title: Shock wave induces biological renal damage by activating excessive inflammatory responses in rat model.
abstract: The study was aimed to investigate the potential mechanism of inflammatory renal damage induced by shock wave. A total of 48 rats, with the right kidney cut, are randomly assigned into control group, ESWL group and ESWL + PDTC group. Rats were treated with shock wave at the left kidney. At post-shock wave 3 and 105 days, all the animals were sacrificed for detecting the expression of tumor necrosis factor (TNF)-α, intercellular adhesion molecule (ICAM)-1, and monocyte chemoattractant protein (MCP)-1. The inflammatory responses were evaluated by detecting the level of myeloperoxidase (MPO) and ED-1. The histological renal injury was also examined. Before the animals were sacrificed, the urine samples were collected for measuring the values of malondialdehyde (MDA), β2-microglobulin, interleukin (IL)-6, and IL-18. At post-shock wave 3 days, the higher expression of ICAM-1 and TNF-α were observed in shock wave-treated kidneys. The level of urine TNF-α, IL-6, and IL-18 were also increased significantly. Using PDTC obviously decreased the expression of ICAM-1 and TNF-α. It also effectively inhibited the degree of oxidative stress and neutrophil infiltration. At post-shock wave 105 days, the expression of MCP-1 and the level of urine β2-microglobulin and IL-18 were increased significantly. The histological analysis also indicated more ED-1-positive cells and serious fibrosis in shock wave-treated kidneys. PDTC significantly suppressed MCP-1 and IL-18 expression, decreased monocyte infiltration, and alleviate the degree of interstitium fibrosis. Shock wave triggered excessive inflammatory responses and aggravated renal biological damage. Several inflammatory factors including ICAM-1, MCP-1, and TNF-α were considered to play important role in this type of renal damage.
authors.affiliation: Department of Urology, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi Province, 710061, China.
authors.forename: Xiang
authors.initials: X
authors.lastname: Li
authors.forename: Qingzhi
authors.initials: Q
authors.lastname: Long
authors.forename: Xinfa
authors.initials: X
authors.lastname: Cheng
authors.forename: Dalin
authors.initials: D
authors.lastname: He
mesh_terms: D000818:Animals; D018932:Chemokine CCL2 / Q000378:metabolism; D005355:Fibrosis; D007249:Inflammation / Q000473:pathology*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D020382:Interleukin-18 / Q000652:urine; D015850:Interleukin-6 / Q000652:urine; D007668:Kidney / Q000473:pathology*; D007962:Leukocytes / Q000166:cytology; D008096:Lithotripsy / Q000009:adverse effects*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism / Q000652:urine
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D020382:Interleukin-18; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde; D009195:Peroxidase