liver disease, and inflammatory bowel disease. This review also discusses a recent study of Saccharomyces spp. in which inflammation was prevented by promotion of proinflammatory immune function via the production of short-chain fatty acids. A summary of gut microbiota alteration with future perspectives is also provided.

Unrestricted cell proliferation is a hallmark of cancer. Purines are basic components of nucleotides in cell proliferation, thus impaired purine metabolism is associated with the progression of cancer. The de novo biosynthesis of purine depends on six enzymes to catalyze the conversion of phosphoribosylpyrophosphate to inosine 5′-monophosphate. These enzymes cluster around mitochondria and microtubules to form purinosome, which is a multi-enzyme complex involved in de novo purine biosynthesis and purine nucleotides requirement. In this review, we highlighted the purine metabolism and purinosome biology with emphasis on the therapeutic potential of manipulating of purine metabolism or purinosome in cancers. We also reviewed current advances in our understanding of mammalian target of rapamycin for regulating purinosome formation or purine metabolism in cancers and discussed the future prospects for targeting purinosome to treat cancers.

Melatonin affects a variety of physiological processes including circadian rhythms, cellular redox status, and immune function. Importantly, melatonin significantly influences T‐cell‐mediated immune responses, which are crucial to protect mammals against cancers and infections, but are associated with pathogenesis of many autoimmune diseases. This review focuses on our current understanding of the significance of melatonin in T‐cell biology and the beneficial effects of melatonin in T‐cell response‐based diseases. In addition to expressing both membrane and nuclear receptors for melatonin, T cells have the four enzymes required for the synthesis of melatonin and produce high levels of melatonin. Meanwhile, melatonin is highly effective in modulating T‐cell activation and differentiation, especially for Th17 and Treg cells, and also memory T cells. Mechanistically, the influence of melatonin in T‐cell biology is associated with membrane and nuclear receptors as well as receptor‐independent pathways, for example, via calcineurin. Several cell signaling pathways, including ERK1/2‐C/EBPα, are involved in the regulatory roles of melatonin in T‐cell biology. Through modulation in T‐cell responses, melatonin exerts beneficial effects in various inflammatory diseases, such as type 1 diabetes, systemic lupus erythematosus, and multiple sclerosis. These findings highlight the importance of melatonin signaling in T‐cell fate determination, and T cell‐based immune pathologies.

Birth oxidative stress is an oxidative response to a sudden transition process from maternal mediated respiration in uterus to autonomous pulmonary respiration outside the uterus. Meanwhile, oxidative stress has been demonstrated to be associated with various pathologies recorded in newborns. So, this research aimed to study the oxidative stress and the development of antioxidant system in newborn piglets. The measured variables include plasma lipid, protein and DNA oxidant injury, the activities of plasma antioxidant enzymes and the jejunal and ileal antioxidant gene expressions at 1, 7, 14, and 21 days after birth. Meanwhile, the nuclear factor erythroid 2-related factor 2 (Nrf2), transcription factor p65, and tumor protein 53 (p53) were determined by western blot. The results showed that newborn piglets suffered seriously from birth oxidative stress because of the naive antioxidant system. In addition, oxidant injury activated Nrf2 signaling pathway, resulting in the expression of antioxidant genes and release of antioxidant enzymes. With the development of antioxidant system, the oxidative balance gradually recovered on Day 7 after birth. In conclusion, birth caused oxidative stress and the oxidative balance gradually recovered with the development of antioxidant system.