Collagen study advances for photoaging skin.

BACKGROUND: Collagen dominates the skin's extracellular matrix (ECM). Type I collagen comprises 80%-90% of the skin's collagen, followed by type III (8%-12%) and type V (5%). Reactive oxygen species, matrix metalloproteinases, and collagen degradation all increase during photoaging, which disrupts the ECM's dynamic balance and lowers the amount of total collagen in the body. In recent years, domestic and foreign researchers have conducted multidimensional and multifaceted studies on collagen and skin photoaging. Collagen and the peptides that are derivates of it are currently being used more and more in biomedicine and medical esthetics. OBJECTIVE: Offering new suggestions for both the avoidance and remedy of photoaging. METHODS: This article reviews collagen and its potential connection to skin photoaging, illustrates the effects of collagen and peptide supplementation derivatives on photoaged skin, and briefly describes other compounds that can also be used to fight photoaging by increasing collagen synthesis in the skin. RESULT: Both internal and external aging are inevitable, and as the main component of extracellular matrix, collagen plays a variety of functions in maintaining skin structure and fighting skin aging, and its role in photoaging is undeniable. Ultraviolet radiation can induce increased fragmentation and degradation of cutaneous collagen, while conversely, supplementation with collagen can effectively counteract photodamage-induced skin impairment. CONCLUSION: Collagen and its derived peptides are indispensable in photoaging skin, holding promising prospects for applications in skin aging.

Cox-2 Antagonizes the Protective Effect of Sevoflurane on Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis through Inhibiting the Akt Pathway.

OBJECTIVE: To uncover the protective role of sevoflurane on hypoxia/reoxygenation-induced cardiomyocyte apoptosis through the protein kinase B (Akt) pathway. METHODS: An in vitro hypoxia/reoxygenation (H/R) model was established in cardiomyocyte cell line H9c2. Sevoflurane (SEV) was administrated in H9c2 cells during the reoxygenation period. Viability, layered double hydroxide (LDH) release, and apoptosis in H9c2 cells were determined to assess H/R-induced cell damage. Relative levels of apoptosis-associated genes were examined. Moreover, phosphorylation of Akt was determined. RESULTS: H/R injury declined viability and enhanced LDH release and apoptotic rate in H9c2 cells. Cyclooxygenase-2 (Cox-2) was upregulated following H/R injury, which was partially reversed by SEV treatment. In addition, SEV treatment reversed changes in viability and LDH release owing to H/R injury in H9c2 cells, which were further aggravated by overexpression of Cox-2. The Akt pathway was inhibited in H9c2 cells overexpressing Cox-2. CONCLUSIONS: Sevoflurane protects cardiomyocyte damage following H/R via the Akt pathway, and its protective effect was abolished by overexpression of Cox-2.

Sendeng-4 Suppressed Melanoma Growth by Induction of Autophagy and Apoptosis.

Sendeng-4 is a traditional Chinese medicine that has been successfully applied to anti-inflammatory diseases in clinical practice. Monomers within Sendeng-4 showed promising antitumor activity against lung cancer, colon cancer, and cutaneous cancer. However, potency of Sendeng-4 in melanoma has not been explored. This study aims to explore the potential application of Sendeng-4 in melanoma treatment. In the present study, we systemically investigate the possibility of Sendeng-4 for treatment of melanoma cancer in vitro by proliferation assay, colony formation, flow cell cytometry, RNA-seq, western blot, and fluorescence-based assay. Our data demonstrated that Sendeng-4 suppresses the proliferation and colony formation capacity of melanoma cells and induces cell cycle block at G2/M phase and eventually cell death. Mechanistically, transcriptome sequencing demonstrates that the PI3K-AKT pathway was significantly inactivated upon Sendeng-4 exposure, which was confirmed by western blot showing decreased phosphorylation of AKT. In addition, decreased BCL-2 expression and increased BAX expression were observed, suggesting programmed cell death via apoptosis. Moreover, LC3-II production as well as autophagosomes formation was observed as demonstrated by western blot and immunofluorescence, indicating elevated autophagy network by Sendeng-4 stimulation. Collectively, we concluded that Sendeng-4 might be used as an anticancer drug for melanoma.