Skin photoaging is mainly induced by ultraviolet (UV) irradiation and its manifestations include dry skin, coarse wrinkle, irregular pigmentation, and loss of skin elasticity. Dietary supplementation of nutraceuticals with therapeutic and preventive effects against skin photoaging has recently received increasing attention. This article aims to review the research progress in the cellular and molecular mechanisms of UV-induced skin photoaging. Subsequently, the beneficial effects of dietary components on skin photoaging are discussed. The photoaging process and the underlying mechanisms are complex. Matrix metalloproteinases, transforming growth factors, skin adipose tissue, inflammation, oxidative stress, nuclear and mitochondrial DNA, telomeres, microRNA, advanced glycation end products, the hypothalamic–pituitary–adrenal axis, and transient receptor potential cation channel V are key regulators that drive the photoaging-associated changes in skin. Meanwhile, mounting evidence from animal models and clinical trials suggests that various food-derived components attenuate the development and symptoms of skin photoaging. The major mechanisms of these dietary components to alleviate skin photoaging include the maintenance of skin moisture and extracellular matrix content, regulation of specific signaling pathways involved in the synthesis and degradation of the extracellular matrix, and antioxidant capacity. Taken together, the ingestion of food-derived functional components could be an attractive strategy to prevent skin photoaging damage.
Previous studies have reported the therapeutic effects of oleuropein (OP) consumption on the early stage of type 2 diabetes. However, the efficacy of OP on the advanced stage of type 2 diabetes has not been investigated, and the relationship between OP and intestinal flora has not been studied. Therefore, in this study, to explore the relieving effects of OP intake on the advanced stage of type 2 diabetes and the regulatory effects of OP on intestinal microbes, diabetic db/db mice (17-week-old) were treated with OP at the dose of 200 mg/kg for 15 weeks. We found that OP has a significant effect in decreasing fasting blood glucose levels, improving glucose tolerance, lowering the homeostasis model assessment–insulin resistance index, restoring histopathological features of tissues, and promoting hepatic protein kinase B activation in db/db mice. Notably, OP modulates gut microbiota at phylum level, increases the relative abundance of Verrucomicrobia and Deferribacteres, and decreases the relative abundance of Bacteroidetes. OP treatment increases the relative abundance of Akkermansia, as well as decreases the relative abundance of Prevotella, Odoribacter, Ruminococcus, and Parabacteroides at genus level. In conclusion, OP may ameliorate the advanced stage of type 2 diabetes through modulating the composition and function of gut microbiota. Our findings provide a promising therapeutic approach for the treatment of advanced stage type 2 diabetes.
Scope
Eugenol (EU), the major aromatic compound derived from clove oil, is being focused recently due to its potential in preventing several chronic conditions. Herein, this study aims to evaluate the potential of EU in obesity prevention and to delineate the mechanisms involved.
Methods and results
Five‐week‐old male C57BL/6J mice are fed with high‐fat diet (HFD) or HFD supplemented with EU (0.2%, w/w) for 13 weeks. EU significantly reduces obesity‐related indexes including final body weight, body weight gain, adipocyte size, visceral fat‐pad weight, and fasting blood glucose. EU prevents HFD‐induced gut dysbiosis, as indicated by the increase of Firmicutes and decrease of Desulfobacterota at phylum level, and the increase of Dubosiella, Blautia, unclassified_f_Oscillospiraceae, and unclassified_f_Ruminococcaceae, and the decrease of Alistipes, Alloprevotella, and Bilophila at genus level. Notably, the obesity‐related indexes are positively correlated with the relative abundances of Bacteroides, unclassified_f_Lachnospiraceae, Colidextribacter, and Bilophila, and negatively correlated with the relative abundances of norank_f_Muribaculaceae and Lachnospiraceae_NK4A136_group. Moreover, the preventive effects of EU on obesity are accompanied by the transcriptomic reprogramming of white adipose tissue.
Conclusion
These findings demonstrate that EU prevents the HFD‐induced adiposity and modulates gut dysbiosis, and highlight the potential of EU in obesity intervention as a functional dietary supplement.
Scope: Curcumin is a natural polyphenol compound with multiple pharmacologic activities. The present study aims to explore the potential therapeutic properties of curcumin on intestinal inflammatory diseases, including its anti-inflammatory, antioxidant, and anti-apoptotic properties, as well as their associations with altered intestinal microbiome. Methods and Results: DSS, i.e., Dextran Sulfate Sodium, (3%) is administered to C57BL/6J mice in the drinking water daily for 6 days in DSS and curcumin groups. Then, mice in curcumin groups are orally administered with 50 or 150 mg kg -1 curcumin for 7 days. On day 13, mice are sacrificed. Results show that oral administration with curcumin relieves macroscopic pathological manifestations, e.g., colon length and histological change. Moreover, it enhances intestinal barrier via increasing expression of tight junction proteins, e.g., occludin, ZO-1, claudin-3; alleviates DSS-induced intestinal apoptosis via suppressing caspase-3 pathway; mitigates intestinal inflammation via inhibiting the MAPK/NF𝜿B/STAT3 pathway. It is also noticed that curcumin is beneficial for modulating abundance of some specific bacteria, including Akkermansia, Coprococcus, Roseburia, and Turicibacter, as well as families such as F16, Enterococcaceae, and Aerococcaceae. Most of the altered bacteria by curcumin are highly correlated with colitis-associated parameters. Conclusion: Curcumin shows therapeutic potential against colitis. It may be served as an alternative medicine or adjuvant therapy in the treatment of colitis.
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