摘要
目的:研究松花粉对甘油诱发大鼠急性肾衰竭(acute renal failure,ARF)的保护作用及机制。方法:采用双侧后肢注射50%甘油溶液(10mL·kg-1)诱发大鼠成急性肾衰竭模型,检测大鼠血清肌酐(Scr)、血清尿素氮(BUN)的含量,肾组织中超氧化物歧化酶(SOD)的活性,谷胱甘肽(GSH)、丙二醛(MDA)的含量,同时测定肾组织中一氧化氮(NO)的含量和诱导型一氧化氮合酶(iNOS)的活性;HE染色观察肾病理组织形态学变化。结果:与空白组大鼠相比,模型组大鼠血清Scr和BUN的含量明显上升,肾组织中SOD的活性和GSH的含量显著降低,MDA的含量显著升高;组织病理检查发现,模型组大鼠肾小管损伤明显,肾皮质细胞部分脱落,肾小球肿胀,间质炎性侵润明显。给予松花粉治疗后,可显著降低ARF大鼠血清Scr和BUN,升高肾组织中SOD的活性、GSH的含量,降低MDA的含量,同时发现,松花粉可明显降低肾组织中NO的含量和iNOS的活性,并显著降低肾组织损伤。结论:松花粉对甘油致大鼠ARF具有治疗作用,其作用机制可能与抑制iNOS的活性,降低体内NO过多产生,降低NO相关的脂质过氧化过程有关。
Objective: To study the protective effect of pollen pini against acute renal failure (ARF) induced by glycerol and its underlying mechanisms in rats. Methods: The rats were intramuscularly injected with 50% glycerol (10 mL·kg-1) in each hind leg to establish kidney damage. After the pini treatment for seven days, the contents of serum creatinine (Scr) and urea nitrogen (BUN), the activities of superoxide dismutase (SOD), inducible nitric oxide synthase (iNOS) and the contents of glutathione (GSH), malondialdehyde (MDA) and NO in the kidney tissue were examined. Results: Compared the model group with the control group, the contents of Scr and BUN in serum, the contents of MDA and NO and the activities of iNOS in kidney tissue were increased, the activities of SOD and the content of GSH were decreased; and the sections showed that the kidney tissue damage was obvious with bigger glomerular volume, swelling and degeneration of endothelial cells and renal interstitial inflammatory cell infiltration. However, pollen pini dose-dependently exhibited significantly decreases contents of Scr and BUN in the plasma, reduced contents of MDA and NO, and decreased activities of iNOS in the kidney tissue, as well as increased activities of SOD and content of GSH in the kidney tissue. The damage decreased after the administration of pollen pini. Conclusion: The results indicated that pollen pini had a protective effect against glycerol-induced ARF in rats. It is considered that this protective effect may be related to its activities on inhibition of iNOS and the level of NO, and its free radical scavenging related to NO.
出处
《药学与临床研究》
2015年第3期232-234,共3页
Pharmaceutical and Clinical Research