Glycyrrhizic acid prevents ultraviolet‐B‐induced photodamage: a role for mitogen‐activated protein kinases, nuclear factor kappa B and mitochondrial apoptotic pathway

• DOI: 10.1111/exd.12964
• Publication Date: 2016-02-02T21:23:51Z
• Authors: Quadri Afnan; Peerzada J. Kaiser; Rather A. Rafiq; Lone A. Nazir; Shashi Bhushan; Subhash C. Bhardwaj; Rajat Sandhir; Sheikh A. Tasduq
• Keywords: HaCaT

Glycyrrhizic acid (GA), a natural triterpene, has received attention as an agent that protective effects against chronic diseases including ultraviolet UV-B-induced skin photodamage. However, the mechanism of its effect remains elusive. Here, we used immortalized human keratinocyte cell line (HaCaT) and small animal model (BALB/c mice), to investigate GA oxidative damage, additionally, delineated molecular mechanisms involved in UV-B-mediated inflammatory apoptotic response. In HaCaT cells, inhibited increase intracellular reactive oxygen species (ROS) down-regulated release pro-inflammatory cytokines interleukin (IL)-1α, -1β -6, tumor necrosis factor (TNF)-α prostaglandin E2 (PGE2). activation p38 JNK MAP kinases, COX-2 expression nuclear translocation NF-κB. Furthermore, apoptosis by attenuating Bax from cytosol mitochondria, thus preserving mitochondrial integrity. GA-treated cells also exhibited elevated antiapoptotic Bcl-2 protein, concomitant with reduced caspase-3 cleavage decreased PARP-1 protein. BALB/c mice, topical application on dorsal exposed UV-B irradiation protected epidermal hyperplasia, lymphocyte infiltration several proteins, p38, JNK, COX-2, NF-κB ICAM-1. Based above findings, conclude protects photodamage inhibiting signalling cascades triggered stress, MAPK/NF-κB activation, well apoptosis. Thus, strong potential be therapeutic/cosmeceutical