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 of local administration of silver nanoparticles for the treatment of pyogenic spondylitis].

OBJECTIVE: To establish a proper animal model of pyogenic spondylitis, to evaluate the efficacy of silver nanoparticles for treatment of spinal pyogenic infections, and to explore the distribution of the particles in the body of the animals. METHODS: Staphylococcus aureus was inoculated into intervertebral discs of rabbits to establish a spinal pyogenic infection model. These rabbits were divided into Group A [0.1 mg/(kg.d)], Group B [1 mg/(kg.d)], and a Control group. Groups A and B were injected with different doses of silver nanoparticles solution daily at locally infected side. Two weeks later, bacterial cultures, radiographic outcomes, histopathology were analyzed. Atomic absorption spectrometry was utilized to measure silver contents in some vital organs of the rabbits to detect the distribution and accumulation of silver particles. RESULTS: Staphylococcus aureus (100 CFU/mL), induced 100% pyogenic spondylitis. 1 mg/kg dose of silver nanoparticles solution could effectively inhibit the occurrence of spinal pyogenic infection with the effective rate of 75%. While the effect of 0.1 mg/kg dose of silver nanoparticles solution was less obvious, the efficiency was only 25%. Significant numbers of silver nanoparticles were observed to accumulate in the animal. In the 1 mg/kg group silver was deposited mainly in the spinal cord, liver, kidneys, spleen, and testicles, while in the 0.1 mg/kg group it accumulated only in the spinal cord. CONCLUSION: Local administration of silver nanoparticles can effectively prevent and treat pyogenic spondylitis; the particles accumulate in the body commensurate with the administered drug concentration.

[Surgical management of vertebral sarcoidosis].

OBJECTIVE: To investigate the clinical characteristics, diagnostic foundation and treatment of vertebral sarcoidosis. METHODS: The clinical data of 13 patients with vertebral sarcoidosis who received anterior debridement and instrumentation were retrospectively analyzed. RESULTS: The onset of progressive pain in the pathological region was common in the 13 patients. Neurologic deficit existed in 4 cases. Radiographic study showed multiple vertebral bone destructions, and no other systemic lesions were found. Surgical indications were progressive vertebral destruction, spinal instability or neurological deficit. Anterior vertebra resection, and autologous bone grafts fusion with internal fixation were done. No operative mortality and major complications occurred. Diagnosis was confirmed in all patients by pathological exam. After the surgery, metacortandracin treatment was given routinely for 1 year. Patients were followed up for 12-52 (median 26) months, and pain and neurological symptoms were alleviated. Visual analog scale (VAS) score was 7-10 (median 8) points preoperatively, which dropped to 0-4 (median 2) points postoperatively. All patients showed successful bone fusion with no recurrence. CONCLUSION: For vertebral sarcoidosis associated with progressive instability and/or neurological symptoms, surgical intervention combined with steroid therapy is safe and effective.