ObjectiveTo investigate the interventive effect of xuebijing for injection combined with nalmefene hydrochloride injection in treatment of acute hepatocyte functional injury after severe thoracoabdominal injuries. MethodsClinal data of 169 patients with severe thoracoabdominal injuries who treated in The 253th Hospital of PLA between January 2009 and June 2013 were collected retrospectively. The trauma indexes of the 169 patients were all higher than 17 scores. Patients were divided into the intervention group (n=112) and the control group (n=57) according to their receptive treatment:patients of control group underwent traditional treatments such as antishock, hemostasis, and so on; but patients of intervention group received xuebijing for injection combined with nalmefene hydrochloride injection (intravenous infusion). Patients of intervention group were tested at the time of arriving at and leaving the emergency department to the inpatient department with alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-α (TNF-α), lipopolysaccharide (LPS), and interleukin-6 (IL-6); the patients of control group were just tested at the time of leaving the emergency department to the inpatient department, then comparison of the indexes between the 2 groups was performed. ResultsIn intervention group, the levels of ALT, AST, TNF-α, LPS, and IL-6 after the interventive treatment were all lower than those of before interventive treatment (P<0.05). Compared with control group, there was no significant difference in the levels of ALT, AST, TNF-α, LPS, and IL-6 before the interventive treatment of intervention group (P>0.05); but the levels ALT, AST, TNF-α, LPS, and IL-6 were all lower after the interven-tive treatment (P<0.05). ConclusionsXuebijing for injection combined with nalmefene hydrochloride injection can evidently improve the acute hepatocyte functional injury after severe thoracoabdominal injuries, and improve the prognosis.
ObjectivesTo systematically review the efficacy and safety of nalmefene hydrochloride for acute cerebral infarction.MethodsPubMed, EMbase, The Cochrane Library, CBM, CNKI, WanFang Data and VIP databases were electronically searched to collect randomized controlled trials (RCTs) on nalmefene hydrochloride for acute cerebral infarction from inception to February 21st, 2018. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies, then, meta-analysis was performed by using RevMan 5.3 software.ResultsA total of 8 RCTs involving 1 038 patients were included. The results of meta-analyses showed that, compared to the routine treatment group, the nalmefene hydrochloride group was significantly associated with an increased reduction in total effective rate (RR=1.14, 95%CI 1.04 to 1.23, P=0.003), GCS (MD=1.30, 95%CI 0.66 to 1.94, P<0.0001), patient satisfaction (RR=1.26, 95%CI 1.03 to 1.55, P=0.03), cerebral blood flow (MD=5.00, 95%CI 3.81 to 6.19, P<0.05), and cerebral blood volume (MD=0.28, 95%CI 0.23 to 0.32, P<0.05). It was also significantly associated with an reduction of NIHSS, CSS, level of inflammatory factors after treatment in 14 days, level of MMP-9 and mean transit time of contrast medium (P<0.05). However, no significant association was observed between two groups in level of inflammatory factors after treatment in 20 days. For safety outcomes, no significant association was found between two groups in mortality, dizziness, and nausea and vomiting.ConclusionsThe current evidence indicates that the nalmefene hydrochloride can be used to treat acute cerebral infarction based on routine treatment of acute cerebral infarction, and the safety is relatively good. Due to limited quality and quantity of the included studies, more high quality studies are required to verify above conclusion.
Objective To study the mechanism of alleviating lung ischemia-reperfusion injury by postischemic treatment with namefene hydrochloride, and explore the optimal timing of drug treatment throughout the disease course. Methods A total of 60 rats were randomly divided into six groups with 10 rats in each group: a sham group, a model group, a nalmefene A (NA) group, a nalmefene B (NB) group, a nalmefene C (NC) group and a nalmefene D (ND) group. The sham group without drug treatment was not treated with ischemia-reperfusion. The lung ischemia-reperfusion model was established by occlusion of the left pulmonary hilum in the model group without drug treatment. After ischemic treatment, the NA, NB, NC and ND groups were respectively injected with nalmefene (15 μg/kg) by the tail vein at 5 min before, 10 min, 30 min and 60 min after pulmonary circulation reperfusion. At the 3rd hour after reperfusion, all rats were sacrificed and the specimens from the upper lobe of the left lung tissue were preserved to observe pulmonary lesions, detect wet/dry weight ratio and the activity of myeloperoxidase (MPO), the expressions of tumor necrosis factor-α (TNF-α), Toll-like receptor 2 (TLR2) mRNA and MyD88 mRNA as well as the expressions of TLR2, MyD88, NF-κB p65 and p-NF-κB p65 in lung tissue. Results There were different degrees of alveolar septal destruction, obvious pulmonary interstitial edema, the infiltration of inflammatory cell, the exudationred of blood cell in the mesenchyme, and the collapse of partial alveolar in the model group and the NA, NB, NC, ND groups. In terms of wet/dry weight ratio, the score of lung tissue injury, the activity of MPO, the expressions of TNF-α, TLR2 mRNA and MyD88 mRNA as well as the expressions of TLR2, MyD88, NF-κB p65 and p-NF-κB p65 in lung tissue, the model group were significantly higher than the sham group (P<0.01); there was no significant difference between the ND group and the model group (P>0.05). The corresponding test values of the nalmefene groups with post-ischemic treatment showed the characteristics of ND group> NC group> NB group> NA group (P<0.01). Conclusion The effect of nammefene on alleviating lung ischemia-reperfusion injury is closely related to the inhibition of TLR2, MyD88, NF-κB p65 and phosphorylation of NF-κB p65 with a characteristic of time-dependent manner.