Anti-Skin Inflammatory and Anti-Oxidative Effects of the Neoflavonoid Latifolin Isolated from Dalbergia odorifera in HaCaT and BJ-5ta Cells.
Linsha DongHwan LeeZhiming LiuDong Sung LeePublished in: International journal of molecular sciences (2023)
Skin is the first line of defense in the body against external stimulation and injury. Inflammation and oxidative stress in skin cells are the initiators and promoters of several skin diseases. Latifolin is a natural flavonoid isolated from Dalbergia odorifera T. Chen. This study aimed to evaluate the anti-inflammatory and antioxidant properties of latifolin. The anti-inflammatory effects were evaluated using tumor necrosis factor-α/interferon-γ (TNF-α/IFN-γ)-treated HaCaT cells, revealing that latifolin inhibited the secretion of Interleukin 6 (IL-6); Interleukin 8 (IL-8); Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted (RANTES); and Macrophage-derived chemokine (MDC) while decreasing the expression of Intercellular Adhesion Molecule 1 (ICAM-1). The results of western blots and immunofluorescence demonstrated that the activation of Janus kinase 2 (JAK2), Signal transducer and activator of transcription 1 (STAT1), Signal transducer and activator of transcription 3 (STAT3), and nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) cells signaling pathways were significantly inhibited by latifolin. The antioxidant properties were evaluated using t -BHP-induced BJ-5ta cells. Latifolin increased the viability of t -BHP-induced BJ-5ta cells. Additionally, fluorescent staining of reactive oxygen species (ROS) showed that the production of ROS was inhibited by latifolin. Additionally, latifolin reduced the phosphorylation of p38 and JNK. The results indicate that latifolin has potential anti-inflammatory and antioxidant properties, and may be a candidate natural compound for the treatment of skin diseases.
Keyphrases
- induced apoptosis
- oxidative stress
- nuclear factor
- cell cycle arrest
- anti inflammatory
- signaling pathway
- cell death
- diabetic rats
- reactive oxygen species
- endoplasmic reticulum stress
- dna damage
- pi k akt
- rheumatoid arthritis
- escherichia coli
- toll like receptor
- immune response
- cell proliferation
- ischemia reperfusion injury
- stress induced
- epithelial mesenchymal transition
- wound healing
- single molecule
- tyrosine kinase
- living cells