(−)-Epigallocatechin gallate (EGCG) and curcumin are two naturally derived agents that have been widely investigated worldwide. They exhibit their anti-tumor effects in many types of cancers. In the current study, the effect of the combination of the two agents on non-small cell lung cancer (NSCLC) cells was investigated. The results revealed that at low concentrations, the combination of the EGCG and curcumin strongly enhanced cell cycle arrest. Flow cytometry analysis showed that the cells were arrested at G1 and S/G2 phases. Two main cell cycle related proteins cyclin D1 and cyclin B1 were significantly inhibited at the present of EGCG and curcumin. EdU (5-ethynyl-2′-deoxyuridine) fluorescence staining showed that the DNA replication was significantly blocked. A clonal growth assay also confirmed a marked repression of cell growth. In a lung cancer xenograft node mice model, combination of EGCG and curcumin exhibited protective effect against weight loss due to tumor burden. Tumor growth was strongly repressed by the combination of the two agents, without causing any serious side-effect. Overall, these results strongly suggest that EGCG in combination with curcumin could be a candidate for chemoprevention agent of NSCLC.
Aim: The expression of Piezo1 in reactive glial cells in the peripherally infected patient's brain was upregulated. This study aimed to determine whether Piezo1 is involved in the immune activation of microglial cells induced by bacterial lipopolysaccharides.Materials and methods: BV2 cells were used as a model of brain microglia. In vitro, Yoda1 was used to activate Piezo1 in BV2 cells, and Piezo1 was simulated for LPS-induced Piezo1 activation to evaluate the role of Piezo1 in microglial inflammatory activation.Key findings: In vitro, LPS upregulates the expression of Piezo1 in microglial cells through TLR4. In the absence of LPS, Yoda1 treatment of microglia produced similar immune function changes as LPS treatment. This indicates that Piezo1 plays a role in LPS-induced microglial immune activation. Specifically, Piezo1-mediated Ca2+ signals are involved in the immune activation of microglia. Piezo1-mediated Ca2+ regulates multiple signaling mechanisms downstream of TLR4, including the JNK1, mTOR and NF-κB signaling pathways, which are related to the immune activation of microglia.Significance: Piezo1 is involved in the immune response of microglia to LPS. Changes in Piezo1 activity may play an indispensable role in the immune response of microglia, and mechanical environmental changes may affect neuroinflammatory progression through Piezo1.
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