Aging skin, wrinkles, pigmentation, and dryness are problems that plague people, and researchers are working to solve them. Recent studies have shown that intestinal microbiota homeostasis can influence skin health, demonstrating the existence of a gut–skin axis. Recently, improving skin health through probiotic interventions has been proposed, and micro-ecological skin care is becoming a popular concept. By regulating skin health and gut–skin axis interactions, probiotics can be used as potential management tools to suppress and improve skin diseases in multiple ways, including decreasing oxidative stress, suppressing inflammatory responses, and keeping immune effects. The purpose of this paper is to provide a comprehensive review of the application and mechanisms of probiotic-mediated gut microbiota homeostasis in skin care and to offer a theoretical basis for the application of probiotics in skin care.

Radical cure colitis is a severe public health threat worldwide. Our previous studies have confirmed that melatonin can effectively improve gut microbiota disorder and mucosal injury caused by sleep deprivation (SD). The present study further explored the mechanism whereby exogenous melatonin prevented SD-induced colitis. 16S rRNA high-throughput sequencing and metabolomics analysis were used to explore the correlation between SD-induced colitis and intestinal microbiota and metabolite composition in mice. Fecal microbiota transplantation (FMT) and melatonin or butyrate supplementation tests verified the core role of gut microbiota in melatonin-alleviating SD-induced colitis. Further, in vitro tests studied the modulatory mechanism of metabolite butyrate. The results demonstrated that SD leads to reductions in plasma melatonin levels and colonic Card9 expression and consequent occurrence of colitis and gut microbiota disorder, especially the downregulation of Faecalibacterium and butyrate levels. The FMT from SD-mice to normal mice could restore SD-like colitis, while butyrate supplementation to SD-mice inhibited the occurrence of colitis, but with no change in the plasma melatonin level in both treatments. However, melatonin supplementation reversed all inductions in SD-mice. In intestinal epithelial cells, the inflammatory ameliorative effect of butyrate was blocked with pretreatments of HDAC3 agonist and HIF-1α antagonist but was mimicked by GSK-3β and p-P65 antagonists. Therefore, the administration of MLT may be a better therapy for SD-induced colitis relative to butyrate. A feasible mechanism would involve that melatonin up-regulated the Faecalibacterium population and production of its metabolite butyrate and MCT1 expression and inhibited HDAC3 in the colon, which would allow p-GSK-3β/β-catenin/HIF-1α activation and NF-κB/NLRP3 suppression to up-regulate Card9 expression and suppress inflammation response.

Sunlight is a vital element in modulating the central circadian rhythm, such as the regulation of the host’s sleep–awake state. Sunlight is also considered to have a significant influence on the circadian rhythm of the skin. Over-exposure or prolonged exposure to sunlight can lead to skin photodamage, including hyperpigmentation, collagen degradation, fibrosis, and even skin cancer. Thus, this review will focus on the adverse effects of sunlight on the skin, not only in terms of photoaging but also its effect on the skin’s circadian rhythm. Mitochondrial melatonin, regarded as a beneficial anti-aging substance for the skin, follows a circadian rhythm and exhibits a powerful anti-oxidative capacity, which has been shown to be associated with skin function. Thus, the review will focus on the influence of sunlight on skin status, not only in terms of ultraviolet radiation (UVR)-induced oxidative stress but also its mediation of circadian rhythms regulating skin homeostasis. In addition, this article will address issues regarding how best to unleash the biological potential of melatonin. These findings about the circadian rhythms of the skin have broadened the horizon of a whole new dimension in our comprehension of the molecular mechanisms of the skin and are likely to help pharmaceutical companies to develop more effective products that not only inhibit photoaging but keep valid and relevant throughout the day in future.

Macrophages polarized into distinct phenotypes play vital roles in inflammatory diseases by clearing pathogens, promoting tissue repair, and maintaining homeostasis. Metabolism serves as a fundamental driver in regulating macrophage polarization, and understanding the interplay between macrophage metabolism and polarization is crucial for unraveling the mechanisms underlying inflammatory diseases. The intricate network of cellular signaling pathway plays a pivotal role in modulating macrophage metabolism, and growing evidence indicates that the Hippo pathway emerges as a central player in network of cellular metabolism signaling. This review aims to explore the impact of macrophage metabolism on polarization and summarize the cell signaling pathways that regulate macrophage metabolism in diseases. Specifically, we highlight the pivotal role of the Hippo pathway as a key regulator of cellular metabolism and reveal its potential relationship with metabolism in macrophage polarization.

The intestinal tract, as the main place for nutrient digestion and absorption, is closely related to the health of livestock and poultry. Melatonin secreted by the pineal gland acts as an endocrine transport signaling molecule to regulate intestinal function. However, the effect on intestinal function after pineal removal is unclear. We raised 24 chicks under 400-700 nm white light with or without pinealectomy for 21 days. We used electron microscopy, HE staining, PAS staining, immunohistochemistry, immunofluorescence staining and western blot to detect intestinal physical and to explore the effect of melatonin secreted by the pineal gland on the intestinal mucosa barrier function. The results showed that after pineal gland removal, the structure of the intestinal villi is severely damaged. Moreover, there was an obviously down-regulation in the villi length, the number of goblet cells and and its secretion of MUC2 protein, the expression level of tight junction proteins (Occludin and ZO-1) and lysozyme secreted by paneth cells, number of PCNA positive cells and macrophage, and an up-regualtion in crypt depth and apoptosis level after pinealectomy, suggesting pinealectomy-mediated melatonin level decrease damaged the intestinal physical, chemical and immune barriers. Our findings provide new theoretical support for the future use of melatonin in intestinal development and new ideas about the relationship between endocrine hormone and intestinal physiology.

Collagen loss is one of the major contributor to signs of skin aging such as dryness, roughness, and wrinkle formation, which is closely linked to a decline in the amount of proline produced in mitochondria. Melatonin has been shown to improve several clinical signs of skin aging, while the mechanism is unclear. In our study, we found that mitophagy, proline synthesis key enzyme NADK2 and proline and collagen levels were significantly reduced, while oxidative stress levels increased in aging skin, and melatonin supplementation could effectively up-regulate mitophagy level and restore proline synthesis and further improved skin aging. However, proline supplementation could also exert an anti-aging effect, while it had no effect on the mitochondrial dysfunction. Moreover, our study indicated that melatonin enters the cell by binding to the MT1 receptor and then enters the mitochondria via the PEPT1 transporter to exert its mitochondrial protective effects. This study helps to elucidate the mechanism of mitochondrial dysfunction-induced skin aging, and provides new theoretical guidance for revealing the mechanism of skin aging and rationally utilizing endocrine hormones to improve skin aging, which has a broad application prospect.