ABSTR AC TS FROM THE CHINESE JOURNAL OF HYPERTENSION The Effects of Renal Sympathetic Denervation on Hypothalamic Mitogen-Activated Protein Kinase and NF-κB in Spontaneously Hypertensive Rats 1 1 1 1 1 1 Li Wang, Cheng-zhi Lu, Yi-jie Ma, Meng-ping Xv, Zhu-qing Li, and Chao Li Department of cardiology, Tianjin First Center Hospital, Tianjin, China. Correspondence: Cheng-zhi Lu (firstname.lastname@example.org). Objective: To study the effects of renal sympathetic denervation (RDN) on blood pressure, hypothalamic mitogen-activated protein kinase (MAPK), and nuclear factor-kappa B (NF-κB) in spontaneously hypertensive rats (SHR). Methods: Thirty-six SHR were randomly divided into baseline, RDN, and sham-operated groups ( n = 12 rats per group). Age-matched Wistar-Kyoto (WKY) rats served controls (n = 12). At 12 weeks of age, rats underwent RDN or sham sur- gery and were killed aer 1 o ft r 6 weeks aer s ft urgery. Blood pressure, plasma levels of neuron-specific enolase (NSE), and p-p38MAPK, p65 NF-κB in the hypothalamus were assessed. Results: At 1 to 5 weeks aer ft RDN, systolic and diastolic blood pressures were significantly decreased. Compared with sham surgery at 1 week and SHR baseline, blood pressure was significantly decreased at 1 week aer RD ft N (all P < 0.05). At 6 weeks aer s ft urgery, there were no statistical differences in the blood pressure among RDN, sham surgery and SHR baseline groups (all P > 0.05). Plasma NSE levels were increased in SHR baseline compared to WKY and were further increased 1 week aer ft RDN (P < 0.05). Phosphorylation of p38 MAPK and p65 NF-κB proteins levels in the hypothalamus were increased in SHR groups compared to WKY controls and were decreased 1 week aer RD ft N compared to SHR baseline (all P < 0.05). Conclusion: RDN decreases blood pressure and hypothalamic p38 MAPK and NFκB levels in SHR. Arachidonic Acid Induces Human Podocyte Apoptosis 1 1 1 1 1 Yang-bin Pan, Shi-xiang Zhen, Hong-tin Ke, Guo-hua Ding, and Jian-xin Wan Department of Nephrology, First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China. Correspondence: Jian-xin Wan (email@example.com). Objective: To study the effects of arachidonic acid (AA) on cell apoptosis, p38 phosphorylation, and p53 levels in cultured human podocytes. Methods: Conditionally immortalized human podocytes were cultured in vitro. Differentiated human podocytes were −8 −5 exposed to AA at variable times (0.5–2.0 hours) and concentrations (10 –10 mol/l). Podocyte apoptosis was assessed by flow cytometry and Hoechst-33342 staining. Levels of p-p38 and p53 were analyzed by Western blotting. −8 −5 Results: Treatment with AA at 10 to 10 mol/l for 2 hours dose-dependently increased podocyte apoptosis as assessed −6 −5 by flow cytometry, along with increased levels of p-p38 and p53 at the higher doses (10 to 10 mol/l, P < 0.05). However, −8 −7 compared to controls, AA treatment at lower doses (10 and 10 mol/l) for 2 hours did not significantly increase podocyte −5 apoptosis or p53 levels. When podocytes were exposed to 10 mol/l AA for 0.5 hours, no significant changes were observed in podocyte apoptosis or p53 levels. Conclusion: AA dose-dependently induces cell apoptosis, and increases p-p38 and p53 levels in cultured human podocytes. 512 American Journal of Hypertension 31(4) April 2018 Downloaded from https://academic.oup.com/ajh/article-abstract/31/4/512/4925895 by Ed 'DeepDyve' Gillespie user on 16 March 2018
American Journal of Hypertension – Oxford University Press
Published: Apr 1, 2018
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