Significantly higher than that in normal controls, suggesting in response to intestinal mucosa membrane damage. Recently, HSF1 has been shown to inhibit the expression of proinflammatory cytokines such as TNF-a and IL-1b by regulating the expression of the HSP, and suppressing key transcription Tubuloside-A factors of inflammatory signaling pathways, such as NF-kB and AP-1. The current data showed that serum concentrations of HSF2 were positively correlated with two proinflammatory factors, TNF-a and IL-1b. After down-regulation expression of HSF2 in Caco-2 cells by RNA interference, the secretions of these two cytokines stimulated by LPS increased dramatically, while enhanced expression of HSF2 by plasmid transfection resulted in significantly decresased production, suggesting that HSF2 might directly or indirectly affect inflammation-related transcription factors and down-regulates inflammatory cytokines to overcome inflammation. It is important to understand the pathogenesis of UC and identify specific biomarkers and biological therapeutic targets. Our results showed that HSF2 was over expressed in UC, and the increases paralleled the severity of disease. This suggests that HSF2 might be an endogenous protective factor against UC. This study will enable HSF2 as a potential novel molecular marker for UC and provide the basis for novel biological therapeutic targets. It has been reported that aging greatly affects vessel tone and arterial stiffness, causing the onset of vascular-related diseases such as hypertension, diabetes mellitus and atherosclerosis, by arterial dysfunction of receptors, ion channels, and signal transduction pathways. In addition, we demonstrated for the first time that aortic VDCC expression in aged rats was much lower than that in young rats, irrespective of the Campesterol presence of hypertension. The finding that VDCC blockers lost their relaxation activity in 40-week rats also suggests that their usefulness as therapeutic treatments in aged patients may be limited and needs to be evaluated. So far, some researchers have investigated the effect of age on vascular function from the view-points of prevention or treatment of cardiovascular and cerebral vascular disorders. Van der Loo et al. reported that aging promoted peroxynitrite formation by increased superoxide anion formation in the vascular endothelium in F344/BN F1 rats, and speculated on the importance of suppression of oxidative stress for age-related vascular dysfunction. Factors affecting age-related endothelial dysfunction were also reported to involve ATPases and NADPH oxidases. Owing to these findings, some preventive studies against ageinduced vascular dysfunction have been performed to improve endothelium-dependent vascular relaxation by antioxidant compounds, e.g., thymoquinone, red wine polyphenols, and vitamin C. Research interests in age-related vascular dysfunction have begun to investigate the change in the physiological vascular response in the muscle layer, since vasomotor activity is regulated by MLC phosphorylation through in part AT1R stimulation. It is well known that the blockade of AT1R by AT1R antagonistic drugs is the most effective target for therapeutics for hypertension.