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Puerins, a kind of nitrogen-containing polyphenol compound with unique structure, is a kind of catechin derivative first isolated from ripened Pu-erh tea. In this paper, the effects of puerins V-VII on breast cancer cells were studied. Four breast cancer cell lines with different receptor phenotypes were used as models, and MTT assay, proteomics detection and apoptosis detection were carried out. The results show that all puerins V, VI and VII had obvious inhibitory effects on the four kinds of breast cancer cells. Proteomics analysis indicates that the differentially expressed proteins were mainly concentrated in the metabolic pathway, followed by cancer pathway and adhesion spot signal pathway under the intervention of puerins V-VII. Apoptosis detection demonstrates that all three puerins compounds could induce the apoptosis of MDA-MB-231 cells. This study first reported the anti-breast cancer activity and preliminary mechanism of puerins V-VII, which provided basic information for studying the anti-cancer active substances of ripened Pu-erh tea. [ABSTRACT FROM AUTHOR]

Aim of the Study. Late-onset Alzheimer's disease (LOAD) is recognized as a degeneration disorder in patients' central nervous system over 65 years old who will experience memory decline and cognitive impairment, causing great harm to the health of the elderly. To investigate the role of KL-FGF23-VD axis in LOAD and its molecular mechanism, we designed experiments from two dimensions of cells and animals. Materials and Methods. LOAD rats and Aβ microglia were constructed by using Aβ1-40 and IBO mixture. The effect of KL-FGF23-VD axis on LOAD was investigated by transfecting overexpressing and interfering with KL gene adenovirus, and IKK-16 was added to Aβ microglia to explore the effect of KL-FGF23-VD axis on regulation of IKK/NF-κB signaling pathway. Results. The results showed that, in KL-OE group, FGF23 was decreased in the hippocampus of LOAD rats compared with control and KL-si, and the trend was opposite in the KL-si group. The KL-FGF23-VD axis can alleviate inflammatory response, reduce the deposition of Aβ, and inhibit activation of the NF-κB pathway and neuron apoptosis in brain tissue of LOAD rats. In Aβ microglia, the expression of KL-FGF23-VD axis was consistent with animal experiments. The KL-FGF23-VD axis can inhibit the expression of Aβ microglia inflammatory factors and the activation of microglia and NF-κB pathway. Meanwhile, IKK expression was decreased in KL-OE group compared with KL-si and Control. In the IKK-16 addition group, the ability of KL-FGF23-VD axis to inhibit the activation of microglia and NF-κB pathway was enhanced. Conclusions. These findings suggest a potential role of the KL-FGF23-VD axis in AD treatment by regulating the IKK/NF-κB pathway. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is a grievous neurology-related disorder that causes many devastating symptoms. Emerging roles of long non-coding RNAs (lncRNA) have been shown to play critical roles in multiple neurological diseases. This research planned to dig the function and latent molecular mechanisms of the lncRNA CCAT1 on OGD/R-disposed injury in astrocytes. We observed that CCAT1 expression was diminished and miR-218 expression was elevated in astrocytes during OGD/R. Additionally, an abundance of CCAT1 obviously amplified cell viability and restrained OGD/R-triggered apoptosis in astrocytes, as characterized by reduced levels of pro-apoptotic proteins Bax and C-caspase-3, concomitant with elevated level of anti-apoptotic Bcl-2 protein. Furthermore, administration of CCAT1 remarkably mitigated OGD/R injury-induced neuro-inflammatory responses, reflected in a reduction of inflammatory cytokines including TNF-α, IL-1β, and IL-6. In action, CCAT1 served as an endogenous sponge effectively downregulating miR-218 expression by binding directly to it, and a negative regulatory relationship between miR-218 and NFAT5. Mechanistically, introduction of miR-218 reversed the inhibitory effects of CCAT1 on OGD/R-induced apoptosis and inflammation damage, which directly resulted from the inhibition of miR-218 and its targeting of NFAT5. Collectively, our study illuminated a new CCAT1/miR-218/NFAT5 regulatory axis in which CCAT1 served as a competing endogenous RNA by sponging miR-218, effectively upregulating NFAT5 expression, thereby alleviating apoptosis and inflammation damage under OGD/R condition. CCAT1 is, therefore, a putative therapeutic target for SCI, based on the results of this study and the potential application of CCAT1 as a neuroprotective agent. [ABSTRACT FROM AUTHOR]