peoniflorin and Psoriasis

Psoriasis is a common chronic relapsing immune-mediated inflammatory disease, the prevalence of which has increased in recent years. At present, there are many treatment methods available for the condition, but the curative effect is unsatisfactory.. This study aimed to evaluate the efficacy, adverse reactions, and recurrence rates of using paeoniflorin capsules for psoriasis treatment.. systematic review and meta-analysis.. Randomized controlled trials comparing total glycosides of paeony (TGP) with other treatments for patients with psoriasis were retrieved by searching EMBASE, MEDLINE, and the Cochrane Central Register of Controlled Trials electronic databases. Cochrane bias risk tool was used to evaluate the quality of randomized controlled trial (RCT) methodology. The primary outcome measure is the effective number. Secondary outcomes included psoriasis area and severity index (PASI), adverse reactions, recurrence, and inflammatory biomarkers.. In all, 30 RCTs with 2,802 participants were included in this meta-analysis. The studies were generally of low methodological quality. Although there was no statistically significant difference between the use of TGP capsule alone and other monotherapies in the treatment of psoriasis (RR: 0.93; 95% CI: 0.76-1.15; p = 0.50), the addition of TGP to other therapies had an advantage over monotherapy with regard to the effective number (RR: 1.31; 95% CI: 1.26-1.37; p < 0.00001), PASI (RR: -3.40; 95% CI: -4.22,-2.57; p < 0.00001), adverse reactions, recurrence rate (RR: 0.42; 95% CI: 0.24-0.74; p = 0.002), and inflammatory inhibition (RR:-12.54; 95% CI: -18.50, -6.59; p < 0.0001).. TGP can be used to treat psoriasis with reduced adverse reactions and recurrence rates. However, the mechanism of TGP in psoriasis treatment requires to be evaluated further in high-quality, large-sample, and rigorous clinical studies.

Topics: Dermatologic Agents; Glucosides; Glycosides; Humans; Monoterpenes; Paeonia; Psoriasis; Randomized Controlled Trials as Topic

To investigate the mechanism underlying the effect of paeoniflorin (PF) on the proliferation and migration of psoriatic keratinocytes. The expressions of long noncoding RNA NEAT1, miR-3194-5p and Galectin-7 in skin tissues from psoriatic patients and healthy controls were detected. Psoriatic HaCat cells were used to investigate the function of NEAT1 and Galectin-7 as well as the effect and mechanism of PF in psoriasis. MTT, colony formation and scratch assays were used to assess the proliferation and migration of psoriatic HaCat cells. Dual-luciferase reporter assay was used to validate the interactions among NEAT1, miR-3194-5p and Galectin-7. NEAT1 and Galectin-7 were lowly expressed and miR-3194-5p was highly expressed in psoriatic patients. PF suppressed the proliferation and migration of psoriatic HaCat cells by elevating the expressions of NEAT1 and Galectin-7. NEAT1 positively mediated the expression of Galectin-7 by targeting miR-3194-5p. PF controls the proliferation and migration of psoriatic HaCat cells via the NEAT1/miR-3194-5p/Galectin-7 axis.

Topics: Apoptosis; Cell Movement; Cell Proliferation; Galectins; Glucosides; HaCaT Cells; HEK293 Cells; Humans; Keratinocytes; MicroRNAs; Monoterpenes; Psoriasis; RNA, Long Noncoding; Signal Transduction; Up-Regulation

Psoriasis is a common inflammatory skin disease characterized by hyperproliferation of epidermal keratinocytes, however, there is still no curative therapy for psoriasis. Paeoniflorin (PF), a Chinese herbal medicine, has shown anti-inflammatory effects.. We aimed to illustrate the effect and associated mechanism of PF on keratinocyte proliferation using the IMQ-induced psoriasis mouse model.. The anti-psoriatic effect of PF in vivo and in vitro was assessed by western blot, RT-PCR, immunofluorescence, cell counting kit-8 and haematoxylin/eosin staining.. In vivo, epidermal thickness, dermal infiltrated lymphocytes and the level of several antimicrobial peptides, pro-inflammatory cytokines, and K17 were significantly reduced in mice with topical application of PF. In vitro, PF inhibited the proliferation of HaCaT cells in a dose-dependent manner, down-regulated K17 expression, and suppressed NF-kappaB activation.. Our findings indicate that PF may inhibit the proliferation of keratinocytes by targeting K17, suggesting that PF might be a potential target in the treatment of psoriasis.

