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目的:观察高盐诱导的高血压大鼠肾组织中可溶性表氧化物水解酶(sEH)的表达并探讨其作用。方法:8周龄Wistar大鼠12只,随机分为正常饮食组(WC组)和高盐饮食组(WH组),分别给予正常饮水和高盐饮水[2%(质量分数)NaCl]喂养21 d,测定大鼠血压、血浆血管紧张素Ⅱ、血钠、血尿素氮、血肌酐水平和24 h尿量、尿钠、尿蛋白,应用免疫组化和Western印迹的方法检测肾组织sEH表达。结果:与WC组相比,WH组大鼠高盐饮食3 d后收缩压显著升高且一直持续到实验结束(P<0.05),24 h尿量、尿钠均显著增加,血钠、血尿素氮水平显著升高(P均<0.01),血肌酐、24 h尿蛋白的差异无统计学意义(P均>0.05),血管紧张素Ⅱ显著下降(P<0.05)。肾组织免疫组化结果显示WH组皮质肾小管sEH表达显著上调,Western blot测定sEH表达量(sEH/β-actin)WH组(1.24±0.13)较WC组(0.38±0.03)显著增加(P<0.01)。结论:高盐饮食后大鼠血压升高、钠水潴留、肾组织sEH表达上调,提示sEH可能在高盐诱导的大鼠高血压发生和发展中发挥重要作用。
Objective: To observe the expression of soluble epoxide hydrolase (sEH) in renal tissue of hypertensive rats induced by high salt and to explore its role. Methods: Twelve Wistar rats aged 8 weeks were randomly divided into normal diet group (WC group) and high salt diet group (WH group), and were given normal drinking water and high salt drinking water [2% (mass fraction) d. The blood pressure, plasma angiotensin Ⅱ, serum sodium, blood urea nitrogen, serum creatinine, 24 h urine output, urinary sodium and urinary protein in rats were measured. The expression of sEH in renal tissue was detected by immunohistochemistry and Western blotting. Results: Compared with the WC group, the systolic blood pressure in WH group increased significantly after 3 days of high-salt diet and continued until the end of the experiment (P <0.05), and the urine volume and urinary sodium increased significantly at 24 h There was no significant difference in serum creatinine and 24 h urinary protein between the two groups (P> 0.05) and the level of angiotensin Ⅱ (P <0.05). The results of immunohistochemistry showed that the expression of sEH in cortex of WH group was significantly increased, and the expression of sEH / β-actin in WH group (1.24 ± 0.13) was significantly higher than that in WC group (0.38 ± 0.03) by Western blot (P < 0.01). CONCLUSION: Elevated blood pressure, sodium and water retention, and up-regulation of sEH expression in renal tissues of rats after high-salt diet suggest that sEH may play an important role in the occurrence and development of hypertension-induced hypertension in rats.