P7C3-A20 treats traumatic brain injury in rats by inhibiting excessive autophagy and apoptosis

Traumatic brain injury is a severe health problem leading to autophagy and apoptosis in the brain.3,6-Dibromo-beta-fluoro-N-(3-methoxyphenyl)-9H-carbazole-9-propanamine(P7C3-A20)can be neuroprotective in various diseases,including ischemic stroke and neurodegenerative diseases.However,whether P7C3-A20 has a therapeutic effect on traumatic brain injury and its possible molecular mechanisms are unclear.Therefore,in the present study,we investigated the therapeutic effects of P7C3-A20 on traumatic brain injury and explored the putative underlying molecular mechanisms.We established a traumatic brain injury rat model using a modified weight drop method.P7C3-A20 or vehicle was injected intraperitoneally after traumatic brain injury.Severe neurological deficits were found in rats after traumatic brain injury,with deterioration in balance,walking function,and learning memory.Furthermore,hematoxylin and eosin staining showed significant neuronal cell damage,while terminal deoxynucleotidyl transferase mediated dUTP nick end labeling staining indicated a high rate of apoptosis.The presence of autolysosomes was observed using transmission electron microscope.P7C3-A20 treatment reversed these pathological features.Western blotting showed that P7C3-A20 treatment reduced microtubule-associated protein 1 light chain 3-Ⅱ(LC3-Ⅱ)autophagy protein,apoptosis-related proteins(namely,Bcl-2/adenovirus E1B 19-kDa-interacting protein 3[BNIP3],and Bcl-2 associated x protein[Bax]),and elevated ubiquitin-binding protein p62(p62)autophagy protein expression.Thus,P7C3-A20 can treat traumatic brain injury in rats by inhibiting excessive autophagy and apoptosis.

PLC在传输带控制系统中的应用

由于传统继电器控制的传输带存在电路复杂、可靠性差、故障诊断与排除困难等缺点,提出了用PLC对传输带控制系统进行设计。介绍了OMRON公司C20P可编程控制器在传输带控制系统中的应用,给出了PLC控制传输带系统的硬件组成和软件设计,其中包括PLC选型、I/O地址分配、I/O端子接线、程序设计和控制原理。

P7C3-A20对创伤性脑损伤的PC12细胞凋亡和氧化的影响

旨在研究3,6-二溴-beta-氟-N-(3-甲氧基苯基)-9H-咔唑-9-丙胺(P7C3-A20)对大鼠肾上腺髓质嗜铬瘤分化细胞株(PC12细胞)创伤性脑损伤(TBI)的修复作用。将细胞分为对照组(A组)、模型组(B组)、0.03μmol·L^(-1)药物治疗组(C组)、0.3μmol·L^(-1)药物治疗组(D组)、3μmol·L^(-1)药物治疗组(E组)和药物空白组(F组),TBI细胞模型通过使用10μL枪头划出横竖相间4 mm的直线来制备。使用CCK8试剂盒检测细胞活力,荧光显微镜观察细胞凋亡、活性氧(ROS)情况,荧光定量PCR仪检测半胱氨酸蛋白酶-3(Caspase-3)、B细胞淋巴瘤/白血病-2基因(Bcl-2)、血红素氧合酶1(HO-1)、NAD(P)H:醌氧化还原酶1(NQO 1)和谷氨酸半胱氨酸连接酶催化亚基(GCLC)的mRNA相对表达量。结果显示:TBI造模后细胞活力极显著降低(P<0.01),0.03μmol·L^(-1)浓度的P7C3-A20能显著提高TBI后的细胞活力(P<0.05),0.3μmol·L^(-1)浓度的P7C3-A20能极显著提高TBI后的细胞活力(P<0.01)。TBI造模后细胞早晚期凋亡细胞比例极显著增加(P<0.01),0.03μmol·L^(-1)浓度的P7C3-A20能显著减少TBI后的早期凋亡细胞比例(P<0.05),极显著减少TBI后的晚期凋亡细胞比例(P<0.01),0.3和3μmol·L^(-1)浓度的P7C3-A20能极显著减少TBI后的早晚期凋亡细胞比例(P<0.01)。TBI造模后活性氧细胞比例极显著增加(P<0.01),0.03和3μmol·L^(-1)浓度的P7C3-A20能显著减少TBI后的活性氧细胞比例(P<0.05),0.3μmol·L^(-1)浓度的P7C3-A20能极显著减少TBI后的活性氧细胞比例(P<0.01)。0.3μmol·L^(-1)浓度的P7C3-A20能极显著减少TBI后Caspase-3的mRNA相对表达量(P<0.01),显著提升TBI后Bcl-2、HO-1、NQO 1和GCLC的mRNA相对表达量(P<0.05)。P7C3-A20对TBI后的PC12细胞有抗凋亡、减轻氧化应激的修复作用。