氯化汞致大鼠肾损伤及原花青素的保护作用

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[目的]观察氯化汞对大鼠肾脏的损伤作用及原花青素的保护作用。[方法]30只Wistar大鼠按体重随机分成5组,第1~4组以大豆油灌胃,第5组以原花青素450 mg/kg灌胃;2 h后,第1组皮下注射生理盐水,第2~5组分别皮下注射2.2、4.4、8.8、8.8μmol/kg氯化汞。第2天重复上述步骤后,收集24 h尿液测定尿汞(Hg)和蛋白含量,以及碱性磷酸酶(ALP)、β-N-乙酰氨基葡萄糖苷酶(NAG)和乳酸脱氢酶(LDH)活力;腹主动脉采血测定血清尿素氮(BUN);切取肾皮质测定Hg含量和还原型谷胱甘肽(GSH)、丙二醛(MDA)水平及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力。[结果]与对照组比较,各染毒组的尿蛋白含量、尿LDH活力、肾皮质Hg含量、GSH、MDA含量及SOD、GSH-PX活力差异均具有统计学意义(P<0.05或P<0.01);4.4、8.8μmol/kg染毒组的尿汞含量、ALP、NAG活力、血清BUN含量的差异均具有统计学意义(P<0.01)。原花青素干预组与8.8μmol/kg染毒组比较,尿LDH、ALP、NAG活力降低,尿蛋白含量下降,肾皮质GSH、MDA含量下降,SOD、GSH-Px活力升高,血清BUN含量下降,差异均具有统计学意义(P<0.05或P<0.01)。[结论]氯化汞可蓄积于大鼠肾脏并产生损伤,原花青素对大鼠氯化汞所致肾损伤具有一定程度的保护作用。 [Objective] To observe the injury effect of mercuric chloride on rat kidney and the protective effect of proanthocyanidins. [Methods] Thirty Wistar rats were randomly divided into five groups according to their body weight. Groups 1 to 4 were orally administered with soybean oil. Group 5 was given gavage with procyanidin 450 mg / kg. After 2 hours, group 1 was injected subcutaneously with normal saline, Groups 2 to 5 were subcutaneously injected with 2.2,4.4,8.8,8.8μmol / kg mercuric chloride. On the second day after the above steps were repeated, urine samples were collected for 24 hours to determine urinary mercury (Hg) and protein content, and alkaline phosphatase (ALP), β-N-acetylglucosaminidase (NAG) and lactate dehydrogenase (LDH) activity was measured. Serum urea nitrogen (BUN) was measured by blood sampling in abdominal aorta. Hg, glutathione (GSH), malondialdehyde (MDA) and superoxide dismutase (SOD) Glutathione peroxidase (GSH-Px) activity. [Results] Compared with the control group, urinary proteinuria, urine LDH activity, renal cortical Hg content, GSH, MDA content and SOD, GSH-PX activity in each exposure group were statistically significant (P <0.05 or P < 0.01). The contents of mercury and ALP, NAG and BUN in 4.4, 8.8μmol / kg exposed groups were significantly different (P <0.01). Compared with 8.8μmol / kg group, the activity of LDH, ALP and NAG decreased, the content of urine protein decreased, the content of GSH and MDA in renal cortex decreased, the activity of SOD and GSH-Px increased and the content of serum BUN decreased All were statistically significant (P <0.05 or P <0.01). [Conclusion] Mercuric chloride can accumulate in the kidney of rats and cause injury. Proanthocyanidins protect renal injury induced by mercuric chloride in rats to some extent.
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