Related Experiment Video
Updated: May 1, 2026
07:40
Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
1.9K
Caffeic Acid Protects Keratinocytes from PM2.5 by Regulating ROS, Mitochondrial Integrity, and JNK Activation.
Herath Mudiyanselage Maheshika Madhuwanthi Senavirathna1, Mei Jing Piao1, Kyoung Ah Kang1
1College of Medicine and Jeju Research Center for Natural Medicine, Jeju National University, Jeju 63243, Republic of Korea.
Biomolecules & Therapeutics
|April 30, 2026
Summary
Caffeic acid (CA) protects skin cells from pollution damage. It reduces oxidative stress and apoptosis caused by particulate matter (PM2.5) by regulating key cell survival pathways.
Area of Science:
- Dermatology and Environmental Toxicology
- Cellular and Molecular Biology
Background:
- Particulate matter (PM2.5) is a significant air pollutant causing skin damage via oxidative stress and apoptosis.
- Caffeic acid (CA) is a natural phenolic compound with known antioxidant and cytoprotective effects.
Purpose of the Study:
- To investigate the protective effects of caffeic acid (CA) against PM2.5-induced cellular injury in human HaCaT keratinocytes.
Main Methods:
- HaCaT keratinocytes were exposed to PM2.5 with and without CA treatment.
- Assessed reactive oxygen species (ROS) levels, lipid peroxidation, protein oxidation, and mitochondrial function.
- Analyzed apoptosis markers including Bcl-2, Bax, caspase-3, caspase-9, and phospho-JNK.
Main Results:
- CA significantly reduced PM2.5-induced ROS accumulation and oxidative damage.
- CA mitigated mitochondrial membrane depolarization and intracellular calcium overload.
- CA attenuated apoptosis by upregulating Bcl-2 and downregulating Bax, caspase-3, caspase-9, and phospho-JNK.
Conclusions:
- Caffeic acid (CA) demonstrates significant protective effects against PM2.5-induced oxidative stress and apoptosis in skin cells.
- CA acts by modulating the Bcl-2/Bax ratio and inhibiting JNK signaling pathways.
- CA shows potential as a therapeutic agent for preventing skin damage from environmental pollutants.
Related Concept Videos
02:34Inhibition of Cdk Activity
4.8K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.8K
01:46Electron Transport Chain: Complex I and II
11.9K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...
11.9K
01:07MAPK Signaling Cascades
7.3K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
7.3K