Cardiovascular remodeling or dysfunction-induced abnormal cardiac output,blood volume and peripheral vascular resistance is an important pathophysiological mechanism for the occurrence and development of hypertension.Cathepsins are widely expressed in human various tissue and cells and they are involved in the pathogenesis of hypertension through activation of renin-angiotensin system,degradation of cytoplasmic matrix,proliferation of smooth muscle cell and hypertrophy of myocyte.The clinical studies have found that cathepsins can be used as a biomarker for hypertension.In recent years,the studies on the functions and mechanisms of cathepsins have provided a new sight and strategy for treatment of hypertension.

Objective:To explore the effect of interleukin-1α (IL-1 α) on the senescence of human umbilical vein endothelial cells (HUVECs) and the function of high mobility group protein 1 (HMGB 1).Methods:HUVECs were randomly divided into a control group,a IL-1α group (10 ng/mL IL-1α),a HMGB 1 group (100 ng/mL HMGB 1),and a HMGB 1 +IL-1α group (100 ng/mL of HMGB 1 plus 10 ng/mL of IL-lα).Senescence associated β-galactosidase (SA β-gal) staining was used to assess the number of senescent cells,Western blot were performed to detect the protein levels of silent information regulator 1(SIRT1),and quantitative real-time PCR (qRT-PCR) was used to detect the mRNA levels of p53,p21 and p 16.Restlts:Compared with the control group,the number of SA β-gal positive cells were significantly increased in the IL-1α group (P＜0.05),while the expression of SIRT1 protein significantly decreased (P＜0.01).Compared with the IL-1 α group,the expression of SA β-gal positive cells in the HMGB 1+IL-1α group was decreased and the mRNA levels of p21 and p53 were down-regulated (all P＜0.05),however,there was no statistical significance in the mRNA expression ofp16 (P＞0.05).Conclusion:IL-1α can induce the senescence of HUVECs,and HMGB1 may inhibit IL-1α-induced endothelial cell senescence via p53-p21 pathway.