Topics: Administration, Cutaneous; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Proliferation; Cytokines; Down-Regulation; Female; Glucosides; HaCaT Cells; Humans; Imiquimod; Keratin-17; Keratinocytes; Keratins; Mice; Monoterpenes; NF-kappa B; Psoriasis; Signal Transduction

The total glucosides of paeony (TGP) are used to treat psoriasis in the clinic. However, its active components and mechanisms are not clear. Paeoniflorin is the main constituent of TGP. Thus, the anti-psoriasis effect of paeoniflorin was studied, and its mechanism was explored.. The effect of paeoniflorin was evaluated using a psoriasis-like model of guinea pigs. The levels of IL-6, IL-17A, IL-22, p38 MAPK, and ERK1/2 in HaCaT cells stimulated by lipopolysaccharide (LPS) were determined using RT-qPCR, enzyme linked immunosorbent assays (ELISAs) and western blot.. Compared with the control group, the model group showed edema, redness, and lesions in the ear upon stimulation with propranolol hydrochloride, and the Baker Score increased by 7-fold. Paeoniflorin ameliorated the lesion and decreased the Baker Score by 37% (p<0.05). In vitro, paeoniflorin significantly inhibited the mRNA expression of IL-6, IL-17A and IL-22 at both 2.08 and 10.41μM (p<0.01), and paeoniflorin had a marginal effect on the protein expression of IL-17A and IL-6. However, it inhibited the protein expression of IL-22 significantly, with inhibition ratios of 48.5% and 47.8% at 2.08 and 10.41μM, respectively (p<0.05). This effect was achieved by inhibiting the phosphorylation of p38 MAPK.. The results of this work demonstrated that paeoniflorin is the active components of TGP and support its use as a therapeutic compound for psoriasis therapy.

Topics: Animals; Blotting, Western; Cell Line; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Gene Expression Regulation; Glucosides; Guinea Pigs; Humans; Interleukin-22; Interleukins; Lipopolysaccharides; Male; Monoterpenes; p38 Mitogen-Activated Protein Kinases; Paeonia; Phosphorylation; Propranolol; Psoriasis; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger

Paeoniflorin (PF) is the main active ingredients of radix paeoniae rubra and radix paeoniae alba, which are used widely in Traditional Chinese Medicine. This study aimed to assess the capacity of PF to inhibit imiquimod (IMQ)-induced psoriasis. Mice treated with IMQ were divided into four groups and administered 240mg/kg/day or 120mg/kg/day of PF, 1mg/kg/day of methotrexate (MTX), or normal saline intragastrically. Weight-matched mice treated with vaseline were used as controls. Morphology, structural features, keratinocyte proliferation and differentiation, inflammatory cell infiltration, levels of Th1/Th2/Th17/Treg cytokine mRNA, and phosphorylation of Th17 differentiation-related proteins were assessed. Mouse spleen cells were incubated under Th17 polarizing conditions, then with PF (2, 20, and 200μg/ml) and cell viability, Th17 differentiation, and Th17 cytokines and the orphan nuclear receptor (RORγt) mRNA levels were assessed. PF alleviated IMQ-induced keratinocyte proliferation and inflammatory cell infiltration, and reduced mRNA levels of Th17 cytokines at day 4 and phosphorylation of Th17 differentiation-related proteins. However, 2, 20, or 200μg/ml PF did not affect spleen cell viability, and 2 and 20μg/ml PF reduced IL-17 secretion under Th17 polarizing conditions. Finally, 2 and 20μg/ml PF inhibited mRNA expression of Th17 cytokines and phosphorylation of Stat3 in spleen cells under Th17 polarizing conditions. These results suggest that PF inhibits IMQ-induced psoriasis by regulating Th17 cell response and cytokine secretion via phosphorylation of Stat3.

