| Objective: Paraquat (PQ), is a world wide range using a rapidherbicide.In the domain of our country agriculture also should be widely, ithas always been PQ poisoning cases in our country it is often seen.PQ toxicityto the human body strong, only trace poisoning can be fatal, and there is nospecific antidote, clinical case fatality rate is extremely high, is now more than20countries banned or severely restricted the use of command. The currentPQ poisoning caused by kidney injury mechanisms are not completelyclear.The experimental research through the establishment of PQ rats exposedto model, the measurement of its serum superoxide dismutase (SOD) andactivity of glutathione (GSH), malondialdehyde (MDA) content, usingimmunohistochemical staining method for the observation of intercellularadhesion molecule-1(ICAM-1) and tumor necrosis factor A (TNF-a) in PQrats exposed to renal tissue expression, and based on this, through theapplication of5-aminosalicylic acid (5-ASA) observed in the above indexesvariation rules, so as to further explore the PQ poisoning on renal injurymechanism and5-ASA on paraquat poisoning rats renal injury in rabbits.Method: Selection of healthy adult male Wistar rats80, weight in200-230g.Rearing room temperature control in22-26C, short termexperimental rearing, after the rats were randomly divided into4groups:①The control group (group A)20rats;②the treated group (group B)20rats;③exposure and treatment group (group C)20rats;④the simple treatmentgroup (group D)20rats. Experiment on the morning of8clock, the group B,Cwere given80mg/kg PQ gavage, the group A,D were given the same volumeof double distilled water gastric perfusion.2hours later, the group C,D weregiven75mg/kg5-ASA intragastric perfusion, the group A,B were given the same volume of double distilled water gastric perfusion. Since the morning ofthe second day, group C,D were given75mg/kg5-ASA intragastric perfusion,the group A,B were given the same volume of double distilled waterintragastric perfusion,1times a day, the longest duration of medication for7days.It’s respectively selected of5rats in group A,B,C,D on day1,day3,day7,day14,given10%chloral hydrate0.35mg/kg intraperitonealinjection anesthesia after open, from the common iliac vein blood sampling3-4ml, high-speed centrifugal10min (4000R/h), taking the determination ofSOD activity and GSH, MDA content; take side kidney quickly were stainedwith HE, were observed under microscope ultrastructural organizationstructure, parallel immunohistochemical staining, observation of ICAM-1andTNF-a in rat renal tissue expression.Result:1.Clinical presentation: the rats in group A and group D were notobserved apparent poisoning performance.The rats in group B after injectionin2hours or hair erect, spirit, irritability, anorexia water poisoningperformance; after that most rats reduced urine output, weight loss, some ratsbreathing difficulties, stools, and a visible bloody secretion.The rats in groupC after5-ASA treatment, poisoning performed better than the group B loss,only occasionally dyspnea symptoms, weight loss is not obvious, stools andnose, eye discharge bloody rare.2. serology test①The rats in group B serum SOD activity after exposure to the lowest in1d,7d time point is still significantly lower than that in group A(P＜0.01),after gradually increased, and14d compared with group A had no statisticalsignificance (P＞0.05).The rats in group C serum SOD activity after injectionin1d,3d,7d time point were much higher than those of group B, hasstatistical significance (P＜0.05); only1d,3d time points compared with thegroup A had statistical significance (P＜0.01). group D compared with groupA, SOD activity after injection in1d,3d,7d time point were not statisticallysignificant (P＜0.01).②The rats in group B after injection in the serum content of GSH1d is the lowest, to3d time point is still significantly lower than that in A group (P＜0.01), after gradually increased, and7d compared with group A had nostatistical significance (P＞0.05).The rats in group C the content of serumGSH after injection in1d,3d,7d time point were much higher than those ofgroup B, has statistical significance (P＜0.05); all time points compared withthe group A were not statistically significant (P＞0.05).Group D comparedwith group A, GSH content after injection in1d,3d,7d time point were notstatistically significant (P＜0.01).