Psoriasis is an autoimmune skin disease in which dendritic cells (DCs) trigger the progression of psoriasis by complex interactions with keratinocytes and other immune cells. In the present study, we aimed to load celastrol, an anti-inflammatory ingredient isolated from Chinese herbs, on mannosylated liposomes to enhance DC uptake as well as to induce DC tolerance in an imiquimod-induced psoriasis-like mouse model. Mannose was grafted onto liposomes to target mannose receptors on DCs. The results demonstrated that compared with unmodified liposomes, DCs preferred to take up more fluorescence-labeled mannosylated liposomes. After loading celastrol into mannose-modified liposomes, they effectively inhibited the expression of maturation markers, including CD80, CD86 and MHC-II, on DCs both in vitro and in vivo. Additionally, after intradermal injection with a microneedle, celastrol-loaded mannose-modified liposomes (CEL-MAN-LPs) achieved a superior therapeutic effect compared with free drug and celastrol-loaded unmodified liposomes in the psoriasis mouse model in terms of the psoriasis area and severity index, histology evaluation, spleen weight, and expression of inflammatory cytokines. In conclusion, our results clearly revealed that CEL-MAN-LPs was an effective formulation for psoriasis treatment and suggested that this treatment has the potential to be applied to other inflammatory diseases triggered by activated DCs.

Psoriasis is an autoimmune inflammatory disease, where dendritic cells (DCs) play an important role in its pathogenesis. In our previous work, we have demonstrated that topical delivery of curcumin-loaded poly (lactic-

In order to explore the effect of extract (SNE) on skin wound healing in mice and its mechanism, hemostasis effect of SNE was measured, the mouse skin wound model was established by full-thickness excision. The morphological changes of the wound were observed after the treatment with SNE and the healing rate was measured. The changes of wound histology were observed by hematoxylin eosin (HE) staining, Masson staining and transmission electron microscope (TEM). The expression of cell factors and related proteins was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Results showed that the SNE possessed hemostatic function. SNE could obviously improve the healing rate of wound in mouse and shorten time of scab removal compared with the none-treatment (NT) group ( < 0.05).The pathological histology analysis results showed complete epidermal regeneration, with remarkable capillary and collagen fiber observed in the SNE group. The expression level of tumor necrosis factor-α (TNF -α), interleukin-1β (IL-1β) and transforming growth factor-β1 (TGF-β1) in SNE group was significantly lower than that of the NT group on 7 d ( < 0.05). Moreover, compared with the NT group, the gene expressions level of Smad7 was significantly increased and the level of type II TGF-β receptors (TGF-βRII), collagen I (COL1A1) and α-smooth muscle actin (α-SMA) were significantly reduced in the SNE group on 28 d ( < 0.05), but the difference was not statistically significant compared to Yunnanbaiyao group (PC group) ( > 0.05). These results indicated that SNE possessed obvious activity of accelerating wound healing and inhibiting scar formation, and its mechanism was closely related to hemostatic function, regulation of inflammatory factors, collagen deposition, collagen fiber remodeling and intervening TGF-β/Smads signal pathway. Therefore, SNE may have promising clinical applications in skin wound repair and scar inhibition.

Objective To investigate the relationship between the expressions of VEGF,ENS, MVD and arteriosclerosis (AS) plaque in atherosclerosis obliterans (ASO) patients. Methods Immunohistochemical staining was used to determine the expression of VEGF, ENS and MVD value in the atherosclerosis plaque of ASO patients hospitalized from October 2007 to August 2010 in our hospital (n =30),and the femoral arterials of control were collected from 22 amputation after traumatic injury. Results The expressions of VEGF (2. 24 ±0.31 vs. 1.87 ±0.27,t =3.58),ENS (1.84 ±0.41 vs. 1. 56 ±0. 38, t =2.09) and MVD value (8.79 ±2.46 slip/HP vs. 6. 05 ±1.68 slip/HP, t =3.64) were significantly higher in the AS plaque of ASO patient than control (P <0.01 or P < 0. 05). We found positive correlations between the expression of VEGF, VEGF/ENS with MVD (r = 0. 391, P < 0. 01; r =0. 583, P < 0. 05) , while negative correlation between the expression of ENS with MVD (r=-0. 328,P <0. 05). Conclusion VEGF promotes the angiogenesis in atherosclerosis plaque,while ENS shows opposite effect The comprehensive performance of them is promoting angiogenesis.