Allicin attenuates UVB-induced photodamage of keratinocytes by inhibiting NLRP3 inflammasomes and activating the PI3K/Akt pathway.

Allicin is a sulfide extracted from garlic bulbs responsible for various physiological and pathophysiological effects, including antioxidant, antibacterial, and anti-parasite activities. However, its efficacy and mechanism of protecting UVB-induced photodamage have not been studied. The research explores Allicin's protective roles and underlying mechanisms in UVB-induced photodamage of keratinocytes. UVB was employed to generate photodamage in the HaCaT cell line. DCFH-DA fluorescent and Biochemical analyses were carried out to evaluate reactive oxygen species (ROS) and oxidative stress on UVB-induced photodamage to HaCaT cells. RT-qPCR and western blot were performed to measure mRNA and protein expression. Allicin pretreatment (10 and 25 µM) improved cell proliferation and reduced apoptotic rates in UVB-induced HaCaT cells. Allicin (10 and 25 µM) inhibited tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) expressions (all, P < 0.001). Allicin reduced the intracellular ROS level and attenuated oxidative stress, with reduced malondialdehyde (MDA) level while increasing the levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSh-Px) (all, P < 0.001) in UVB-induced HaCaT cells. Allicin pretreatment inhibited autophagy and reduced the protein expression of Beclin-1 while increasing the p62 protein expression (all, P < 0.001). We also observed that Allicin pretreatment reduced the NLRP3-related protein, such as Caspase-1 (P < 0.001) and increased the protein expressions of the PI3K/Akt pathway molecules, such as PI3K and Akt (all, P < 0.001). Our research data demonstrated that Allicin might inhibit UVB-induced photodamage of keratinocytes via inhibiting NLRP3 inflammasomes and activating the PI3K/Akt pathway.