RESUMEN
The relationship between the levels of renalase and changes in proteinuria,hypertension,renal function,renal tubular epithelial cell apoptosis and B-cell lymphoma-2 (Bcl-2) expression was investigated in patients (chronic nephritis,primary nephrotic syndrome or other kidney disease) that underwent renal biopsy.The study group comprised 72 patients undergoing renal biopsy.Patient profiles and renal function were collected.Concentrations of renalase and Bcl-2 were measured by immunohistochemistry.Tubular injury was detected by periodic acid Schiff staining (PAS) and renal tubular epithelial cell apoptosis was assessed by TUNEL assay.The expression of renalase was significantly lower in renal biopsy specimens than in normal kidney tissues.There was a positive linear relationship between renalase and some serum and cardiac indices;a negative correlation was found between age,eGFR,Ccr and 24-h urinary protein.Renal tubule injury index and tubular epithelial cell apoptosis index showed a negative linear correlation with renalase.The results showed that renalase probably increased the expression of Bcl-2.By two independent samples t-test,renalase levels were significantly increased in the non-hypertension group than in the hypertension group.One-way ANOVA showed that renalase expression was higher in samples with Lee's grade Ⅲ than in those with Lee's grade V.The expression of renalase was significantly decreased in patients who underwent renal biopsy,and was also associated with blood and renal function.The research proved that renalase may reduce renal tubular injury and apoptosis of renal tubular epithelial cells through the mitochondrial apoptosis pathway,finally achieving the purpose of delaying the progress of renal failure.
RESUMEN
The relationship between the levels of renalase and changes in proteinuria,hypertension,renal function,renal tubular epithelial cell apoptosis and B-cell lymphoma-2 (Bcl-2) expression was investigated in patients (chronic nephritis,primary nephrotic syndrome or other kidney disease) that underwent renal biopsy.The study group comprised 72 patients undergoing renal biopsy.Patient profiles and renal function were collected.Concentrations of renalase and Bcl-2 were measured by immunohistochemistry.Tubular injury was detected by periodic acid Schiff staining (PAS) and renal tubular epithelial cell apoptosis was assessed by TUNEL assay.The expression of renalase was significantly lower in renal biopsy specimens than in normal kidney tissues.There was a positive linear relationship between renalase and some serum and cardiac indices;a negative correlation was found between age,eGFR,Ccr and 24-h urinary protein.Renal tubule injury index and tubular epithelial cell apoptosis index showed a negative linear correlation with renalase.The results showed that renalase probably increased the expression of Bcl-2.By two independent samples t-test,renalase levels were significantly increased in the non-hypertension group than in the hypertension group.One-way ANOVA showed that renalase expression was higher in samples with Lee's grade Ⅲ than in those with Lee's grade V.The expression of renalase was significantly decreased in patients who underwent renal biopsy,and was also associated with blood and renal function.The research proved that renalase may reduce renal tubular injury and apoptosis of renal tubular epithelial cells through the mitochondrial apoptosis pathway,finally achieving the purpose of delaying the progress of renal failure.
RESUMEN
<p><b>BACKGROUND</b>An acute respiratory distress syndrome (ARDS) is still one of the major challenges in critically ill patients. This study aimed to investigate the effect of inhibiting c-Jun N-terminal kinase (JNK) on ARDS in a lipopolysaccharide (LPS)-induced ARDS rat model.</p><p><b>METHODS</b>Thirty-six rats were randomized into three groups: control, LPS, and LPS + JNK inhibitor. Rats were sacrificed 8 h after LPS treatment. The lung edema was observed by measuring the wet-to-dry weight (W/D) ratio of the lung. The severity of pulmonary inflammation was observed by measuring myeloperoxidase (MPO) activity of lung tissue. Moreover, the neutrophils in bronchoalveolar lavage fluid (BALF) were counted to observe the airway inflammation. In addition, lung collagen accumulation was quantified by Sircol Collagen Assay. At the same time, the pulmonary histologic examination was performed, and lung injury score was achieved in all three groups.</p><p><b>RESULTS</b>MPO activity in lung tissue was found increased in rats treated with LPS comparing with that in control (1.26 ± 0.15 U in LPS vs. 0.77 ± 0.27 U in control, P < 0.05). Inhibiting JNK attenuated LPS-induced MPO activity upregulation (0.52 ± 0.12 U in LPS + JNK inhibitor vs. 1.26 ± 0.15 U in LPS, P < 0.05). Neutrophils in BALF were also found to be increased with LPS treatment, and inhibiting JNK attenuated LPS-induced neutrophils increase in BALF (255.0 ± 164.4 in LPS vs. 53 (44.5-103) in control vs. 127.0 ± 44.3 in LPS + JNK inhibitor, P < 0.05). At the same time, the lung injury score showed a reduction in LPS + JNK inhibitor group comparing with that in LPS group (13.42 ± 4.82 vs. 7.00 ± 1.83, P = 0.001). However, the lung W/D ratio and the collagen in BALF did not show any differences between LPS and LPS + JNK inhibitor group.</p><p><b>CONCLUSIONS</b>Inhibiting JNK alleviated LPS-induced acute lung inflammation and had no effects on pulmonary edema and fibrosis. JNK inhibitor might be a potential therapeutic medication in ARDS, in the context of reducing lung inflammatory.</p>
