C-Peptide Ameliorates Particulate Matter 2.5-Induced Skin Cell Apoptosis by Inhibiting NADPH Oxidation.

Area of Science:

• Dermatology
• Cell Biology
• Environmental Health

Background:

• Particulate matter 2.5 (PM$_{2.5}$) exposure causes skin aging, thickening, and inflammation.
• Oxidative stress is a key mechanism in PM$_{2.5}$-induced skin damage.
• Connecting peptide (C-peptide), a byproduct of insulin biosynthesis, has known biological functions.

Purpose of the Study:

• To investigate the protective effects of C-peptide against PM$_{2.5}$-induced skin cell damage.
• To elucidate the role of oxidative stress and NADPH oxidase (NOX) activity in this protective mechanism.

Main Methods:

• Human HaCaT keratinocytes were exposed to PM$_{2.5}$ with and without C-peptide treatment.
• Assessed oxidative stress markers: NADPH oxidation, intracellular reactive oxygen species (ROS) production.
• Measured NOX activity, NOX1 and NOX4 expression, DNA damage, lipid peroxidation, and protein carbonylation.
• Evaluated apoptosis levels.

Main Results:

• C-peptide significantly mitigated PM$_{2.5}$-induced NADPH oxidation and ROS production.
• C-peptide suppressed PM$_{2.5}$-induced NOX activity and NOX1/NOX4 expression.
• C-peptide protected against PM$_{2.5}$-induced DNA damage, lipid peroxidation, and protein carbonylation.
• C-peptide reduced PM$_{2.5}$-induced apoptosis.

Conclusions:

• C-peptide mitigates PM$_{2.5}$-induced skin cell damage by inhibiting oxidative stress.
• C-peptide's protective effects are mediated through the suppression of NOX activity and ROS production.
• C-peptide demonstrates potential as a therapeutic agent against environmental skin aging caused by PM$_{2.5}$.