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目的观察百草枯中毒大鼠肾组织中血红素氧合酶-1(HO-1)的表达,探讨其病理生理机制。方法 SD大鼠126只随机分为空白对照组、中毒组和褪黑素组,各42只。中毒组、褪黑素组予以百草枯(25mg/kg)腹腔注射染毒,对照组予以等量生理盐水腹腔注射,15min后褪黑素组予以褪黑素(10mg/kg)腹腔注射,对照组、中毒组予以等量生理盐水腹腔注射。于1、3、6、12h,1、2、3、5d时各组随机取6只处死。苏木精伊红(HE)染色观察各组肾组织病理学变化,采用免疫组识化学和RT-PCR观察肾组织HO-1蛋白和mRNA表达。结果①与对照组相比,中毒组染毒后3h即可见充血、水肿及空泡变性等病理变化,1d达顶峰,病理损伤评分3.30±0.31(P<0.05),其后缓解趋势不明显;而褪黑素组病理变化明显减轻且缓解趋势明显,1d时病理损伤评分2.70±0.26,与中毒组相比差异有统计学意义(P<0.05)。②与对照组相比,中毒组染毒3h在皮质部肾小管上皮细胞的细胞膜及细胞浆HO-1呈阳性表达,免疫组识化学评分(IHS)3.33±1.75,HO-1mRNA表达增强,与对照组相比差异有统计学意义(P<0.05),1d达顶峰,HIS为7.00±2.00,之后减弱,5d仍有阳性表达,但与对照组相比差异无统计学意义(P>0.05);褪黑素组HO-1表达较中毒组明显增强,IHS评分6h～3d差异具有统计学意义(P<0.05),5d不再有统计学意义(P>0.05)。结论 HO-1在百草枯中毒大鼠肾组织中呈高表达,褪黑素能明显改善百草枯中毒肾脏病理损伤,增强HO-1表达可能是其作用途径之一,而氧化损伤可能是百草枯中毒肾损伤病理生理机制之一。
Objective To observe the expression of heme oxygenase-1 (HO-1) in the kidney of paraquat poisoning rats and to explore its pathophysiological mechanism. Methods 126 SD rats were randomly divided into blank control group, poisoning group and melatonin group, 42 rats each. The rats in the poisoning group and the melatonin group were given intraperitoneal injection of paraquat (25mg / kg), the control group were injected intraperitoneally with the same amount of saline, and the rats in the melatonin group were injected intraperitoneally with melatonin (10mg / kg) 15 minutes later. , Poisoning group was given the same amount of saline intraperitoneal injection. At 1, 3, 6, 12h, 1, 2, 3 and 5d, 6 mice were sacrificed at random. Hematoxylin and eosin (HE) staining was used to observe the histopathological changes in each group. The expression of HO-1 protein and mRNA in renal tissues was detected by immunohistochemistry and RT-PCR. Results ① Compared with the control group, the pathological changes such as hyperemia, edema and vacuolar degeneration were observed in the poisoning group 3 h after exposure, reaching the peak on the 1st day and the pathological damage score was 3.30 ± 0.31 (P <0.05), and then the remission tendency was not obvious. However, the pathological changes of melatonin group were significantly alleviated and the remission tendency was obvious. The score of pathological injury on the 1st day was 2.70 ± 0.26, which was significantly different from that of the poisoning group (P <0.05). ② Compared with the control group, the poisoning group showed positive expression of HO-1 in the cell membrane and cytoplasm of the tubular epithelial cells at 3h after exposure to the poisoning group. The immunohistochemistry score (IHS) was 3.33 ± 1.75, the expression of HO-1 mRNA was enhanced, (P <0.05). The peaked on the 1st day, the HIS was 7.00 ± 2.00, then weakened and remained positive on the 5th day, but there was no significant difference compared with the control group (P> 0.05) ; The expression of HO-1 in melatonin group was significantly higher than that in poisoning group. The difference of IHS score between 6h and 3d was statistically significant (P <0.05), and there was no statistical significance at 5d (P> 0.05). Conclusions HO-1 is highly expressed in the kidney of paraquat poisoning rats. Melatonin can significantly improve the pathological damage of kidney and increase the expression of HO-1 in paraquat poisoning. Oxidative damage may be caused by paraquat One of the pathophysiological mechanisms of renal injury.