Home Blog of Signal Transduction DNA Damage/DNA Repair Sirtuin Salidroside Ameliorates Ultraviolet-Induced Keratinocyte Injury by Inducing SIRT1-Dependent Autophagy

Category

Archives

Popular Post

ESKM, a novel therapeutic agent for sensitive and resistant PH+ leukemias

The mechanism of resistance to JAK2 inhibitor in myeloproliferative neoplasms patients

Effects of PARP inhibitors in BRCA gene-mutated ovarian cancer

DASATINIB; An inhibitor of Receptor Tyrosine Kinase

GP130/JAK/STAT3 signaling pathway induces multiple myeloma

Salidroside Ameliorates Ultraviolet-Induced Keratinocyte Injury by Inducing SIRT1-Dependent Autophagy

Introduction: Autophagy is an important process for maintaining intracellular homeostasis and is deregulated in ultraviolet B (UVB)-induced skin injury. Salidroside (SAL) is an active ingredient extracted from Rhodiola rosea, which is a herbal medicine that has shown protection against ultraviolet (UV) radiation. Here, we investigated the functions and mechanisms of SAL on UVB-induced skin cell oxidative damage and autophagy.

Methods: Human immortalized keratinocyte cell line HaCaT was used as a cell model of UV injury. HaCaT cells were exposed to UVB irradiation and then incubated with SAL to investigate cell viability, lactate dehydrogenase (LSD) in culture media, intracellular reactive oxygen species (ROS) level, oxidative stress, autophagy, and regulatory effects on SIRT1 protein.

Results: SAL pretreatment (25, 50 and 100 μM) increased cell viability and inhibited LDH release in UVB-challenged HaCaT cells. SAL (100 μM) significantly reduced intracellular ROS level and suppressed oxidative stress, with increased MDA content and increased SOD activity. In addition, SAL pretreatment enhanced autophagy in UVB-irradiated HaCaT cells, increased protein expressions of Beclin-1 and ATG7, and decreased protein expression of P62. We also found that pretreatment with SAL increased the SIRT1 protein in irradiated HaCaT cells. SAL protected UVB-induced damage in a dependent manner on autophagy and SIRT1, as SAL-induced increase in viability was significantly attenuated by specific autophagy inhibitor Wortmannin (1 μM) or SIRT1 inhibitor EX-527 (100 nM).

Discussion: The present study results speculate that SAL suppresses UVB-induced injury and autophagy by enhancing SIRT1 expression.

Related Products

Cat.No. Product Name Information
S1541 Selisistat (EX 527) Selisistat (EX 527, SEN0014196) is a potent and selective SIRT1 inhibitor with IC50 of 38 nM in a cell-free assay, exhibits >200-fold selectivity against SIRT2 and SIRT3. Phase 2.

Related Targets

Sirtuin