P. granatum Peel Polysaccharides Ameliorate Imiquimod-Induced Psoriasis-Like Dermatitis in Mice via Suppression of NF-κB and STAT3 Pathways

Abstract

Psoriasis is a chronic and refractory inflammatory and autoimmune-mediated cutaneous disease affecting approximately 2%–3% of the global population. Most of the current therapies could relieve symptoms rapidly, while the side effects cannot be negligible. Hence, it is urgent to explore much safer and more effective treatments. In the current work, we evaluated the potential beneficial effect of Punica granatum peel polysaccharides (PPPs) in an imiquimod-elicited psoriasis-like mouse model and unraveled their mechanism of action. Firstly, PPPs were isolated from P. granatum peels, and then the molecular weight was determined and monosaccharide analysis was performed. The results revealed that PPPs significantly ameliorated psoriasis-like skin lesions and reduced the Psoriasis Area and Severity Index (PASI) scores and transepidermal water loss (TEWL). PPPs also attenuated the expressions of CD3 and Ki67 in psoriasis-like mouse skin and suppressed the serum or skin levels of pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), IL-1β, IL-8, IL-17, and IL-23. Moreover, PPPs were able to upregulate the mRNA and protein expressions of aquaporin-3 (AQP3) and filaggrin (FLG) in the skin of mice. In addition, PPPs inhibited the NF-κB and STAT3 signaling pathways. Overall, these results indicated that PPPs ameliorated the symptoms of psoriasis through inhibition of the inflammatory cytokines by suppressing the NF-κB and STAT3 signaling pathways and improved skin barrier protection via enhancing AQP3 and FLG. These observations potentially contribute to providing theoretical and experimental evidence for the clinical application of PPPs for psoriasis.

Oral Intake of Linseed Oil Inhibits Skin Barrier Dysfunction in Obese Mice

“…Therefore, we hypothesize that linseed oil enhanced skin barrier function in obese mice by another factor. In addition, the epidermal thickening and proliferation of Ki-67 positive cells observed in the Control group are consistent with an earlier study, which showed increased Tnfα levels [16], as well as skin barrier dysfunction, in inflamed skin. Furthermore, skin inflammation in the context of obesity is also associated with increased Tnfα expression [25].…”

Enhancement of Human Epidermal Cell Defense against UVB Damage by Fermentation of Passiflora edulis Sims Peel with Saccharomyces cerevisiae

“…Excessive UVB irradiation can cause the excessive secretion and up-regulation of inflammatory signalling factors such as TNF-α, IL-1β and IL-8 in keratinocytes [ 15 ], leading to skin inflammation, which in turn affects the normal function of the skin barrier, leading to skin homeostasis imbalance, dry and red appearance, and desquamation [ 16 , 17 ]. In the epidermis, KLK-7 [ 38 ], FLG, caspase 14 [ 39 ] and AQP3 [ 40 ] are proteins closely related to the skin barrier that can help the keratinocytes maintain good skin barrier function. The abnormal activation of KLK-7 affects the barrier function of the stratum corneum [ 28 ].…”

Oral exposure to citrinin significantly exacerbates the pathophysiology of a mouse model of imiquimod‐induced psoriasis via direct activation of dendritic cell

“…Corresponding results were seen in the pathological evaluation, revealing that epidermal thickness was significantly increased by citrinin administration. Psoriasis is characterized as excessive inflammatory cytokine production and destruction of the skin barrier function (Chen et al, 2021). As the present study focused on the early development of psoriasis, TEWL as a barometer of skin barrier function was not so enhanced only by the imiquimod treatment, whereas citrinin exposure significantly enhanced the TEWL compared with the vehicle treatment.…”