Topics: Aminoquinolines; Animals; Cell Differentiation; Cell Proliferation; Cell Survival; Cytokines; Gene Expression Regulation; Glucosides; Imiquimod; Keratinocytes; Mice; Monoterpenes; Nuclear Receptor Subfamily 1, Group F, Member 3; Phosphorylation; Psoriasis; RNA, Messenger; Skin; STAT3 Transcription Factor; Th17 Cells

Psoriasis is one of the most common immune-mediated chronic inflammatory skin disorders, characterized by hyperproliferation of keratinocytes, dilation and growth of dermal capillary vasculature, and cellular infiltration of T cells, dendritic cells (DCs), and neutrophils. Paeoniflorin (PF), the principal component of total glucosides of paeony (TGP), displays anti-inflammatory and antioxidant properties in several animal models. In this study, we investigated the anti-inflammatory effects and mechanisms of PF in imiquimod (IMQ)-induced psoriasis-like mouse model. The effects of PF on inflammatory cytokine expression in peripheral blood mononuclear cells (PBMCs) from patients with psoriasis vulgaris were also observed. Our results indicated that PF effectively attenuated the clinical and histopathologic changes in IMQ-induced psoriasis-like mouse model. Furthermore, PF reduced the infiltration of T cells, CD11c(+)DCs, and neutrophils in lesional skin. In addition, PF also significantly decreased the mRNA expression of inflammatory cytokines, such as IL-17, INF-γ, IL-6, and TNF-α, in IMQ-induced psoriasis-like mouse model and PBMCs from patients with psoriasis vulgaris. Hence, our data suggest that PF can inhibit leukocyte infiltration and decrease the expression of inflammatory cytokines such as IL-17, INF-γ, IL-6, and TNF-α. PF might be a candidate drug for the treatment of psoriasis.

Topics: Aminoquinolines; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cells, Cultured; Glucosides; Humans; Imiquimod; Inflammation Mediators; Leukocytes, Mononuclear; Male; Mice; Mice, Inbred BALB C; Monoterpenes; Psoriasis; Random Allocation

Psoriasis is a common chronic immune-mediated inflammatory disease. It is well known that macrophages, neutrophils and T-helper 1 (Th1)/T-helper 17 (Th17) cells play important roles in skin lesions by provoking inflammation. Paeoniflorin (PF) is the major effective component extracted from the root of Paeonia lactiflora, which has been widely used in China to treat inflammatory and autoimmune diseases, including psoriasis. Although PF shows a clinical therapeutic effect on psoriasis patients, how PF affects infiltrated immune cells in psoriasis skin lesions is still unknown. In this study, using a generated imiquimod (IMQ)-induced psoriasis-like mouse model, we found that PF ameliorates inflammation and skin lesions. Subsequent analyses showed that PF decreases the number of F4/80(+)CD68(+) macrophages and their related cytokine production (TNF-α, IL-1β, IL-6, IL-12 and inducible nitric oxide synthase (iNOS)) in the skin of IMQ-challenged mice. Moreover, PF suppresses the number of CD11b(+)Gr-1(+) neutrophils and the expression of macrophage inflammatory protein-2 (MIP-2; a counterpart of human IL-8, which is responsible for the recruitment of neutrophils in mice). Finally, PF also down-regulates Th1- and Th17-related cytokine expression. Therefore, our new findings reveal that PF alleviates psoriatic skin lesions by inhibiting inflammation, which provides new insights into the immunomodulatory effect of PF in psoriasis treatment.

Topics: Aminoquinolines; Animals; Anti-Inflammatory Agents; Cytokines; Female; Glucosides; Imiquimod; Macrophages; Mice, Inbred BALB C; Monoterpenes; Neutrophils; Psoriasis; Skin