Anti-ICAM1 monoclonal antibody, clone NFN-222

Objective: Endothelial cellular senescence is an important contributor to the endothelial dysfunction and atherosclerosis. Our previous studies suggested that salidroside (SAL) can alleviate atherosclerosis and protect endothelial cells against oxidative stress induced damage. However, the effect and mechanism of SAL on endothelial cellular senescence is still unclear. Here, we investigated the underlying mechanisms of SAL on preventing endothelial cellular premature senescence. Methods and results: We established a hyperhomocysteinemia (HHcy)mouse model via high methionine diet (HMD) to explore the protective effect of SAL. According to our results, the HMD elevated the concentration of serum homocysteine. HHcy induced the collagen deposition and the up-regulation of senescence markers, i.e. p16(INK4A) and p21(CIP1), in intima-medial of aorta. In addition, SAL also inhibited the expression of CD68 and intercellular adhesion molecule 1 (ICAM1) in aorta. In senescent human umbilical vein endothelial cells (HUVECs) induced by H2O2, SAL treatment alleviated the expression of p16(INK4A) and p21(CI)(P1) and reduced the activity of senescence-associated (SA)-beta-gal. Conclusion: our data suggested that SAL decreased the expression of inflammatory cytokines and up-regulated the expression of SIRT3, which might be the underlying mechanism of SAL on preventing endothelial cells from premature senescence.

Chronic obstructive pulmonary disease (COPD) is a multifactorial chronic inflammatory disease of the respiratory system. A key phenomenon of COPD pathogenesis is inflammation. The goal of the present study was to investigate the association of COPD with alleles and genotypes of the genes that encode chemokines and chemokine receptors (CCL11, CX3CR1, CCR5, CCL5, CXCL12, CCL2, and CCL17), adhesion molecules (PECAM1 and ICAM1), and serum amyloid A1 (SAA1). It was found that COPD was associated with the C allele and the TC genotype of SAA1 (rs1136743C>T) (P = 0.0001, OR = 1.58 and P = 0.00001, OR = 2.15, respectively); this association was confirmed in the subgroups differentiated by smoking status. Markers of COPD risk were also the CG genotype of PECAM1 (rs281865545G>C) (P = 0.028, OR = 1.36) and the GG genotype of ICAM1 (rs5498A>G), which were significantly associated with the disease in smokers (P = 0.005, OR = 1.66). The AA genotype of CCL2 (rs1024611A>G) was associated with the disease in nonsmokers (P = 0.037, OR = 1.82). The GG genotype of PECAM1 (rs281865545G>C) and the AA genotype of CX3CR1 (rs3732378A>G) were associated with higher vital capacity (P = 0.014 and P = 0.04, respectively). Subjects with the GG genotype of ICAM1 (rs5498A>G) exhibited lower forced expiration volume in 1 s and lower forced vital capacity (P = 0.025 and P = 0.029, respectively).