Preparation and anti-inflammatory effect of mercury sulphide nanoparticle-loaded hydrogels.

We successfully prepared mercury sulphide nanoparticle hydrogels by physical encapsulation method. The successfully prepared mercuric sulphide nanoparticle hydrogel was a zinc folate hydrogel, which showed an obvious porous structure with interconnected and uniformly distributed pores and a pore size range of about 20 µm. The maximum drug loading of the hydrogels was 3%, and the in vitro cumulative release degree was in accordance with the first-order kinetic equation Mt = 149.529 (1 - e-0.026t). The particles in mercuric sulphide nanoparticle hydrogels significantly down-regulated the expression of the cell surface co-stimulatory molecule CD86 (p < .0001). Meanwhile, the inflammatory response was regulated through the NF-κB pathway in LPS-induced inflammatory cells. Later, it was observed that mercuric sulphide nanoparticle hydrogels could significantly counteract the inflammatory and immune models through a mouse ear swelling model, a rat foot-plantar swelling model and a rheumatoid arthritis model. This design targets the immunomodulatory, and anti-inflammatory effects through nanocomposite hydrogel technology. It reduces the drawbacks of low mercury utilisation and susceptibility to accumulation of toxicity. It aims to provide an experimental basis for the development of mercuric sulphide and the treatment of inflammatory and immune-related diseases.HighlightsMercury sulphide nanoparticle hydrogel has an optimal mercury sulphide nanoparticle content of 2%, is structurally homogeneous and stable, and does not exhibit significant liver or kidney toxicity.Mercuric sulphide nanoparticle hydrogel exerts anti-inflammatory effects in cells and rats, and regulates the expression of macrophage surface molecules and factors related to the NF-κB pathway.Mercuric sulphide nanoparticle hydrogel improves the condition of ankle synovial joints in a rat model of rheumatoid arthritis.

COP1 is downregulated in renal cell carcinoma (RCC) and inhibits the migration of RCC ACHN cells in vitro.

Constitutive photomorphogenic 1 (COP1) belongs to the COP­de-etiolated (DET)­fusca (FUS) protein family and has been demonstrated to suppress prostate adenocarcinomas and other types of tumor, such as liver and gastric cancer. The present study investigated the expression of COP1 and its downstream factor, ets variant 1 (ETV1) in renal cell carcinoma (RCC) tissue samples, and evaluated the correlation of COP1 expression levels with the clinicopathological characteristics of RCC. In addition, the role of COP1 in the proliferation and migration of RCC ACHN cells was investigated. The results demonstrated significantly downregulated COP1 expression levels in the RCC intratumors, which was negatively associated with clinicopathological characteristics, such as tumor size, tumor­node­metastasis (TNM) stage and lymph node or distant metastasis. COP1 was demonstrated to markedly reduce the colony size of RCC ACHN cells, and inhibit the migration and invasion of ACHN cells. In addition, ETV1 and matrix metalloproteinase 7 (MMP7) mRNA and protein expression levels were significantly downregulated by the overexpressed COP1. Thus, the results of the present study demonstrate the reduced expression of COP1 and the upregulated expression of ETV1 in RCC tissue samples, which was associated with a high tumor-node-metastasis stage of RCC. Furthermore, the overexpression of COP1 in the RCC ACHN cells inhibited the migration and invasion of ACHN cells, and downregulated ETV1 and MMP7 expression levels. The present study demonstrated the tumor suppressive role of COP1 in RCC by inhibiting cell migration.

[Chemoattractive effects of chemokine-like factor 1 on human arterial smooth muscle cells].

OBJECTIVE: To investigate the chemotactic effect of chemokine-like factor 1 (CKLF1) on human arterial smooth muscle cells (ASMCs). METHODS: The recombinant eukaryotic expression vectors pEGFP-N1-CKLF1 (test group) and pEGFP-N1 (control group) were transiently transfected into 293T cells. The supernatants were harvested 72 h after transfection for bioactivity study. The chemotactic effect of CKLF1 on ASMCs were assayed by cellular chemotactic experiments. RESULTS: ASMCs number migrated from the test and control groups diluted by none and 10-fold supernatants had statistical significance (114+/-4 vs 41+/-4, P<0.05; 74+/-4 vs 34+/-3, P<0.01), but have no statistical significance (28+/-4 vs 25+/-5, P>0.05; 26+/-5 vs 23+/-5, P>0.05) between the two groups diluted by 100-fold and 1 000-fold supernatants. When ASMCs were treated at different concentrations of 0 and 2 microg/L of pertussis toxin (PTX), the cell number migrated from the test and control groups diluted by 10-fold supernatants, they had statistical significance (74+/-4 vs 34+/-3, P<0.01; 45+/-3 vs 34+/-3, P<0.01). And when ASMCs were treated at 10 microg/L of PTX, the cell number migrated from both groups diluted by 10-fold supernatants, they had no statistical significance (37+/-4 vs 34+/-3, P>0.05). CONCLUSION: CKLF1 has significant chemotactic effects on ASMCs and such a CKLF1-induced chemotaxis could be inhibited by PTX at concentration of 10 microg/L.