Prospective experimental studies on the renal protective effect of ulinastatin after paraquat poisoning

Abstract

BACKGROUND: Paraquat (PQ) is an effective herbicide and is widely used in agricultural production, but PQ poisoning is frequently seen in humans with the lung as the target organ. Currently, there are many studies on lung injury after PQ poisoning. But the kidney as the main excretory organ after PQ poisoning is rarely studied and the mechanisms of this poisoning is not very clear. In this study, we observed the expression of caspase-3 and livin protein in rat renal tissue after PQ poisoning as well as the therapeutic effects of ulinastatin. METHODS: Fifty-four Sprague-Dawley (SD) rats were randomly divided into three experimental groups: control group (group A), paraquat poisoning group (group B) and ulinastatin group (group C), with 18 rats in each group. Rats in group B and group C were administered intragastrically with 80 mg/kg PQ, rats in group C were injected peritoneally with 100 000 U/kg ulinastatin once a day, while rats in group A were administered intragastrically with the same volume of saline as PQ. At 24, 48, 72 hours after poisoning, the expression of livin in renal tissue was detected by Westen blotting, the expression of caspase-3 was detected by immunohistochemistry, and the rate of renal cell apoptosis was tested by TUNEL detection. The histopathological changes were observed at the same time. RESULTS: Compared to group A, the expression of caspase-3 in the renal tissue of rats in groups B and C increased significantly at any time point. Compared with group B, the expression of caspase-3 in renal tissue of rats in group C decreased. Compared with group A, the expression of livin in renal tissue in rats of groups B and C increased significantly at any time point (P<0.01), especially in group C (P<0.01). TUNEL method showed that the rate of renal cell apoptosis index was higher in group B at corresponding time points than in group A (P<0.01), and was lower in group C at corresponding time points than in group B (P<0.01). CONCLUSION: UTI has a protective effect on the renal tissue of rats after paraquat poisoning through up-regulating the expression of livin and down-regulating the expression of caspase-3, but the regulation path still needs a further research.

Effect of hemoperfusion cartridge on different internal environmental indicators

“…For each HP treatment, total toxic removed by HP cartridge is not equal and clearance kinetics of HP cartridge for various poisons are not the same. [2] Zhang et al [11][12][13] found that for the clearance of paracetamol, sodium salicylate, digoxin, phenobarbital, etc by carbon renal HP, the clearance rate decreased with time. Mui et al [14] reported that the adsorption capacity of activated carbon for drugs reached the maximum from the beginning to 20 minutes and the absorbing ability decreased with time.…”

“…There were some similarities between the clearance ability of blood glucose and that of drugs for HP cartridge. [11,14] Indirectly it provided the specific time of HP treatment for patients with acute poisoning by detecting the difference. Future studies can focus on indirect judgement of toxic clearance by detecting the difference of the blood glucose levels before and after HP cartridge.…”

Heat shock protein 70 protects the lungs from hyperoxic injury in a neonatal rat model of bronchopulmonary dysplasia

“…The presence of Hsp70 in the culture medium can inactivate dendritic cells and some reports have revealed that Hsp70 can promote the production of regulatory T cells (Tregs), which play a role in the development of tolerance and immunoregulation [20]. In some animal experiments and clinical observations, the expression of HSPs are found in lung tissue cells which imply that Hsp70 may plays an important role in the repair and protection of lung injury [21,22].…”

Recent research progress on the role of ulinastatin in chronic kidney disease

“…Studies have shown that paraquat can still be detected in the kidney as the main excretory organ of paraquat after 21 days of poisoning 25 . Zhang et al found that apoptosis is the main mechanism that causes renal tubular necrosis, renal interstitial congestion and edema after paraquat poisoning, while UTI can take a part in renal protection 29 . The related mechanisms are mainly characterized by up‐regulating the expression of livin protein (inhibitor of apoptosis) and down‐regulating the expression of caspase‐3 protein 29 (a key enzyme of apoptosis) (Figure 1).…”

“…Zhang et al found that apoptosis is the main mechanism that causes renal tubular necrosis, renal interstitial congestion and edema after paraquat poisoning, while UTI can take a part in renal protection 29 . The related mechanisms are mainly characterized by up‐regulating the expression of livin protein (inhibitor of apoptosis) and down‐regulating the expression of caspase‐3 protein 29 (a key enzyme of apoptosis) (Figure 1). Liu et al used the TUNEL method to assess the degree of apoptosis in the renal cortex in a model of post‐traumatic cardiac arrest 30 .…”