Abstract:Objective: To observe the effect of simvastatin on brain tissue after renal ischemia reperfusion injury and its mechanism. Methods: A rat model of renal ischemia reperfusion injury (RIRI) was prepared by clamping the bilateral renal arteries for 45 minutes(10% chloral hydrate intraperitoneal anesthesia, open the abdominal cavity, exposed bilateral renal artery and vein, clamping the bilateral renal artery and vein with artery clamp, 45min after removal of the artery clamp to restore blood flow, and then suture the abdominal wall). 36 rats were randomly divided into the following groups, 12 rats in each group: sham operation group; renal ischemia reperfusion group; simvastatin group. Detection of serum creatinine (Scr), urea nitrogen (BUN), brain tissue malondialdehyde (MDA) and nitric oxide (NO) content, superoxide dismutase (SOD) and inducible nitric oxide synthase (iNOS) activity in brain tissue was detected in endothelial nitric oxide synthase (eNOS) protein expression level. Results: Compared with the sham operation group, the contents of Scr, BUN, MDA, NO and iNOS activity in the ischemic group increased (P<0.05), while the activity of SOD decreased (P<0.05). Compared with the ischemia reperfusion group, the content of SCr, BUN and MDA decreased, iNOS activity was decreased (P<0.05), but the activity of SOD and the content of NO increased (P<0.05). The content of eNOS protein in renal ischemia reperfusion group was higher than that in sham operation group (P<0.05), and the content of eNOS protein in simvastatin group was higher than that in the renal ischemia reperfusion injury group (P<0.05). Conclusion: Simvastatin can protect the brain from ischemia reperfusion injury. It may be related to decreased the activity of iNOS, and increase the expression of eNOS protein and the content of NO.
荆娇, 张永忠, 闫文升, 马海玲, 张玉清, 焦宗伟. 辛伐他汀对肾缺血再灌注损伤大鼠脑组织OFR NO和NOS的影响[J]. 河北医学, 2017, 23(6): 941-943.
JING Jiao, ZHANG Yongzhong, YAN Wensheng, et al. Effects of Simvastatin on OFR, NO and NOS in Brain Tissue of Rats with Renal Ischemia Reperfusion Injury. 河北医学, 2017, 23(6): 941-943.
[1] Endo A, Kuroda M. Citrinin, an inhibitor of cholesterol synthesis[J].Antibiot (Tokyo), 1976, 29(8):841~843. [2] 金健,朴尚国,金顺英等.普伐他汀对肾缺血再灌注损伤的保护作用及其机制的探讨[J].中华肾脏病杂志,2014,30(3):138~144. [3] 刘国庆.辛伐他汀对大鼠脑创伤后内皮祖细胞动员和损伤脑组织血管再生影响[M].天津:天津医科大学,2009. [4] Xia Xiao-hong, Shen Yu-xue,Shi Ji-cai,et al.Antibody of endothelin in renal ischemia/reperfusion injury in rats[J].Chinese Journal of Pathophysiology, 1999, 15(5): 415~417. [5] 高永强,杨巧莲,王伟.大鼠局灶性脑缺血模型制备及取脑方法实验研究[J].包头医学院学报,2009,29(4):6~9. [6] 仝飞,夏晓红.短暂反复缺血预处理对大鼠肾缺血再灌注损伤的保护作用及其机制研究[D].石家庄:河北医科大学,2011. [7] Yi Shi-hua. L - arginine and research progress of cardiovascular disease[J].Cardiovascular epidemiology,2000, 21(4): 234~236 [8] Laude K, Favre J, Thuillez C,et al. NO produced by endothelial NO synthase is a mediator of delayed preconditioning-induced endothelial protection[J].Am Physiol Heart Circ Physiol, 2003, 284(6): 2053~2060. [9] Varela M, Garvin JL. Acute and chronic regulation of thick ascending limb endothelial nitric oxide synthase by statins[J].AmSoc Nephrol, 2004, 15:269~275. [10] Takemoto M, Sun J, HIRoki J, et al. Rho-kinase mediates hypoxia induced downregulation of endothelial nitric oxide synthase[J].CIRculation, 2002, 106:57~62. [11] Laufs U, La Fata V, Plutzky J, et al. Upregulation of endothelial nitric oxide synthase by HMG -CoA reductase inhibitors[J].CIRculation, 1998, 97 (12):1129~1135.