Atrial natriuretic peptide protects vertebral endplate chondrocytes against H2O2­induced apoptosis and oxidative stress through activation of the Nrf2/HO­1 signaling pathway.

The present study aimed to investigate the effect of atrial natriuretic peptide (ANP) on cell apoptosis and oxidative stress in H2O2­induced vertebral endplate chondrocytes (EPCs), and to assess the associated mechanisms involved. Cell viability and apoptosis were evaluated using the Cell Counting Kit­8 method and TUNEL assay, respectively. In addition, the scavenging capability was detected using various enzymatic assays, and the quantity of nitric oxide (NO) and malondialdehyde (MDA), and activity of superoxide dismutase (SOD) were assessed. The expression levels of apoptosis­related proteins, activation of the nuclear factor erythroid 2­related factor 2 (Nrf2)/heme oxygenase­1 (HO­1) signaling pathway induced by H2O2 and the effect of treatment with ANP on vertebral EPCs were detected by western blotting. The results revealed that ANP protected EPCs from H2O2­induced cell damage. H2O2­induced intracellular MDA was decreased by ANP, and the levels of SOD and NO were increased in the presence of ANP. ANP also inhibited the H2O2­induced alterations in the expression levels of cleaved­caspase­3, Bax and Bcl­2. Finally, ANP blocked H2O2­induced oxidative stress through activating the Nrf2/HO­1 signaling pathway. These findings suggested that ANP may effectively protect EPCs through inhibition of H2O2­induced oxidant injury and cell death by activating the Nrf2/HO­1 signaling pathway.

Experimental study on the repair of ureteral functional regeneration with highly bioactive extracellular matrix stent.

BACKGROUND: The research of extracellular matrix stent (ECM) has made some progress in the repair of urethra and bladder defects. OBJECTIVES: To observe the effects of highly bioactive ECM scaffold on the regeneration and repair of defects in long-segment ureteral replacement. MATERIAL AND METHODS: An animal model of long-segment ureteral defect was established and four-layer tubular highly bioactive ECM materials were prepared. After the ureteral defect was repaired through surgery, the rabbits in the negative control group were administered a non-bioactive stent, and rabbits in the observation group were treated with an ECM stent. RESULTS: Comparison of macro-indicators: The negative control group had a higher infection rate, a lower survival rate and more complications than the observation group (p < 0.05). The frequency of ureteral peristalsis in the negative control group was lower than in the observation group. In addition, the rate of urinary dysfunction was higher, and the ratio of ureteral diameter was lower in the negative control group than in the observation group (all p < 0.05). Comparison of histopathology: Three months after the operation, the vascular, smooth muscle and mucous membrane of the ureter in the observation group regenerated to close to normal ureteral tissue. There was no significant difference between the ureter regeneration in the repair area and the normal ureter tissue in the observation group 3 months after the operation. The number of regenerated muscle fibers in the observation group was significantly higher than that of the negative control group. Compared with the negative control group, the fibrous capsule was thicker, the percentages of CD31, CD3, CD68, CD80+, and CD163+ were higher, the scope of new smooth muscle fiber was expanded, fusion with the host muscle fibers was higher, and the neuromuscular junction (NMJ) structure was stronger in the observation group (all p < 0.05). CONCLUSIONS: A highly bioactive ECM stent can better regenerate the local anatomical structure and physiological function.