③The rats in group B after injection in the serum content of MDA1d isthe highest point in time, to7d was significantly higher than that of group A(P＜0.01), and then decreased gradually, and14d compared with group A wasnot significant (P＞0.05).The rats in group C the content of serum MDA afterinjection in1d,3d,7d time point were significantly lower than those in groupB (P＜0.05),1d only,3d time points compared with the group A had statisticalsignificance (P＜0.05).Group D compared with group A, MDA content afterinjection in1d,3d,7d time point were not statistically significant (P＜0.01).3. Experimental rat kidney tissue morphological changes①Macroscopic observation: the rats of group A kidney ruddy color, filmwithout swelling; the rats of group B kidney by color dark, swelling of themembrane; the rats of group C kidneys compared with group B color is red,swelling of the membrane is lighter; group D rat kidney ruddy color, filmwithout swelling.②Endoscopic observation: the rats of group A kidney glomerulus,tubules, renal interstitial showed no abnormality; the rats of group B in renaltissues of rats with renal tubular change, gradually visible epithelial edema,vacuolar degeneration, necrosis, within the lumen of the necrosis particles; therats of group C in renal tissues of rats than in the group B less, and laterappeared; group D in renal tissue of rats with no abnormal.4.Experiment rat kidney tissue ICAM-1and TNF-a immunohistochedetection results4.1ICAM-1in rat renal tissue expression and distribution ①The expression of ICAM-1: in the renal tissue of rats of group A, onlyin the renal tubular cell membrane is a small amount of ICAM-1expression,in the glomeruli, renal peritubular capillaries and vascular endothelial cellswere not found in ICAM-1marked expression②In the renal tissue of rats of group B, visible on ICAM-1in renaltubular and glomerular cell membrane is widely expressed, compared with thegroup A had statistical significance (P＜0.01) in7d, reached the peak,thereafter expression decreased, but the expression of14d was higher than thatof group A, compared with the group A had statistical significance (P＜0.05)③In the renal tissue of rats of group C, visible on ICAM-1in renaltubular and glomerular membrane expression, and the expression is from1d to14d time point were significantly lower than those in group B, compared withthe group B had statistical significance (P＜0.05); but the expression in1d to14d time point is higher than that of group A (P＞0.01)④In the renal tissue of rats of group D,compare with group A,ICAM-1expression was not significantly different4.2TNF-a in rat renal tissue expression and distribution①In the renal tissue of rats of group A, only in the renal tubularendothelial cells within the cytoplasm showed occasional TNF-a expression inglomerular capillaries around, such as renal interstitial area has obviousexpression of TNF-a.②In the renal tissue of rats of group B, TNF-a is mainly expressed inrenal tubular endothelial cells within the cytoplasm, since1d started increasedsignificantly, to the7d reached the peak, and to the14d still have obviousexpression, compared with group A had statistical significance (P＜0.01).③In the renal tissue of rats of group C, TNF-a is mainly expressed inrenal tubular endothelial cells within the cytoplasm, the application of5-ASAfrom1d to14d its expression than those in group B was significantlyattenuated, with statistical significance (P＜0.05); compared with A group,from1d to14d TNF-a expression was higher, with statistical significance (P＜0.01). ④In the renal tissue of rats of group D, TNF-a also is mainly expressedin renal tubular endothelial cells within the cytoplasm, was not significantlydifferent compare with group A.Conclusion:1. PQ gavage can cause can cause kidney damage, the main findings ofrenal tubular epithelial cell injury, showed that the PQ gavage is theestablishment of acute kidney injury animal model method.2. PQ rats exposed to plasma SOD activity and GSH content decreased,the increase of MDA content, showed that rats exposed to in vivo in thepresence of oxidative damage and oxidation and antioxidant imbalance, PQmay lead to kidney injury mechanism；PQ rats exposed to ICAM-1in renaltissue and expression of TNF-a may change, indicated that the two kinds ofcytokines on PQ induced renal injury may play an important role in.3. Rats exposed to in the application of5-ASA after treatment, cansignificantly increase the PQ poisoning rats serum SOD activity and GSHcontent, lower the content of MDA,5-ASA can reduce kidney tissueperoxidative damage.4.5-ASA probably by inhibiting the generation of oxygen free radical ordirect oxygen free radical scavenging and anti-inflammatory machine, indirectin vivo inhibition of ICAM-1and TNF-a expression, so as to reduce PQinduced renal injury. |
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