Huang Jun, Jiang Wentao, Pan Junping, Xu Xuetao
Department of Pediatrics, Chaohu Hospital Affiliated to Anhui Medical University, Hefei, Anhui,238001, China.
Functional Laboratory, Anhui Medical College, Hefei, Anhui,238001, China.
Cell Mol Biol (Noisy-le-grand). 2023 Oct 31;69(10):150-154. doi: 10.14715/cmb/2023.69.10.21.
To provide clinical evidence for the management of hypoxic-ischemic encephalopathy (HIE) by analyzing the role of soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) and colony-stimulating factor-1 (CSF1) in the disease. We purchased 15 Sprague-Dawley (SD) rat pups and randomized them into five groups (n=3), of which one group was untreated as the control group and the other four were modeled by HIE. After modeling, a group was treated as a model group without any treatment, another group was injected with sLOX-1-silencing lentiviral vector (sLOX-1-si group), and the third and fourth were injected with CSF1-silencing lentiviral vector (CSF1-si group) and an equal amount of normal saline (blank group), respectively. After the corresponding intervention, the rat tissue in each group was obtained to observe the pathological injury by HE and TUNEL staining. In addition, sLOX-1, CSF1, 5-hydroxytryptamine (5-HT), dopamine (DA), and norepinephrine (NE) levels in brain tissue of each group were determined. The model group showed more severe pathological damage of the hippocampus and higher neuronal apoptosis than the control group. Besides, higher sLOX-1 and CSF1 levels and lower 5-HT, DA and NE contents were identified in the model group versus the control group (P<0.05). Compared with the blank group, sLOX-1-si and CSF1-si groups showed significantly alleviated hippocampal damage, inhibited neuronal apoptosis, reduced 5-HT, DA, NE, Bax, and cl-caspase-3, and increased Bcl-2 (P<0.05). Silencing sLOX-1 and CSF1 expression ameliorated the pathological injury of HIE and inhibited neuronal apoptosis.
通过分析可溶性凝集素样氧化型低密度脂蛋白受体-1（sLOX-1）和集落刺激因子-1（CSF1）在缺氧缺血性脑病（HIE）中的作用，为HIE的治疗提供临床依据。我们购买了15只Sprague-Dawley（SD）大鼠幼崽，并将它们随机分为五组（n = 3），其中一组不进行处理作为对照组，另外四组通过HIE建模。建模后，一组作为未治疗的模型组，另一组注射sLOX-1沉默慢病毒载体（sLOX-1-si组），第三组和第四组分别注射CSF1沉默慢病毒载体（CSF1-si组）和等量生理盐水（空白组）。经过相应干预后，获取每组大鼠组织，通过HE和TUNEL染色观察病理损伤。此外，测定每组脑组织中sLOX-1、CSF1、5-羟色胺（5-HT）、多巴胺（DA）和去甲肾上腺素（NE）的水平。模型组海马的病理损伤比对照组更严重，神经元凋亡更高。此外，与对照组相比，模型组的sLOX-1和CSF1水平更高，5-HT、DA和NE含量更低（P<0.05）。与空白组相比，sLOX-1-si组和CSF1-si组海马损伤明显减轻，神经元凋亡受到抑制，5-HT、DA、NE、Bax和cl-caspase-3减少，Bcl-2增加（P<0.05）。沉默sLOX-1和CSF1表达可改善HIE的病理损伤并抑制神经元凋亡。
