摘要:目的:探讨卡配因抑制剂3（MDL28170）对新生大鼠缺氧缺血性脑损伤(HIBD)神经细胞凋亡的影响。方法:建立新生SD大鼠HIBD模型,治疗组于缺养缺血后即刻、2 h、4 h腹腔内注射MDL28170,对照组及手术组同时予生理盐水。缺氧缺血后24 h用免疫组化方法观察大脑皮质及海马CA1区Caspase3 蛋白表达、TUNEL法检测细胞凋亡,观察组织病理改变并计算海马神经元死亡数,透射电镜观察细胞超微结构。结果:缺氧缺血后24 h缺血侧大脑皮质及海马CA1区Caspase3和TUNEL阳性细胞数较对照组明显增加,透射电镜证实有凋亡细胞;MDL28170可减少阳性细胞数量,抑制神经元死亡,差异有显著性(Plt;0.05)。结论:MDL28170可通过抑制神经凋亡而对新生大鼠HIBD具有一定保护作用。Abstract: Objective: To investigate the effect of (Calpain inhibitor3) MDL28170 on neural apoptosis in a neonatal model of hypoxicischemic brain damage (HIBD). Methods: A neonatal model of HIBD was established, 7dayold SD rats were divided into three groups. The treatment group received MDL28170(ip) at 0 h,2 h,4 h after HI, whereas the other two groups were administered normal saline simultaneously. The expression of caspase3 (by immunohistochemistry), neural apoptosis (by TUNEL) in cortex and hippocampus ipsilateral to the insult were observed 24 h after HI; hippocampal CA1 neural loss and electromicroscopic changes were assessed at the same time. Results: Apoptotic body was observed by electromicroscopy. Caspase3 positive cells and apoptotic cells increased significantly in the ipsilateral cortex and hippocampal CA1 region compared to the control, and MDL28170 reduced the number of positive cells, attenuated CA1 neural loss with significance (Plt;0.05). Conclusion: It is suggested that MDL28170 may protect the brain of neonatal rats after HIBD by suppressing neural apoptosis.
ObjectiveTo systematically review the efficacy of pidotimod in children.MethodsPubMed, The Cochrane Library, EMbase, CNKI, CBM, VIP and WanFang Data databases were searched online to collect randomized controlled trials (RCTs) on pidotimod in children from inception to January, 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 310 RCTs involving 30 525 children were included. The results of meta-analysis showed that, compared with conventional therapy, conventional therapy combined with pidotimod could not improve the efficacy of children with respiratory infections (RR=1.78, 95%CI 0.99 to 3.20, P>0.05). However, pidotimod could significantly reduce the number of respiratory tract infection (MD=−2.79, 95%CI −3.12 to −2.46, P<0.05), shorten the time of respiratory tract infection (MD=−4.15, 95%CI −4.72 to −3.58, P<0.05), and the time of fever (MD=−1.47, 95%CI −1.77 to −1.17, P<0.05) in recurrent respiratory tract infection. Pidotimod could also reduce the time of fever (MD=−0.90, 95%CI −1.60 to −0.20, P<0.05) in children with mycoplasma pneumoniae pneumonia, the time of fever (MD=−1.51, 95%CI −1.91 to −1.11, P<0.05) in children with hand-foot-mouth disease, and reduce the incidence of anaphylactoid purpura followed up for 6 months (RR=0.42, 95%CI 0.30 to 0.61, P<0.05) in children with anaphylactoid purpura. However, there was no significant difference between two groups in the recurrence of asthma for 1 year follow-up (RR=0.80, 95%CI 0.60 to 1.06, P>0.05).ConclusionCurrent evidence shows that pidotimod may be effective for children with respiratory tract infection, asthma, hand-foot-mouth disease, could reduce disease relapse and relieve symptoms related to illness.