Microstructure: Surface and cross-sectional studies of hydroxyapatite formation on the surface of white Portland cement paste in vitro

The formation of hydroxyapatite was investigated at the surface and at the cross-section of white Portland cement paste samples before and after immersion in simulated body fluid. Scanning electron microscope images showed that hydroxyapatite were found at the surface of white Portland cement after immersion in simulated body fluid. Hydroxyapatite grains of mostly ≈1 μm size with some grain size of ≈2-3 μm were seen after 4 days immersion period. More estabilshed hydroxyapatite grain size of ≈3 μm grains were observed at longer period of immersion at 7 and 10 days. The cross-section of the samples was investigated using line scanning technique and was used to determine the hydroxyapatite layer. A strong spectrum of phosphorus is detected up to 6-8 μm depth for samples after 4, 7 and 10 days immersion in simulated body fluid when compared to weak spectrum detected before immersion. The increase in the phosphorus spectrum corresponds to the hydroxyapatite formation on the surface of the samples after the samples were placed in simulated body fluid.     

Hesperidin Exhibits Protective Effects against PM2.5-Mediated Mitochondrial Damage,Cell Cycle Arrest,and Cellular Senescence in Human HaCaT Keratinocytes

Particulate matter 2.5 (PM_2.5) exposure can trigger adverse health outcomes in the human skin, such as skin aging, wrinkles, pigment spots, and atopic dermatitis. PM_2.5 is associated with mitochondrial damage and the generation of reactive oxygen species (ROS). Hesperidin is a bioflavonoid that exhibits antioxidant and anti-inflammatory properties. This study aimed to determine the mechanism underlying the protective effect of hesperidin on human HaCaT keratinocytes against PM_2.5-induced mitochondrial damage, cell cycle arrest, and cellular senescence. Human HaCaT keratinocytes were pre-treated with hesperidin and then treated with PM_2.5. Hesperidin attenuated PM_2.5-induced mitochondrial and DNA damage, G₀/G₁ cell cycle arrest, and SA-βGal activity, the protein levels of cell cycle regulators, and matrix metalloproteinases (MMPs). Moreover, treatment with a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, along with hesperidin markedly restored PM_2.5-induced cell cycle arrest and cellular senescence. In addition, hesperidin significantly reduced the activation of MMPs, including MMP-1, MMP-2, and MMP-9, by inhibiting the activation of activator protein 1. In conclusion, hesperidin ameliorates PM_2.5-induced mitochondrial damage, cell cycle arrest, and cellular senescence in human HaCaT keratinocytes via the ROS/JNK pathway.