ABSTRACT
Objective To evaluate the effect of inhibition of ubiquitin carboxy terminal hydrolase LI (UCHL1) on cerebral ischemia/reperfusion injury in mice. Methods Male BALB/c mice were randomly divided into sham group, ischemia/reperfusion (I/R) group, UCHL1 small interfering RNA (siRNA)group and scramble siRNA (control) group, 10 mice in each group. I/R model was established by reperfusion 24 hours after middle cerebral artery occlusion (MCAO) 60 minutes. In the siRNA group and control group, 10 JJLI UCHL1 siRNA or scramble siRNA was injected into the brain through the lateral ventricle 24 hours before MCAO. The expression of UCHL1 was detected by RT-PCR and Western blotting; the volume of cerebral infarction and the rate of edema were assessed by 2, 3, 5-triphenyl tetrazolium chloride (TTC) staining; and the score of neurological symptoms was assessed by neurobehavioral scoring. Results Compared with the sham group, the level of UCHL1 mRNA and protein in ischemic penumbra of I/R group were significantly higher (P< 0.05), while the expression of UCHL1 protein and mRNA in siRNA group were significantly lower (P< 0.05); at the same time, the volume of cerebral infarction, edema rate and neurobehavioral damage in I/R group increased significantly, while the volume and edema rate of cerebral infarction and neurobehavioral damage in siRNA group further increased (P< 0.05). Conclusion Inhibition of UCHL1 can aggravate the cerebral ischemia/reperfusion injury in mice, suggesting that the induction of UCHL1 after MCAO has a protective effect on the cerebral ischemia/reperfusion injury in mice.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate if the duration from poisoning to treatment (no treatment period) is related to the prognosis of patients with severe acute organophosphorus pesticide poisoning (SAOPP).</p><p><b>METHODS</b>One hundred and seventy-four patients with the pre-hospital systematic treatment served as the treatment group while 160 patients going to the hospital by themselves without treatment or rejecting gastrolavage served as the control group. Patients in both groups were treated by gastrolavage, pralidoxime chloride, atropine and other expectant treatment. The duration of no treatment period, death, and severe complication were observed. The time of disappearance of symptoms, the recovery time of acetyl cholinesterase (AChE), atropinization time, atropine dosage, pralidoxime chloride dosage, naloxone dosage, hospitalization days and other targets were also observed.</p><p><b>RESULTS</b>The duration of no treatment period in treatment group [(1.2 +/- 0.3) h] was significantly shorter than that in control group [(2.8 +/- 0.5) h, (P < 0.01)]. The mortality rate in treatment group was 6.32% while that in control group 22.5% (P < 0.01). The incidence of respiratory failure, heart injury, brain injury, atropine poisoning, intermediate syndrome, liver injury in treatment group (12.64%, 5.75%, 8.62%, 1.72%, 4.60%, 5.17% respectively) were lower than those in control group (25.63%, 13.75%, 17.50%, 6.25%, 7.50%, 9.38% respectively, P < 0.05 or P < 0.01). The time of symptoms disappearance, the recovery time of AChE, atropinization time, atropine dosage, pralidoxime chloride dosage, naloxone dosage, hospitalization days in treatment group were significantly superior to those in control group (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>The pre-hospital systematic treatment can improve the prognosis of the patients with SAOPP, which is worth popularizing and using.</p>