Tanshinone II A Attenuates TNF-α-Induced Expression of VCAM-1 and ICAM-1 in Endothelial Progenitor Cells by Blocking Activation of NF-κB.

Background/aims: Tanshinone IIA (Tan IIA) is effective in the treatment of inflammation and atherosclerosis. The adhesion of inflammatory cells to vascular endothelium plays important role in atherogenic processes. This study examined the effects of Tan IIA on expression of adhesion molecules in tumor necrosis factor-α (TNF-α)-induced endothelial progenitor cells (EPCs).

Ox-LDL can enhance the interaction of mice natural killer cells and dendritic cells via the CD48-2B4 pathway.

The importance of the interaction between natural killer (NK) cells and dendritic cells (DCs) in the expansion of antiviral and antitumor immune responses is well documented; however, limited information on NK/DC interaction during atherosclerosis is available. Inflammation plays an important role in the development of atherosclerosis, and oxidized low-density lipoprotein (ox-LDL) is believed to play a critical role in the development and progression of atherosclerosis. In this study, we developed a NK/DC coculture system to examine the role of ox-LDL in modulating the interaction of mice NK cells and DCs.

[Sero-epidemiologic investigation on tick-borne diseases of humans and domestic animals in Zhejiang province].

Objective: To investigate the seroprevalence of tick-borne diseases in humans and domestic animals from rural areas of Zhejiang province.

Methods: Anji county, Jindong district and Tiantai county were selected for samples collection according to their geographic locations and historical prevalence of tick-borne diseases. Blood samples of humans and domestic animals were collected in the three sites.

PPAR-gamma agonist inhibits Ang II-induced activation of dendritic cells via the MAPK and NF-kappaB pathways.

The renin-angiotensin system exerts a profound regulatory effect on the functional features of dendritic cells (DCs), thus suggesting a new target of angiotensin II (Ang II) action in the immune system. This study analyzed whether peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activation in DCs regulated Ang II-induced activation of DCs and exploited the possible molecular mechanisms, especially focused on the signaling pathways of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappaB). Ang II stimulation of human monocyte-derived DCs resulted in an intermediate state of DC maturation and function via modulating the balance of the negative or positive regulation of the signaling pathways of extracellular regulated kinase (ERK), p38 MAPK and NF-kappaB, but not c-Jun N-terminal kinase (JNK).