Polydatin and resveratrol, as major active components in Polygonum cuspidatum, have anti-inflammatory, antioxidant and antitumor functions. However, the effect and mechanism of polydatin and resveratrol on enterovirus 71 (EV71) have not been reported. In this study, resveratrol revealed strong antiviral activity on EV71, while polydatin had weak effect. Neither polydatin nor resveratrol exhibited influence on viral attachment. Resveratrol could effectively inhibit the synthesis of EV71/VP1 and the phosphorylation of IKKα, IKKβ, IKKγ, IKBα, NF-κB p50 and NF-κB p65, respectively. Meanwhile, the remarkably increased secretion of IL-6 and TNF-α in EV71-infected rhabdosarcoma (RD) cells could be blocked by resveratrol. These results demonstrated that resveratrol inhibited EV71 replication and cytokine secretion in EV71-infected RD cells through blocking IKKs/NF-κB signaling pathway. Thus, resveratrol may have potent antiviral effect on EV71 infection.
The tripartite motif (TRIM) proteins have been intensively studied as essential modulators in various biological processes, especially in regulating a wide range of signaling pathways involved in immune responses. Most TRIM proteins have E3 ubiquitin ligase activity, mediating polyubiquitination of target proteins. Emerging evidence demonstrates that TRIM proteins play important roles in innate immunity by regulating pattern recognition receptors, vital adaptor proteins, kinases, and transcription factors in innate immune signaling pathways. Additionally, the critical roles of TRIM proteins in adaptive immunity, especially in T cell development and activation, are increasingly appreciated. In this review, we aim to summarize the studies on TRIMs in both innate and adaptive immunity, focusing on their E3 ubiquitin ligase functions in pattern recognition receptor signaling pathways and T cell functions, shedding light on the developing new strategies for modulating innate and adaptive immune responses against invading pathogens and avoiding autoimmunity.
Depression is a potentially life-threatening mental disorder with unknown etiology. Several microRNAs (miRNAs) have been shown to play critical roles in the etiology of depression. Here, we aim to elucidate the anti-depressive behavior of miR-124 suppression in prefrontal cortex (PFC). Quantitative real-time PCR (RT-PCR) was used to evaluate the expression of miR-124 and SIRT1 in the PFC of a chronic unpredictable mild stress (CUMS) model. The PFC of C57BL/6J mice was bilaterally injected with lentiviral vectors (LV) for ectopic expression of SIRT1, miR-124, or miR-124 inhibitor (si-miR-124). The anti-depressive behavior was observed after injection of LV-SIRT1 or LV-si-miR-124 into the PFC, using behavior tests including latency to feed, food and water intake, sucrose preference test, and forced swimming test. MiR-124 overexpression and inhibition resulted in upregulation and down-regulation of SIRT1 and cyclic AMP responsive element binding protein 1 (CREB1), respectively. MiR-124 overexpression exacerbated depression-like behaviors and decreased SIRT1. Further, dual-luciferase assay confirmed that SIRT1 was a target of miR-124. Taken together, a potential molecular regulation of miR-124 on SIRT1 is revealed by our study and miR-124 suppression in PFC is a potential strategy to reduce depression-like behavior.
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