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超低频脉冲磁场抑制癌瘤和提高细胞免疫功能的实验研究 总被引:4,自引:0,他引:4
在报道用电子显微镜观测超低频脉冲磁场(峰值磁场0.6~2.0T,磁场梯度10~100T·m-1,脉冲宽度20~200ms,重复频率0.16~1.34Hz)抑制鼠S-180肉瘤和加强免疫细胞溶癌作用以后,报道了用Faulgen染色法测定肉瘤细胞核的DNA倍性,和用电镜技术和细胞结构的体视学分析磁场对癌细胞形态的影响,观测到磁场影响癌细胞的代谢:磁场使癌细胞的恶性程度降低,抑制其高速和异形生长;磁场抑制癌细胞的分裂和DNA的复制;磁场提高细胞免疫功能,加强淋巴细胞、浆细胞反应. 相似文献
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Na Lin Liu-Lin Xiong Rong-ping Zhang Hong Zheng Lei Wang Zhong-Yi Qian Piao Zhang Zhi-wei Chen Fa-Bao Gao Ting-Hua Wang 《Apoptosis : an international journal on programmed cell death》2016,21(5):621-640
Alzheimer’s disease (AD) can incur significant health care costs to the patient, their families, and society; furthermore, effective treatments are limited, as the mechanisms of AD are not fully understood. This study utilized twelve adult male tree shrews (TS), which were randomly divided into PBS and amyloidbetapeptide1-40 (Aβ1-40) groups. AD model was established via an intracerebroventricular (icv) injection of Aβ1-40 after being incubated for 4 days at 37 °C. Behavioral, pathophysiological and molecular changes were evaluated by hippocampal-dependent tasks, magnetic resonance imaging (MRI), silver staining, hematoxylin–eosin (HE) staining, TUNEL assay and gene sequencing, respectively. At 4 weeks post-injection, as compared with the PBS group, in Aβ1-40 injected animals: cognitive impairments happened, and the hippocampus had atrophied indicated by MRI findings; meanwhile, HE staining showed the cells of the CA3 and DG were significantly thinner and smaller. The average number of cells in the DG, but not the CA3, was also significantly reduced; furthermore, silver staining revealed neurotic plaques and neurofibrillary tangles (NFTs) in the hippocampi; TUNEL assay showed many cells exhibited apoptosis, which was associated with downregulated BCL-2/BCL-XL-associated death promoter (Bad), inhibitor of apoptosis protein (IAP), Cytochrome c (CytC) and upregulated tumor necrosis factor receptor 1 (TNF-R1); lastly, gene sequencing reported a total of 924 mobilized genes, among which 13 of the downregulated and 19 of the upregulated genes were common to the AD pathway. The present study not only established AD models in TS, but also reported on the underlying mechanism involved in neuronal apoptosis associated with multiple gene expression. 相似文献
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Zi-Bin Zhang Liu-Lin Xiong Lu-Lu Xue Yan-Ping Deng Ruo-Lan Du Qiao Hu Yang Xu Si-Jin Yang Ting-Hua Wang 《Cell death & disease》2021,12(3)
Neonatal hypoxic–ischemic (HI) injury derived from asphyxia during perinatal period, is a serious complication of neonatal asphyxia and the main cause of neonatal acute death and chronic neurological injury. Aberrant autophagy occurs in many nervous system diseases, but its role and underlying mechanism in HI injury is largely unknown. Here, we successfully constructed a newborn rat model of HI brain injury, and the knockout-miR-127-3p (KO-miR-127-3p) rats were structured by using CRISPR/Cas9. Subsequently, the in vitro functional experiments, in vivo zea-longa scores, as well as bioinformatics analyses and biological experiments were applied. The expression of autophagy-related proteins, including ATG12, P62, Beclin-1, LC3II in HI cortex with miR-127-3p knockout was significantly decreased, and autophagic vacuoles were disappeared. Moreover, miR-127-3p has a specific regulatory effect on CISD1 expression, another crucial molecule in autophagy process. Accordingly, the overexpression of CISD1 effectively inhibited the autophagic cell death and physiological dysfunction in the brain of HI injury, whereas si-CISD1 reversed the neuroprotective effects of KO-miR-127-3p. Our findings explained the underlying mechanism for HI injury, and miR-127-3p targeting CISD1 signal could be supposed as a new treatment strategy to prevent and treat HI injury.Subject terms: Autophagy, Molecular biology 相似文献
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