Abstract
Phycocyanin (Pc) is one of the active pigment constituents of Spirulina microalgae. It has been used for its potent antioxidant and anti-inflammatory properties. However, the protective effects of Pc against ultraviolet-B (UVB)-induced primary skin cells damage are still undefined. In the present study, we investigated whether Pc prevented UVB-induced apoptotic cell death in human dermal fibroblasts (HDF) and human epidermal keratinocytes (HEK). Pc induced the transcription of heme oxygenase-1 (HO-1). Furthermore, Pc treatments resulted in a marked increase in nuclear factor erythroid-derived 2 (NF-E2)-like 2 (Nrf-2) nuclear translocation. Also, Pc protected UVB induced apoptosis and reduced the p53 and Bax levels, as well as caspase-3 activation. Pc treatment showed a significantly enhanced effect on the phosphorylation of protein kinase C (PKC) α/β II, but not that of p38 mitogen-activated protein kinase (MAPK) or Akt. Induction of HO-1 induced by Pc was suppressed by Go6976, a selective inhibitor of PKC α/β II. In addition, knockdown of HO-1 by small interfering (siRNA) caused a significant increase in poly (ADP-ribose) polymerase 1 (PARP-1) cleavage and caspase-3 activation after Pc pretreatment. Taken together, our results demonstrate that Pc-induced expression of HO-1 is mediated by the PKC α/β II-Nrf-2/HO-1 pathway, and inhibits UVB-induced apoptotic cell death in primary skin cells.
Highlights
Phycocyanin (Pc), a major pigment constituent of the phycobilisomes in Spirulina, has been suggested to exhibit radical scavenging properties [1], to reduce inflammatory responses [2,3], and reduce oxidative stress [1,4]
Nrf-2 protein might be phosphorylated by several signal transduction pathways, including the inhibition of Heme oxygenase-1 (HO-1) enzyme activity by the substrate antagonist protoporphyrin-tin (SnPP) was found mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K)/Akt, protein kinase C
We further explored whether Pc exerts its cytoprotective effect against UVB-induced cell death via the protein kinase C (PKC) α/β II dependent activation of the Nrf-2/HO-1 signaling pathway
Summary
Phycocyanin (Pc), a major pigment constituent of the phycobilisomes in Spirulina, has been suggested to exhibit radical scavenging properties [1], to reduce inflammatory responses [2,3], and reduce oxidative stress [1,4]. Exogenous administration of HO-1 by gene transfer protected lung cells from free radical-induced lethality and exhibited anti-inflammatory effects in the lungs [16]. It has been reported that activation of Nrf-2 and the subsequent transcription of Nrf-2-related antioxidantapoptotic proteins confers photoprotection response by inhibiting cytokines on UVB-mediated cell death has been suggested earlierpro-inflammatory in UV-irradiated mice[20]. Nrf-2 protein might be phosphorylated by several signal transduction pathways, including the inhibition of HO-1 enzyme activity by the substrate antagonist protoporphyrin-tin (SnPP) was found mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K)/Akt, protein kinase C to increase(PKC), epidermal apoptotic cell numbers and upregulation nuclear. In this study, we determined whether Pc regulates apoptotic cell death has been suggested earlier in UV-irradiated mice in which the inhibition of the Nrf-2/HO-1 activation and whether the cytoprotective effect of Pc on the UVB-induced cell death. HO-1 expression in human dermal fibroblasts (HDF) and human epidermal keratinocytes
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