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目的:研究中药复方四毒清防治内毒素性肾功能衰竭的作用机制。方法:将小鼠随机分成对照组、LPS组、四毒清防治组和四毒清组,用水(0.2mL/10gBW)或四毒清(1000g/L,0.2mL/10gBW)灌胃3d,每天2次,第3d灌胃后2h,腹腔注射LPS(30mg/kg,0.2mL/10gBW)或生理盐水(0.2mL/10gBW),腹腔注射后2h,再用水或四毒清(0.2mL/10g)灌胃1次。测定各组小鼠血清肌酐(Cr)和尿素氮(BUN)的含量,观察肾脏超微结构,肾组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性的变化,并用半定量RT-PCR方法测定肾组织细胞间黏附分子-1(ICAM-1)mRNA的表达。结果:LPS引起小鼠血清Cr和BUN含量明显升高,肾脏近曲小管出现明显病理改变。四毒清有效降低LPS攻击小鼠血清Cr和BUN的含量,明显减轻近曲小管的损伤。LPS组小鼠肾组织MDA含量和ICAM-1mRNA的表达显著高于对照组,而四毒清防治组肾组织MDA含量和ICAM-1mRNA的表达明显低于LPS组,四毒清处理能显著升高肾组织SOD的活性。结论:中药四毒清防治内毒素性肾功能衰竭的作用机制与其升高肾组织SOD的活性、减轻肾组织氧化损伤并抑制肾脏ICAM-1mRNA的表达有关。
Objective: To study the mechanism of Chinese traditional medicine compound Siduqing in preventing and treating endotoxin-induced renal failure. METHODS: Mice were randomly divided into control group, LPS group, Siduqing prevention group and Siduqing group. The rats were orally administered with water (0.2mL/10gBW) or Siduqing (1000g/L, 0.2mL/10gBW) for 3 days. 2 times, intraperitoneal injection of LPS (30mg/kg, 0.2mL/10gBW) or physiological saline (0.2mL/10gBW) 2 hours after intragastric administration on the 3rd day, 2h after intraperitoneal injection, and then water or Tetrasanqing (0.2mL/10g) Gavage once. The levels of serum creatinine (Cr) and urea nitrogen (BUN) were measured in each group. The ultrastructure of the kidney, the content of malondialdehyde (MDA) in the kidney and the activity of superoxide dismutase (SOD) in the kidney were observed, and semi-quantitative was used. The expression of intercellular adhesion molecule-1 (ICAM-1) mRNA was measured by RT-PCR. RESULTS: LPS caused a significant increase in serum Cr and BUN levels in the mice and obvious pathological changes in the renal proximal tubules. Siduqing effectively reduced the serum Cr and BUN levels in LPS challenge mice and significantly reduced the damage of proximal tubules. The expression of MDA and the expression of ICAM-1mRNA in renal tissue of mice in LPS group were significantly higher than those in control group, while the content of MDA and ICAM-1mRNA in renal tissues of Sifuqing prevention group was significantly lower than that in LPS group. Kidney SOD activity. Conclusion: The mechanism of Siduqing in the prevention and treatment of endotoxin-induced renal failure is related to the increase of SOD activity in renal tissue, the reduction of renal oxidative damage and the inhibition of renal ICAM-1 mRNA expression.